Public Health Nutrition in Developing Countries (Woodhead Publishing India)

Public health nutrition in developing countries

Public health nutrition in developing countries

Edited by

Sheila Chander Vir

WOODHEAD PUBLISHING INDIA PVT LTD New Delhi

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Cambridge

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Oxford

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Philadelphia

Published by Woodhead Publishing India Pvt. Ltd. Woodhead Publishing India Pvt. Ltd., G-2, Vardaan House, 7/28, Ansari Road Daryaganj, New Delhi – 110002, India www.woodheadpublishingindia.com Woodhead Publishing Limited, 80 High Street, Sawston, Cambridge, CB22 3HJ UK Woodhead Publishing USA 1518 Walnut Street, Suite1100, Philadelphia www.woodheadpublishing.com First published 2011, Woodhead Publishing India Pvt. Ltd. © Woodhead Publishing India Pvt. Ltd., 2011 This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission. Reasonable efforts have been made to publish reliable data and information, but the authors and the publishers cannot assume responsibility for the validity of all materials. Neither the authors nor the publishers, nor anyone else associated with this publication, shall be liable for any loss, damage or liability directly or indirectly caused or alleged to be caused by this book. Neither this book nor any part may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, microfilming and recording, or by any information storage or retrieval system, without permission in writing from Woodhead Publishing India Pvt. Ltd. The consent of Woodhead Publishing India Pvt. Ltd. does not extend to copying for general distribution, for promotion, for creating new works, or for resale. Specific permission must be obtained in writing from Woodhead Publishing India Pvt. Ltd. for such copying. Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation, without intent to infringe. Woodhead Publishing India Pvt. Ltd. ISBN: 978-93-80308-06-7 Woodhead Publishing Ltd. ISBN: 978-0-85709-004-1 Typeset by Sunshine Graphics, New Delhi Printed and bound by Replika Press, New Delhi

Dedicated to my mother Shanta Metre and father, Padma Bhushan W. B. Metre, in fond memory of their love, blessings, inspiration and encouragement.

Contents

Contents

Foreword Preface List of Contributors

xxv xxix xxxiii

Part - I 1.

Principles of epidemiology and epidemiologic methods

1

Sanjay P. Zodpey

2.

1.1 Introduction 1.2 What is epidemiology? 1.3 Development in epidemiologic methods 1.4 Epidemiological reasoning 1.5 Classifying epidemiologic study methods References

1 1 2 3 4 24

Nutrition epidemiology for developing countries

25

Usha Ramakrishnan and Ines G. Casanova

3.

2.1 Introduction 2.2 Epidemiological studies 2.3 Nutritional epidemiology – measurement 2.4 Importance of nutrition epidemiology in developing countries 2.5 Nutrition epidemiology and public health nutrition References

25 26 33 43 44 47

Undernutrition in children

50

Sheila C. Vir 3.1 3.2

Undernutrition, child survival and millennium development 50 goals Undernutrition in children – stunting, underweight and 52 wasting

Contents

viii 3.3 3.4

Undernutrition and age trend Stunting, underweight and wasting – an overview of the global situation 3.5 Determinants of undernutrition 3.6 Maternal and child undernutrition – evidence for actions 3.7 Addressing undernutrition in children – a life cycle approach References

4.

Dual nutrition burden in women: causes, consequences, and control measures

52 56 61 68 75 80

86

Prema Ramachandran 4.1 4.2 4.3 4.4

Introduction 86 Emergence of dual nutrition burden in India 87 Nutritional status of pregnant and lactating women 90 Interventions to improve dietary intake and nutritional status 95 in women 4.5 Factors responsible for the emerging problem of overnutrition 97 4.6 Undernutrition – overnutrition linkages 101 4.7 Summary and conclusion 104 References 106

5.

Measuring undernutrition and overnutrition in children

108

Dheeraj Shah and H.P.S. Sachdev 5.1 Introduction 5.2 Anthropometric techniques 5.3 Comparison of indices with references 5.4 Cut-offs 5.5 Growth references 5.6 Undernutrition References

6.

Essential new-born care and child survival

108 109 131 135 136 145 149

151

Richa Singh Pandey and Sheila C. Vir 6.1 6.2 6.3 6.4 6.5

Neonatal period – a risky start to childhood Millennium development goal 4 (MDG-4) and neonatal mortality Neonatal mortality – an Indian perspective Neonatal mortality – direct and underlying determinants Continuum of care – a comprehensive approach to saving newborn lives

151 153 154 155 156

Contents

6.6 6.7

Essential newborn care interventions Delivering essential newborn care (ENBC) interventions through public health systems – opportunities and challenges 6.8 Addressing neonatal health in India – initiatives by Government of India 6.9 Integrated Management of Childhood Illnesses (IMCI) – the global strategy 6.10 Integrated Management of Neonatal Care and Childhood Illnesses (IMNCI) 6.11 Conclusion References

7.

Integrating breastfeeding in public health programming – scientific facts, current status and future directions

ix 157 166 168 170 171 172 173

175

Kajali Paintal 7.1 7.2

Introduction Breastfeeding – the science for integrating scientific facts into programming 7.3 Trends in exclusive breastfeeding practices 7.4 Integrating breastfeeding into public sector programmes 7.5 Programme design – community based 7.6 Large scale community-based programmes – lessons learned References

8.

Complementary feeding of infants and young children

175 178 187 190 207 211 215

223

Veenu Seth and Aashima Garg 8.1

Complementary feeding practices – a critical determinant 223 of undernutrition in young children 8.2 Optimal infant and young child feeding 225 8.3 Complementary feeding – issues and guidelines 226 8.4 Initiating complementary feeding 227 8.5 Adequacy and frequency of complementary feeding 228 8.6 Energy and other nutrient intake from complementary foods 228 8.7 Causes of faulty complementary feeding practices 232 8.8 Desirable features of satisfactory complementary feeding 235 8.9 Measuring the status of complementary feeding 238 8.10 Complementary feeding status – global and India 240 8.11 Low-cost complementary feeding 241 8.12 Different ‘home based’ complementary foods 242

Contents

x

8.13 Promoting improved complementary feeding practices – programs, strategies and challenge ahead References

9.

246 249

Options and strategies to reach under-two children 252 through complementary feeding with ARF in the South Asian countries Tara Gopaldas 9.1 9.2

Introduction Nutritional needs, deficiencies and the role of complementary foods in the age group of under twos 9.3 Options for providing nutrition to overcome deficiencies 9.4 Technology for development of premixes and complementary foods 9.5 Mechanisms to improve acceptability, palata-bility, utilization and outreach of the donated complementary food in the public sector References

10. Diarrhea and undernutrition

252 253 259 261 266

271

274

Shariqua Yunus 10.1 Introduction 10.2 Definition of diarrhea 10.3 Types of diarrhea 10.4 Causes of diarrhea 10.5 Diarrhea, morbidity, malnutrition and mortality 10.6 Management of diarrhea 10.7 Prevention of diarrhea References

274 274 275 276 276 280 285 290

11. Prevention and management of protein energy malnutrition

292

Siddarth Ramji 11.1 Introduction 11.2 Clinical syndromes of malnutrition 11.3 Prevention of malnutrition 11.4 Managing malnutrition 11.5 Guidelines for management of mild-moderate malnutrition 11.6 Conclusion References

292 292 293 301 307 307 308

Contents

12. Severe acute malnutrition in children

xi

310

Kamal Raj 12.1 An overview 12.2 Clinical features 12.3 Severe acute malnutrition and mortality 12.4 Management of severe acute malnutrition (SAM) 12.5 Monitoring and evaluation of SAM management program References

13. Prevention and management of overweight and obesity in children

310 311 311 313 336 338

341

Anura Kurpad and Sumathi Swaminathan 13.1 13.2 13.3 13.4

Introduction Maintenance of energy balance The epidemic of obesity in children Developmental aspects of growth, weight gain and later obesity 13.5 Assessment of overweight and obesity in children 13.6 Risk factors for overweight and obesity 13.7 Consequences of overweight or obesity 13.8 Children at special risk of obesity 13.9 Prevention 13.10 Management and treatment References

341 342 343 345 348 350 355 356 357 360 362

14. Human immunodeficiency virus (HIV) and nutrition 372 Minnie Mathew 14.1 14.2

Introduction The clinical course of infection, immune system and infection 14.3 Treatment for HIV infection 14.4 HIV and implications on nutrition status 14.5 Nutritional requirements for People Living with HIV (PLHIV) 14.6 HIV and appropriate support References

15. Vitamin A metabolism

372 374 375 377 383 391 403

405

Ravinder Chadha 15.1

Introduction

405

xii

Contents

15.2 Discovery of vitamin A 15.3 Occurrence and sources 15.4 Metabolism and storage of vitamin A 15.5 Functions of vitamin A and carotenoids 15.6 Recommended Dietary Allowances (RDA) 15.7 Assessment of vitamin A status References

405 406 409 414 420 422 428

16. Vitamin A deficiency: prevention and control

432

Sheila C. Vir 16.1 16.2 16.3 16.4 16.5 16.6 16.7

Vitamin A – an essential micronutrient Consequences of vitamin A deficiency Epidemiology of vitamin A deficiency Vitamin A deficiency (VAD) – a public health problem Public health significance of vitamin A deficiency disorders International focus on prevention of vitamin A deficiency Intervention strategies for preventing vitamin A deficiency disorders (VADD) References

17. Vitamin A prevention and control programme in India – past efforts and current status

432 432 435 441 443 446 447 466

473

Sheila C. Vir and Richa Singh Pandey 17.1 17.2 17.3 17.4

Vitamin A deficiency status in India Measures taken for prevention and control of VAD Vitamin A supplementation programme Establishment of the biannual fixed month strategy – an overview of a state initiative 17.5 Elimination of vitamin A deficiency – future direction References

18. Iodine metabolism and indicators of iodine status

473 476 477 487 498 499

502

Madan M. Godbole and Rajan Sankar 18.1 18.2 18.3 18.4

Introduction Metabolism – iodine absorption and transport Iodine requirement and intake Iodide trapping, organification, coupling, TH synthesis and release (Figure 18.1) 18.5 Storage and availability of throid hormones (TH) 18.6 Iodine metabolism and their mechanism of action

502 503 504 504 505 507

Contents

xiii

18.7 Role of iodine in biological functions 18.8 Importance of iodine nutrition for human populations 18.9 Iodine requirement 18.10 Assessment of iodine status (Impact indicator) 18.11 Conclusion References

509 510 511 514 518 519

19. Sustaining iodine deficiency disorders (IDD) control 523 programme Chandrakant S. Pandav 19.1 Introduction 19.2 Controlling of IDD – a three prong strategy References

20. Iodine deficiency and iodine deficiency disorders (IDD) control program

523 524 533

535

Sheila C. Vir 20.1 Epidemiology of iodine deficiency 20.2 Iodine deficiency disorders – a public health problem 20.3 Elimination of iodine deficiency disorders (IDD) – international focus 20.4 Fortification of salt with iodine 20.5 Universal salt iodization (USI) 20.6 Monitoring IDD control programme 20.7 Monitoring progress towards sustainable elimination of IDD as a public health problem 20.8 Supplementation with iodised oil in special situations of insufficient access to iodized salt References

21. Universal salt iodization (USI)

535 537 542 542 545 549 556 558 559

562

M.G. Venkatesh Mannar 21.1 Introduction 21.2 Taking universal salt iodization to scale 21.3 Components of effective USI programmes 21.4 USI – An example of successful fortification 21.5 Conclusions References

562 563 567 572 572 573

xiv

Contents

22. National iodine deficiency disorders control programme of india

575

Sheila C. Vir 22.1 22.2

History and current policy Universal salt iodization (USI) – an integral part of NIDDCP 22.3 Increasing production of iodized salt for edible purposes 22.4 Advocacy and demand creation for increased production, universal access and consumption of adequately iodized salt 22.5 Innovative efforts to accelerate USI 22.6 Elimination of IDD – impact and progress 22.7 Elimination of IDD – challenges ahead References

575 579 579 590

592 597 602 603

Part - II 23. Metabolism of iron, folic acid and vitamin B12

607

K. Madhavan Nair 23.1 23.2 23.3 23.4 23.5 23.6 23.7 23.8 23.9 23.10 23.11 23.12 23.13 23.14 23.15 23.16 23.17 23.18 23.19 23.20 23.21

Introduction Iron Distribution Functional compartment Heme proteins Heme enzymes Non-heme iron proteins Storage compartment Transport compartment Recycling of iron in the body Iron losses Dietary iron bioavailability Other factors influencing iron absorption Recommended daily allowance (RDA) Iron homeostasis Mechanism of intestinal absorption of iron at the enterocyte Mechanism of iron uptake in cells other than enterocytes Molecular regulation of cellular iron Assessment of iron status Stages in the development of iron deficiency and iron status parameters Iron toxicity

607 607 608 609 609 610 611 613 614 614 614 616 617 617 618 619 621 621 623 623 625

Contents

xv

23.22 Folic acid 23.23 Chemistry 23.24 Dietary sources and recommended intake 23.25 Availability of food folate 23.26 Food folate – digestion and absorption 23.27 Functions 23.28 Folic acid and anemia 23.29 Assessment of folate status 23.30 Vitamin B12 23.31 Chemistry 23.32 Dietary sources and recommended intake 23.33 Absorption and transport 23.34 Bioavailability of dietary vitamin B12 23.35 Body content 23.36 Dietary deficiency of vitamin B12 23.37 Malabsorption of vitamin B12 23.38 Biochemical function 23.39 Neurological manifestations 23.40 Assessment of vitamin B12 status References

626 626 627 627 628 628 629 630 630 630 631 631 632 632 632 633 633 635 635 636

24. Iron deficiency and iron deficiency anemia in young children

638

Sheila C. Vir and Prakash V. Kotecha 24.1

Iron deficiency and iron deficiency anemia in young children 24.2 Anemia, iron deficiency and iron deficiency anemia 24.3 Iron balance in children 24.4 Patho-physiology of anemia in children under three years of age 24.5 Consequences of iron deficiency and iron deficiency anemia in children 24.6 Measures for preventing iron deficiency and anemia 24.7 Conclusion References

638 643 645 645 647 649 658 658

25. Iron and multiple micronutrient supplementation in 663 children: evidence from systematic reviews Tarun Gera 25.1 25.2

Introduction Iron and multiple micronutrient supplementa-tion and anemia

663 664

xvi

Contents

25.3 Effect of iron and multiple micronutrient supplementation on mental development in children 25.4 Iron and multiple micronutrient supplementa-tion in children and growth References

26. Nutritional anemia during pregnancy, early childhood and adolescence: the critical development periods

668 670 672

674

Subadra Seshadri 26.1 Introduction 26.2 Prevalence of anemia: global and the Indian population 26.3 Causes of nutritional anemia 26.4 Iron homeostasis 26.5 Iron requirements 26.6 Assessment of anemia 26.7 Functional effects of anemia 26.8 Approaches for the prevention and control of anemia 26.9 Summary References

27. Iron deficiency and iron deficiency anemia in adolescent girls

674 677 680 687 689 694 697 701 705 707

713

Sheila C. Vir 27.1 Prevalence of iron deficiency and anemia among adolescent girls 27.2 Causes of iron deficiency and iron deficiency anemia in adolescent girls 27.3 Consequences of iron deficiency and iron deficiency anemia 27.4 Prevention and control of iron deficiency and iron deficiency anemia 27.5 Anemia in adolescent girls in India and efforts launched at state level References

28. Zinc – an essential micronutrient for health and development

713 715 721 723 730 732

737

Sunil Sazawal and Pratibha Dhingra 28.1 Introduction

737

Contents

xvii

28.2 Biological functions of zinc 28.3 Public health significance 28.4 Zinc epidemiology 28.5 Clinical manifestations of zinc deficiency 28.6 Dietary sources, intake, absorption and bioavailability 28.7 Physiology of zinc 28.8 Evidence from zinc supplementation studies on child health 28.9 Zinc supplementation in pregnancy 28.10 Effect of zinc on immune response in the elderly 28.11 Zinc toxicity 28.12 Assessment of zinc status 28.13 Scaling up programs to improve zinc nutrition 28.14 Conclusion References

737 738 738 739 739 740 745 753 754 754 755 758 763 764

29. Vitamin A and zinc supplements for child survival – 772 experiences and challenges ahead Anand Lakshman 29.1 29.2 29.3 29.4

Introduction Magnitude of the problem The challenge Vitamin A and zinc deficiencies – implications on child mortality 29.5 Approaches to address vitamin A deficiency 29.6 Addressing zinc deficiency 29.7 Economic analysis of cost and benefit of vitamin A and zinc supplementation 29.8 Implications and conclusions References

30. Addressing micronutrient malnutrition through food fortification

772 772 774 775 777 785 790 792 792

795

Saraswati Bulusu and Annie S. Wesley 30.1 30.2 30.3 30.4 30.5 30.6 30.7

Introduction Micronutrient malnutrition – an overview Complementary strategies to overcome micronutrient malnutrition Food fortification History of food fortification Technical considerations Technology for food fortification

795 796 799 800 800 801 803

xviii

Contents

30.8 30.9 30.10 30.11

Fortificants Planning food fortification intervention Global experiences with food fortification Food fortification in a developing country—Experiences from India 30.12 Fortification of selected food items 30.13 Innovative experiments with fortification 30.14 Public–private partnerships 30.15 Monitoring and evaluation 30.16 Regulations and standards 30.17 Conclusion References

31. Agriculture, food and nutrition security

804 809 810 813 825 831 835 837 837 839 839

844

Deeksha Kapur 31.1 31.2

Introduction Food and nutrition security: understanding the basic concepts 31.3 Agriculture: central to food and nutrition security 31.4 Food insecurity and vulnerability 31.5 Factors underlying the current state of food and nutrition security 31.6 Policies and programmes for reducing food insecurity and vulnerability in the Indian context References

32. Food and nutrition situation in India

844 845 850 852 858 865 876

879

K. Vijayaraghavan 32.1 Introduction 32.2 Food security 32.3 Dietary consumption pattern in India 32.4 Trends in nutrient intake 32.5 Nutritional status – trends in children and adults 32.6 Conclusion References

33. Food and nutrition in natural and manmade disasters

879 881 885 886 892 896 896

898

Deepti Gulati 33.1

Natural and manmade disasters

898

Contents

xix

Understanding concepts of vulnerability disasterpreparedness and building capacities 33.3 Food insecurity and malnutrition – identification and measurement 33.4 Nutritional interventions 33.5 Nutritional requirements 33.6 Addressing food security 33.7 Types of disasters and disaster management in India References

903

33.2

34. Nutrition for the aged

908 913 921 925 927 929

932

Kumud Khanna and Seema Puri 34.1 Introduction 34.2 Definition of old age 34.3 Greying of nations 34.4 Characteristic trends of ageing in India 34.5 Physiological ageing 34.6 Pathological ageing 34.7 Nutrition and ageing 34.8 Dietary guidelines for older persons 34.9 Ageing in the development agenda 34.10 Initiatives in old age care 34.11 Initiatives by the voluntary sector References

35. Nutrition related non-communicable chronic disorders

932 932 933 934 939 942 943 949 950 953 953 954

956

Kamala Krishnaswamy and Avula Laxmaiah 35.1 35.2

Introduction Prevalence of non-communicable diseases at global and national level 35.3 Cardiovascular diseases 35.4 Nutrition transition and NCDs 35.5 Macronutrients 35.6 Risk factors for diet related NCDs 35.7 Overweight and obesity and dietary factors 35.8 Blood lipids (Dyslipedaemia) 35.9 Metabolic syndrome 35.10 Hypertension 35.11 Fetal and childhood malnutrition 35.12 Vegetables and fruits in the diet

956 957 957 960 960 963 964 966 967 967 969 969

xx

Contents

35.13 Prevention and control of NCDs 35.14 Actions 35.15 Childhood and adolescent nutrition 35.16 Community-based programmes for primary prevention 35.17 Health education and role of mass media 35.18 Secondary and tertiary prevention 35.19 Conclusions References

971 974 976 976 977 977 977 978

36. Planning result-oriented public health nutrition programs: theory and practice

982

Ashi K. Kathuria 36.1 Introduction 36.2 Program planning – an overview 36.3 Theory, concepts, frameworks 36.4 Steps in program planning 36.5 Estimating and securing financial resources 36.6 Planning for program monitoring and evaluation 36.7 Planning for program ending or termination 36.8 Conclusion References

37. Monitoring and evaluation of public health nutrition programmes

982 985 988 997 1018 1020 1024 1026 1027

1030

Jerard M Selvam and Sheila C. Vir 37.1 37.2 37.3 37.4 37.5 37.6 37.7

Introduction to Monitoring and Evaluation (M & E) Monitoring Evaluation of programmes Designing the evaluation Programme efficiency analysis Quantitative and qualitative techniques used in evaluation Monitoring and evaluation – decision making and moving forward References

1030 1031 1044 1049 1056 1058 1064 1064

38. District and village planning – a decentralised 1066 implementation approach in public health in India Shraddha Dwivedi, Madhulekha Bhattacharya and Ashish Mukherjee 38.1

Introduction

1066

Contents

38.2 National Rural Health Mission (NRHM) and District Health Action Plans 38.3 District Planning Development Cycle 38.4 Development of a district plan – capacity building and situation analysis 38.5 Village planning – understanding the community/village situation – a shift from central to decentralised planning 38.6 Village plan to district level plan 38.7 Conclusion References

39. Nutrition–Health education and communication for improving women and child nutrition

xxi 1068 1072 1075 1077 1082 1082 1084

1085

Shubhada Kanani 39.1 39.2 39.3 39.4

Introduction 1085 An operational definition of nutrition–health education 1085 Why is nutrition–health education important? 1086 Shift in focus from nutrition education to behavior change 1087 communication 39.5 Design and implementation of a nutrition health education 1094 program with a communications perspective 39.6 Evaluation of NHE programs 1103 39.7 NHE in action – successful program experiences 1104 References 1112

40. From research to programs: Applying knowledge 1114 to improve nutrition outcomes Purnima Menon 40.1 Introduction 40.2 Program theory 40.3 Framing the links between research and programs 40.4 Categories of program-oriented research References

1114 1115 1116 1118 1129

41. Research methods in public health nutrition: Critical factors

1133

Arun K. Nigam and Padam Singh 41.1 Introduction 41.2 Designing a research study – critical factors 41.3 Hypothesis testing and P value

1133 1135 1137

xxii

Contents

41.4 Cut-off levels for different levels of significance in one-tailed and two-tailed test 41.5 Research designs 41.6 Sampling 41.7 Determination of sample size 41.8 Analysis 41.9 Softwares References

42. Reducing malnutrition: An analysis of the Integrated Child Development Services (ICDS) scheme

1140 1140 1141 1143 1147 1152 1153

1154

Deepika N. Chaudhery 42.1 Background 42.2 Program background: design and implementation framework 42.3 Key nutrition, early childcare and preschool education and health related services 42.4 Training in ICDS 42.5 Program evolution 42.6 Evidence from program evaluations and program limitations 42.7 Contribution of ICDS in improving nutrition and health services and behaviors of children and women: evidence from innovative approaches within ICDS 42.8 Moving forward: revisit and refine key strategies References

43. National Rural Health Mission

1154 1155 1159 1162 1163 1165 1171

1187 1192

1195

Deoki Nandan 43.1 43.2 43.3 43.4 43.5 43.6 43.7 43.8 43.9

Introduction The vision of the mission The objectives of the mission The expected outcomes from the mission as proposed for reflection in statistical data Goals, strategies and outcomes of the Mission Institutional mechanisms in the National Rural Health Mission Accredited Social Health Activists (ASHA) Implementation Framework and Plan of Action for NRHM Nutrition: a determinant of health

1195 1195 1196 1196 1197 1199 1200 1203 1206

Contents

43.10 Improving the public health delivery system 43.11 Indian Public Health Standards (IPHS) 43.12 Public health infrastructure 43.13 Improving availability of critical manpower 43.14 Capacity building 43.15 Monitoring and review 43.16 Flexible financing 43.17 NRHM progress made References Index

xxiii 1206 1207 1208 1209 1210 1210 1211 1212 1213 1214

Foreword

Public health nutrition has increasingly gained attention as an important subject in the field of development. It is recognized as a specialized discipline of nutrition that deals with expanding and integrating the understanding of nutrition issues across various levels – individual, family, community, national and global – geared towards solving nutrition problems of individuals and communities. Malnutrition is known to contribute to approximately one-third of child deaths. High levels of malnutrition in developing countries is a major area of concern inhibiting achievement of the Millennium Development Goals (MDGs). Alleviation of malnutrition in developing countries poses to be a major challenge and needs urgent attention. In the developing world, a total of 129 million children under the age of five years are underweight; 27 percent of these are in Asia and 21 percent in Africa. Stunting affects 195 million children under the age of five years in the developing world; and more than 90 percent of stunted children live in Asia and Africa. Many of these children have a poor start in life with 13 million infants being born with intrauterine growth restriction annually, resulting in low birth weight. Deficiencies of micro-nutrients, such as iodine, iron, vitamin A, folic acid and zinc, caused mainly due to inadequate dietary intake and frequent infections, affect the population in developing world. There is immense hope in reducing malnutrition in a positive international development environment. The multiple causes of malnutrition are well known, new technologies are available and vast knowledge has been generated on effective interventions from programmes that have successfully accelerated reduction of malnutrition in countries such as Thailand, and more recently, Vietnam and Brazil. Experiences from successful programmes emphasize that political commitment and support, leadership and strategic capacity development, provision of basic and essential services, combined with community ownership for improving nutrition indicators are key ingredients for accelerated reduction of malnutrition. The enormous challenge for the developing world is the scaling up of malnutrition reduction programmes

xxvi

Foreword

in order to achieve multiple MDGs. Adaptations of known effective interventions in the national and local context would save time and reduce the risk of implementing strategies that are unlikely to yield results. Understanding existing gaps and the key elements of successful programming are critical for formulating, implementing and evaluating effective programmes. This book on Public Health Nutrition is timely and collates information on the current situation of malnutrition in the developing world. It not only presents recent technical developments in nutrition science but also highlights the application of proven sound recommendations for programme implementation. The book will be helpful to health and nutrition professionals, as well as, policy makers, programme designers and project implementers, in dealing with various nutrition issues effectively. The editor, taking into consideration the defined scope and focus of the book, has brought together authors who not only have indepth technical knowledge of the subject but also have first-hand experience in planning and implementation of public health nutrition programmes. The book is reader friendly and the lessons learned from programmes are emphasized in box formats where appropriate. It also focuses on broader health and social issues that need to be addressed for achieving the goal of reducing malnutrition. Interestingly, the book also covers other issues of public health nutrition that relate to a wide variety of situations such as neonatal care, safe drinking water, diarrhoea and HIV. In addition, one section of the book concentrates on programming, with chapters on programme planning and implementation, communication, monitoring and evaluation, linking evidence-based research to programming. These chapters will enable practitioners to apply nutrition science to appropriate programme designing and its implementation. The editor, Dr Sheila C. Vir, has over 25 years of experience working with UNICEF and has contributed significantly in the field of public health nutrition. The passion in the subject is evident from the effort put in by her for undertaking this monumental task of bringing together over thirty selected experts to contribute to this book. She should be congratulated for this exceptional publication in public health nutrition. The book will be a very useful reference not only for nutritionists and public health specialist but also for pediatricians, development professionals, programmers and international agencies. It should be of interest to politicians, policy makers, bureaucrats, economists and agriculture scientists. Non-government organizations and civil society organizations will also find this book interesting, informative and thought provoking. It is hoped that this book will help adaptation of

Foreword

xxvii

proven successful interventions from across the developing world and accelerate and scale up their implementation towards reducing malnutrition. It is indeed my great pleasure and honour to write the foreword for this book.

10th October 2010 Prof Emeritus Kraisid Tontisirin MD, Ph D Chairman of the Policy Board, The Thailand Research Fund, Bangkok Formerly Director Nutrition and Consumer Protection Division, Food and Agriculture Organisation of the United Nations (FAO), Rome

xxix

Preface

Public Health Nutrition in Developing Countries focuses on application of public health and nutrition sciences for formulating strategies and actions for preventing and solving the serious problem of malnutrition in developing countries. Presented are experiences, evidences and developments in addressing public health nutrition problems, over the last three to four decades. The lessons learnt from past experiences are highlighted to facilitate understanding of the basis of policy formulation, development of strategies, designing and implementation of programmes within a result-based framework. Along with these, a description of universally recommended processes and impact indicators is presented for measuring progress and outcomes of a wide range of public health nutrition interventions. In this context, the metabolism of a few selected nutrients are described to explain the rationale for the selection of a specific set of indicators in relation to specific nutrition intervention programmes. This book presents an update on public health nutrition problems of developing countries along with a description of approaches used and efficacy of trials undertaken for addressing them. It highlights the experiences emerging from up-scaling intervention trials to programme models and elaborates on the principles of public health nutrition programme planning and implementation. The book covers emerging global experiences for a wide spectrum of public health nutrition issues, ranging from those addressing women and child undernutrition and micronutrient deficiencies, nutrition care in HIV, and management of nutrition in emergency situations. It therefore aims to provide not only an update on current knowledge but also to generate interest in upcoming challenges and scenarios for future programmes. Presentation of case studies from developing countries is incorporated to draw the attention of policy makers and programmers, and academics to actual experiences, processes, value additions, lessons learned and to potential challenges that remain to be addressed. The book intends to elaborate on the ‘how’ of addressing public health nutrition programming, to inform strategic planning, design and implementation of effective plans that would accelerate the reduction of malnutrition. Specific reference is made to policy formulation processes

xxx

Preface

and programme experiences in India since the country has historically taken a global lead in launching various public health nutrition programmes. The book highlights the emerging double-burden of undernutrition and overnutrition in developing countries. The association of malnutrition with the increasing challenge of communicable and non-communicable diseases has also been described. Additionally, the problem of nutrition of the aged population faced by many countries undergoing demographic transition is also dealt with. Separate sections are devoted to nutritional epidemiology, undernutrition in children and women and major micronutrient deficiency programmes such as iron, vitamin A, iodine and zinc. However, there is some intended overlap in micronutrient sections since different perspectives of similar subjects are addressed. It is envisaged that this book, produced in two volumes, will provide public health experts, nutrition programmers, medical and nutrition graduates, nurses, programme managers with NGOs, or food industry and policy makers with information on technical and programmatic aspects of public health nutrition and thereby enhances skills in formulating and implementing appropriate solutions and actions. I am indebted to innumerable women living in the developing world who greatly inspired me to address issues of public health nutrition with a new perspective. Women play a central role in influencing the nutrition status not only of children but of the entire family. This is well reflected in the profound statement of Swami Vivekananda, “there is no chance for the welfare of the world unless the condition of women is improved. It is not possible for the bird to fly on one wing”. For improving nutrition situation in developing countries, we need to move beyond accessibility to food. Simultaneously, the social, educational and economic empowerment of women needs to be addressed. A multi-dimensional approach is essential for overcoming malnutrition. As editor, I would like to acknowledge the contributors who are eminent scholars and leading programme specialists for their excellent contributions to this book. Their deep knowledge and vast experience has added immense value to the content of the book. I am particularly grateful to the authors for the colossal effort they have put in preparing the manuscripts. Furthermore, I would like to express my appreciation for the support provided by my team at the Public Health Nutrition and Development Centre (PHNDC), New Delhi. The invaluable assistance of Ms. Ritu Jain, Research Nutritionist, PHNDC, in reviewing literature and analyzing data, as well as, her continuous support in networking with the authors is appreciated. The support of Ms. Rachita Gupta, Research Nutritionist, PHNDC, in the final stage of this book is valued. I sincerely appreciate the contribution of Ms. Falguni Gokhale (Director, Design Directions) for the design of the cover page of this book.

Preface

xxxi

I am deeply indebted to my mentor, late Professor A.H.G. Love, for his guidance during my doctoral work at the Institute of Clinical Sciences, Queen’s University of Belfast, and for generating my interest in the subject of public health nutrition. The production of this book would not have been possible without the untiring love, care and support of my husband Dr. Chander Vir whose constant and unrelenting motivation helped me work towards my mission to promote public health nutrition issues in developing countries. My special thanks to my brother-in-law, Dr. Ishwar Dass, IAS, who constantly inspired and encouraged me to complete this book. The support, enthusiasm, patience and understanding of my daughters Parul and Anubha and my son-in-law Amit Garg is appreciated and acknowledged. I also sincerely appreciate and acknowledge the support, understanding and continuous encouragement from my extended family. My special acknowledgement to the United Nations Children’s Fund (UNICEF) with whom I have been associated for almost three decades, first as Project officer and now as a consultant. This association has provided me with the opportunity to learn in an ever evolving development environment. This book could not have been produced without the cooperation of the publishers, Woodhead Publishing India Ltd. My sincere thanks to the publishing house team members—Mr. Ravindra Saxena and Mr. Sumit Aggarwal. Sheila C. Vir MSc Ph D Director, Public Health Nutrition and Development Centre, New Delhi, India January 2011

List of Contributors

Prof Bhattacharya Madhulika Professor Community Health Administration National Institute of Health and Family Welfare(NIHFW) New Delhi, India Dr Bulusu Saraswati Nutrition specialist, UNICEF Field Office Hyderabad, India Dr Casanova Ines G. Department of Nutrition and Health Sciences Rollins School of Public Health Emory University Atlanta, USA Dr Chaddha Ravinder Associate Professor Department of Food and Nutrition Lady Irwin College University of Delhi New Delhi, India Dr Chaudhary Deepika Nayar Deputy Regional Director, Asia The Micronutrient Initiative New Delhi, India Prof Das Tara Gopal Director Tara Consultancy Services Bengaluru, India Dr Dhingra Pratibha Senior Research Scientist

Center for Micronutrient Research New Delhi, India Prof Dwivedi Shraddha Professor and Head Department of Preventive and Social Medicine MLN Medical College Allahabad, India Ms Garg Aashima Nutrition Specialist UNICEF Field Office Jaipur, India Dr Gera Tarun Consultant Department of Pediatrics Fortis Hospital New Delhi, India Prof Godbole Madan M Professor and Head Department of Endocrinology Sanjay Gandhi Post Graduate Institute of Medical Sciences Lucknow, India Gulati Deepti Senior Programme Associate, Global Alliance for Improved Nutrition (GAIN) New Delhi, India Ms Jain Ritu Research Nutritionist Public Health Nutrition and Development Centre New Delhi, India

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List of Contributors

Prof Kanani Shubhada Professor Department of Foods and Nutrition Faculty of Home Science Maharaja Sayajirao University of Baroda Gujarat, India Prof Kapur Deeksha Professor Department of Nutritional Sciences School of Continuing Education Indira Gandhi National Open University New Delhi, India Ms. Kathuria Ashi K. Senior Nutrition Specialist The World Bank New Delhi, India

Dr Laxmaiah Avula Deputy Director (Epidemiology) Division of Community Studies National Institute of Nutrition Hyderabad, India Dr Mathews Minnie Former Senior Program Advisor United Nations World Food Programme New Delhi, India Dr Menon Purnima Senior Research Fellow Division of Poverty, Health and Nutrition International Food Policy Research Institute New Delhi, India

Dr Khanna Kumud Director Institute of Home Economics University of Delhi New Delhi, India

Mr Mukherjee Ashish Executive Director Centre for Development Finance Institute of Financial Management and Research Chennai, India

Dr Kotecha Prakash V Country Representative A2Z USAID Micronutrient Project Academy for Education Development New Delhi, India

Dr Nair K. Madhavan Scientist and Head Micronutrient Research Group Department of Biophysics National Institute of Nutrition Hyderabad, India

Dr Krishnaswamy Kamala Former Director National Institute of Nutrition Hyderabad, India

Prof Nandan Deoki Director National Institute of Health and Family Welfare (NIHFW) New Delhi, India

Prof Kurpad Anura Dean and Professor Department of Nutrition St. John’s Research Institute Bengaluru, India Dr Lakshaman Anand Coordinator, Planning and Knowledge Management The Micronutrient Initiative (Asia office) New Delhi, India

Dr Nigam Arun K Executive President Institute of Applied Statistics & Development Studies Lucknow, India Dr Paintal Kajali Nutrition Specialist UNICEF New Delhi, India

List of Contributors Prof Pandav Chandrakant Head and Professor Centre for Community Medicine AIIMS New Delhi, India Dr Puri Seema Associate Professor Department of Food and Nutrition Institute of Home Economics University of Delhi New Delhi, India Dr Vijayaraghavan Kamasamudram Former Head Department of the Division of Community studies National Institute of Nutrition Hyderabad, India Dr Raj Kamal Emergency Nutrition Specialist Child Nutrition & Development Section UNICEF, New Delhi, India

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Dr Sankar Rajan Regional Manager and Special Adviser in South Asia Global Alliance for Improved Nutrition (GAIN) New Delhi, India Dr Sazwal Sunil Associate Professor Department of International Health Program on Global Disease Epidemiology and Control Johns Hopkins Bloomberg School of Public Health USA Prof Selvam Jerard M. Professor and Head Department of Epidemiology The Tamil Nadu DrMGR Medical University Chennai, India

Dr Ramachandran Prema Director Nutrition Foundation of India New Delhi, India

Prof Seshadri Subadra Senior Nutrition Consultant Former Professor and Head at Department of Food and Nutrition Faculty of Home Science Maharaja Sayajirao University of Baroda Gujarat, India

Dr Ramakrishnan Usha Associate Professor Hubert Department of Global Health Rollins School of Public Health Emory University Atlanta, USA

Dr Seth Veenu Associate Professor, Department of Food and Nutrition Lady Irwin College University of Delhi New Delhi, India

Prof Ramji S Professor Department of Pediatrics Maulana Azad Medical College New Delhi, India

Dr Shah Dheeraj Associate Professor Department of Pediatrics, University College of Medical Sciences New Delhi, India

Prof Sachdev Harshpal S. Senior Consultant Pediatrics and Clinical Epidemiology Sitaram Bhartia Institute of Research and Science New Delhi, India

Dr Singh Padam Head Research & Evaluation EPOS Health India New Delhi, India

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List of Contributors

Dr Pandey Richa S. Nutrition Specialist UNICEF Field Office Lucknow, India Dr Swaminathan Sumathi Research Supervisor Department of Epidemiology and Statistics St. John’s Research Institute Bengaluru, India Dr Mannar M.G. Venkatesh President The Micronutrient Initiative Ottawa, Canada Dr Vir Sheila C. Former Programme Officer ,UNICEF (India) Director

Public Health Nutrition and Development Centre New Delhi, India Dr Wesley Annie S. Senior Program Specialist The Micronutrient Initiative Ottawa, Canada Dr Yunuss Shariqua Programme Officer – Health and Nutrition United Nations World Food Programme New Delhi, India Prof Zodpey Sanjay P. Director, Public Health Education Public Health Foundation of India and Director, Indian Institute of Public Health, Delhi New Delhi, India

* The content of the text presents views of the author and not necessarily reflect outlook of the organization.

1 Principles of epidemiology and epidemiologic methods Sanjay P. Zodpey

Sanjay P. Zodpey, MBBS, MD, PhD, is a Public Health Specialist and Epidemiologist. Currently, he is Director, Public Health Education, Public Health Foundation of India (PHFI), New Delhi and Director at Indian Institute of Public Health, Delhi. Earlier, he was Vice Dean at the Government Medical College, Nagpur, Maharashtra, India. His areas of interest include clinical epidemiology, evidence-based health care, health policy, health systems research, program evaluation and public health governance. Dr Zodpey has been involved in several major international and national research initiatives that have contributed significantly to the field of public health.

1.1

Introduction

The scientific progress in health care research, application and policy formulation begins with a study among the population. The understanding of health events and outcomes in larger groups facilitates researchers in obtaining the ‘true’ and ‘complete’ picture of the situation. Several methods of scientific enquiry have been devised for the study among populations. Based upon the nature of enquiry, the study methods are broadly categorized as qualitative and quantitative. Qualitative methods equip researchers to gather an in-depth understanding of human behaviour and the reasons that govern human behaviour. Quantitative studies involve an ardent numerical foundation and seek to provide ‘hard’ and measurable evidence. Nutrition lends itself to several exploratory and explanatory tools. These tools aim to capture the health status of the population and measure its determinants.

1.2

What is epidemiology?

The term ‘epidemiology’ is coined from the Greek, implying ‘study among the population’. Indeed, the science of epidemiology is essentially based on

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the study of phenomena that affect the population at large. A widely quoted definition is offered by Last in ‘The Dictionary of Epidemiology’ where the term is defined as “The study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to control of health problems”. The definition succeeds in capturing the essence of epidemiology as based among the people at large. It aims to study not just disease or disease processes, but it is directed towards the entire gamut of health related states across the spectrum. It also addresses events that may influence the presence in such a state or which may force a departure from it. Lastly, it completes the picture by emphasizing upon the very purpose of epidemiology of working towards the control of health problems. The history of advancement in the science of epidemiologic methods has been hand-in-hand with public health. Epidemiology is a rapidly expanding and essential quantitative tool in the wide science of public health.

1.3

Development in epidemiologic methods

Contrary to popular belief, the epidemiologic method of scientific enquiry is not a recent addition in the repertoire of the expert. In 1747, James Lind conducted his famous study with 12 participants Box 1.1 Aims of epidemiology [5] First, to identify the etiology or cause of a disease and the relevant risk factors, i.e. factors that increase a person’s risk for a disease. Second, to determine the extent of disease found in the community. Third, to study the natural history and prognosis of disease. Fourth, to evaluate both existing and newly developed preventive and therapeutic measures and modes. Fifth, to provide the foundation for developing public policy relating to environmental problems, genetic issues, and other considerations regarding disease prevention and health promotion. Uses of epidemiology ● ● ●

● ● ●

Identifying health related event Identifying the risk factor and its linkages Establishing the causal relationship between risk factors and health related events Completing the natural history and clinical picture of disease Designing an intervention for addressing the problem Evaluating the effectiveness of intervention

aboard a naval ship. He tried to address scurvy, a significant public health problem among the sailors at that time. The understanding of the basic principles of epidemiology has undergone a significant refinement since this experiment by James Lind. Rapid strides have been made, especially in the last 50 years. The advent of computers and the ability to handle

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complex mathematical processes has fuelled the recent advancements. It is now practically impossible to imagine this progress in public health practices without any assistance from epidemiological methods. The science of epidemiology is a reflection of the inquisitiveness of human nature. It seeks out answers to the elementary questions that are posed to researchers and policy-makers. In this attempt, epidemiology has been influenced by several other scientific domains. The rapid expansion of this field and the need for specialized methods has promoted several new offshoots. The trial conducted by James Lind was a foray into alleviating a nutritional problem by using scientific techniques. Similarly, the means to study chronic diseases and account for multifactorial causation and long latency assisted the development of multivariate methods in epidemiology. Likewise, several fields like infectious diseases, geriatrics, cancer, nutrition, occupational and environmental medicine are developing and contributing to the development of tools and measures. The influence of these disciplines on epidemiology is immense and a welcome addition. Before embarking upon a discussion on the basic principles of the subject, the readers may bear in mind that although epidemiology is a large contributor towards the advancement of public health, it is not the only contributor. The creation of a complete picture for a public health problem mandates an understanding of the social and behavioural sciences as well. These may be studied by their unique methods, not necessarily just epidemiology.

1.4

Epidemiological reasoning

Epidemiological thinking follows a set pattern. Epidemiological reasoning attempts to rule out alternate explanations for the association between the cause and the effect. Let us understand this reasoning with an example from nutrition. For example, we may want to study the relationship between dietary fat consumption and obesity. The systematic collection and analysis of epidemiological data involves the determination of whether the probability of development of obesity in the presence of high dietary fat consumption is merely a chance or random event. The two conditions could be absolutely unconnected and by a stroke of luck may have been present in the study sample. There could be other alternate explanations. A systematic error that has crept into the study (bias) may be responsible for the conclusion. This systematic error could be due to a faulty ascertainment of dietary fat intake in all the study subjects. Alternatively, the association between high dietary fat consumption and obesity may be due to the effects of additional factors (confounding) like physical inactivity. If the issues of chance, bias and confounding can be satisfactorily addressed

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in the study, the investigators seek to make a judgment on causality that is, attributing a cause–effect relationship between high dietary fat consumption and obesity. Such a judgment would be made after considering several ancillary factors like the strength of the association, consistency of findings from all other studies and biologic plausibility. These factors are considered in tandem before arriving at a judgment of causality between the exposure and the outcome. The stronger the association between the cause and the effect, the higher is the likelihood of a causal relation between the exposure and the outcome. The presence of a biologic explanation for the purported causal effect (biologic plausibility) may aid in the process of attributing causality. Also, there must be a temporal sequence between the cause and the effect. The causal factor must precede the effect before attributing a causal relationship between the factors. The judgment of causality also considers the specificity of the association between the cause and the effect. The inference of causality is further strengthened by examining the coherence and analogy of the association between the cause and the effect. Similarly, if a particular finding is evidenced in several studies, in different locations and by different researchers, there is a stronger possibility of the existence of a causal relationship.

1.5

Classifying epidemiologic study methods

The simplest classification of epidemiologic studies is into observational and experimental studies (Table 1.1). Observational studies are those studies where the investigator observes and reports on the events without attempting to alter or control the events. On the other hand, in the experimental studies, the researcher controls the intervention within the study participants. The investigator offers the specific intervention under study and proceeds to study the change in the outcome. These studies or methods often compliment one another. Table 1.1 Study designs in epidemiology

I. Observational designs

(a) (b) (c) (d) (e)

Case reports and case series Ecologic studies Cross-sectional studies Cohort studies Case-control studies

II. Experimental studies

Controlled trials and uncontrolled trials

The study methods that are close approximations to the ideal experimental conditions are considered relatively higher in the chain of evidence. For example, a double-blinded randomized controlled trial

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(RCT) substantiating the beneficial effects of oral zinc supplementation in the treatment of acute diarrhea is considered superior to a simple longitudinal study on the problem. This hierarchy of study designs which rates experimental studies over observational studies may have some relevance, but it is necessary to understand that the choice of study designs must not be influenced by the hierarchy of evidence alone. The actual choice of a certain epidemiologic design is influenced by the current state of knowledge about the disease and the nature of the research question. There may be instances where a well-conducted casecontrol study may provide sufficient evidence and may not warrant the conduction of a RCT. Research usually proceeds from simpler designs that serve to identify and describe the problem to complex designs that address causality. The choice of a study design is also influenced by the frequency of the disease in the community, the ability to quantify the variables linked to the disease and the operational feasibility.

1.5.1

Observational designs

Case reports and case series Though conventionally not classical epidemiologic in their origins, these represent the earliest evidence that is accumulated within clinics and hospitals. Case reports are narratives of unique or rare occurrences during routine practice. Their uniqueness may represent a chance occurrence or may be an unrecognized dimension of a disease. For example, a case report may detail a case of vitamin B 12 deficiency associated with severe depression. This severe depression may be actually linked to the B 12 deficiency or may be a chance occurrence. A case-series lists similar experiences in several patients. Both forms may serve as initial pointers towards identifying newer effects of a disease or even the emergence of a totally unrelated new disease. A case-series of clustering of pneumocystis carinii pneumonia (a rare cause of pneumonia) was published from Los Angeles, United States in 1981. Subsequent research led to the identification of a new virus which was called as the HIV virus. The case report and case series may thus be viewed as the earliest descriptors of a disease. They serve to provide the foundation and rationale for the conduction of further epidemiologic studies. Ecological study Ecological studies are population-level studies that assist primarily in hypothesis generation. Ecological studies, unlike other study forms,

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are not conducted at the individual level. These are conducted at the population level. For example, an ecological study may be conducted to explore the relationship between food prices and the occurrence of vitamin deficiency in the pediatric age group. This comparison may be drawn between various states in the country and it may be evident that with a rise in price of food grains, there is a corresponding elevation in the vitamin deficiency rate. Such a study may therefore yield ground to base a new hypothesis which may be examined by a study design. Because this study is conducted at the population level, it is not possible to draw interpretations at the individual level. This is because it is not possible to state with certainty that the particular child who is suffering from vitamin deficiency is so affected because of food prices or some other cause. This ecological fallacy is the chief drawback in this study design. Cross-sectional studies Cross-sectional studies seek to collect information about a health event and its putative risk factors or outcomes at an individual level and at a specific point of time. In this respect, these studies closely resemble a photograph as they capture all the essential information in a single brief contact with the participant. Cross-sectional studies are distinguished from longitudinal studies by providing only a single opportunity for collecting the information on the disease and the outcome. They do not have a builtin directionality like the prospective study designs and retrospective study designs to be discussed later in this chapter. They differ from ecological studies in studying the health event within individual participants, in contrast to ecological studies which attempt to study the relationships at group level. Cross-sectional studies may have a descriptive as well as an analytical component associated with it. The descriptive component attempts to explore the ‘what’, ‘when’ and ‘where’ of a disease. The crosssectional studies are well-developed to answer this descriptive dilemma. The cross-sectional studies may also be analytical in seeking to provide information about the presence and strength of association between the disease and the study variable, thus permitting the testing of a hypothesis. Analytical cross-sectional studies describe as to ‘why’ the disease in occurring. The study is conducted within a population that is well-enumerated and described. Though it is not an absolute necessity, the conduction within a known group greatly facilitates in drawing inferences about the possible relationship between a variable and the health status. At the time of the data collection, instant estimate (summary) of the presence or absence of the disease is linked with the presence or absence of the variable that

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Box 1.2 Descriptive study – A study designed only to describe the distribution of an event (exposure or outcome), to describe the frequency of specific events or diseases in a particular population without seeking to explain the distribution by looking for association. The descriptive component attempts to explore the ‘what’, ‘when’ and ‘where’ of a disease. Analytical study – A study designed to examine associations, often with the aim of identifying possible causes for an outcome. Analytical cross-sectional studies describe as to ‘why’ the disease is occurring.

seeks to describe the disease. This summary at a point of time is collected for every individual to yield the pattern of the disease in the entire community. By providing this summary measure (prevalence), the crosssectional study gives a representative picture of the disease status in the entire community. Box 1.3 Prevalence is concerned with quantifying the number of existing cases in a population at a designated time. The prevalence of disease in a population is defined as the total number of cases of the disease in the population at a given time. When this estimate is derived for an exact time period, like on a specific date, the measure is more accurately referred to as a point-prevalence measure. The analogous term for a longer time interval like a season or a week may be referred to as period-prevalence. Incidence is the frequency of occurrence of the new cases in a defined population, arising during a given time period. Incidence, in contrast to prevalence, is a measure of new cases that occur in a population. The rate that is thus calculated is referred to as cumulative incidence rate (Number of incident cases/ total population at risk at beginning of follow-up period). Cumulative incidence assumes that there is a uniform and complete follow-up of the entire population at risk, from the beginning of the observation period to the end of the observation period. Incidence density, a similar measure, overcomes this contextual difficulty by substituting the exact amount of time for which each individual is followed-up in the study.

Box 1.4 Basic steps in conduction of a cross-sectional study ●

● ● ● ● ●

Defining the target population and baseline characteristics of the area and population. Conducting literature review to understand current state of knowledge upon subject. Formalizing the study objectives and methodology. Sampling the study population and identifying the study participants. Developing the study tools and standard operating procedures for data collection. Analysing data and interpreting results.

The preliminary step before the conduction of any population-based epidemiologic study, including cross-sectional studies, is to obtain the basic characteristics of the area (defining the population) where the study is planned. This preliminary step is vital because it provides a proper

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perspective to the study by justifying its need. It also assists in the process of planning the data-collection mechanisms that can be employed within the setting. Finally, at the stage of drawing interpretations, it assists the researcher in providing the appropriate context for formulation of the recommendations. The second step is also common to all studies. It involves the conduction of a thorough literature review. Literature reviews involve searching the print and electronic media for information and research conducted upon the subject. A thorough literature review facilitates the subsequent steps in the study conduction and also clarifies to the researcher the current state of knowledge upon the subject. The search should not be limited to indexed journals or to the print media alone. Adequate references may also be searched using online databases. After the researcher is well-acquainted with the study problem and the current status of knowledge on the subject, the researcher may embark upon formalizing the objectives for the study. The study objectives are a set of well-defined and usually quantifiable measures. The study design and methods are planned in accordance with these objectives. Subsequent to the finalization of the objectives, the study methods are formalized. These involve the selection of a study tool and the necessary training of the data collection team. The choice of standard operating procedures for data collection would contribute towards the internal validity of the findings. Internal validity is the approximate truth about inferences drawn from a study. It refers to the confidence we place in the findings of a study. Internally valid studies would generate results/findings which would be applicable to the participating population. External validity, on the other hand, deals with the generalizibility of the study results, in populations that are distinct from the study population. In other words, if the findings of a study demonstrate an increase in the growth velocity of malnourished children with the feeding of energy – protein dense diet, external validity answers the question about whether malnourished children in other locations, countries and conditions will respond similarly with an improvement in the growth velocity as predicted by the study. The analysis of a cross-sectional study proceeds along two general lines. These are guided as to whether the cross-sectional study is planned to be a descriptive cross-sectional study or an analytical cross-sectional study. A descriptive cross-sectional study will seek to provide a preliminary analysis by the calculation of means, medians or ratios as appropriate. The most commonly used measure is a prevalence measure that is derived and can be stratified for age, sex and other demographic variables. An analytical cross-sectional study, in addition to the prevalence measure, will seek to identify the absence or presence of association

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between the putative exposure factor and the outcome measure. If an association is present, it then seeks to quantify the strength of the association. This may be in the form of odds ratio or rate ratio. For example, in a study addressing association between increased cholesterol and Coronary Heart Disease (CHD), we can calculate prevalence of CHD disease in those exposed to high-cholesterol diet and compare it with prevalence with those not consuming high-cholesterol diet to estimate the odds of suffering from CHD given high-cholesterol intake. Also, we can do stratified analysis for various level of cholesterol (high, medium, low) for presence or absence of CHD to estimate the strength of association. The cross-sectional study (Table 1.2) has several points of interest. The chief advantage of this form of study is that it is a one-time exercise. As a result, it has a high degree of operational advantages for the research team. It is also a valuable exercise in generating a preliminary hypothesis. But it suffers from a disadvantage in being unable to attribute the exposure to the effect. For example, a cross-sectional study may identify that there is an association between a mal-absorption syndrome and vitamin D deficiency. The study is however unable to determine whether the vitamin D deficiency is caused by the mal-absorption per se. It may also be that the vitamin D deficiency may have caused enzymatic changes and then may have contributed to mal-absorption. Thus, the one-time visit of the investigator for a cross-sectional study may be an operational advantage, but fails to establish the sequence of events. Cohort study Cohort studies are a frequently encountered research design in public health nutrition literature. The basic constituent of a cohort study is a follow-up of a group of people who constitute the ‘cohort’. A cohort is a group of people with some common characteristic. If this common characteristic is chosen to be year of birth, we may have a cohort of all the children born in 2008. If this characteristic selected is the area of residence, we could constitute a cohort of all the residents of a particular locality or township. Consider a research question where the investigator plans to determine whether the rates of vitamin D deficiency are similar or different in those consuming calcium supplements. The first step in a cohort study would be to define the cohort. This could be done to include all the residents of a fixed geographical area, say village X. The subsequent step would be to classify the members of the cohort (village X) into two groups on the basis of the particular exposure factor (calcium supplementation; taken or not taken) into exposed and the un-exposed groups. We can classify all the people taking calcium supplements as the ‘exposed’ group

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Table 1.2 Effect measures in cross-sectional studies and definitions of common terms[3] Disease (+) Exposure (+) Exposure (–) Total

A C a+c

Means and standard deviations Medians, percentiles and other quantiles Proportions and ratios Odds Ratio Prevalence ratio Rate Ratio (exposure) Rate Differences (prevalence difference) Rate Differences (exposure difference) Excess risk among exposed Population Excess Risk Attributable fraction (exposed) Population attributable fraction Prevented fraction (exposed) Prevented fraction (population)

Disease (–)

Total

b d b+d

a+b c+d a+b+c+d

ad/bc {a/(a+b)}/{c/(c+d)} {a/(a+c)}/{b/(b+d)} {a/(a+b)} - {c/(c+d)} {a/(a+c)} - {b/(b+d)} {a/(a+b)} - {c/(c+d)} {(a+c)/n} - {c/(c+d)} {a/(a+b) - c/(c+d)}/ {a(a+b)} × 100 {(a+c)/n - c/(c+d)}/ {(a+c)/n} × 100 [{c/(c+d) - a/(a+b)}/{c/(c+d)}] × 100 [{c/(c+d) - (a+c)/n}/{c/(c+d)}] × 100

Definitions of common terms

Mean is the sum of the values for observations/number of observation. It is wellsuited for mathematical manipulation. Median is the point where the number of observations above equals the number below. It is not easily influence by extreme values. Mode is most frequently occurring value. It has simplicity of meaning. Range is from lowest to highest value in distribution. It include all values. Standard deviation is the absolute value of the average difference of individual values from the mean. It is also well-suited for mathematical manipulation. Percentile, deciles, and quartiles are proportions of all observations falling between specified values. They describe the “unusualness” of a value without assumptions about the shape of a distribution. Rate measures the occurrence of an event (disease) per unit of person-time. Proportion measures the percentage/fraction of people who develop new event (disease) during a specified period of time. Ratio measures the odds of having an event in question (disease) relative to not having the event. Risk Ratio: Compares the incidence of risk of an outcome in two groups/ populations. It measures how much more likely members of one group develops outcome of interest than members of the other group. It estimates the magnitude if the effect of the exposure on the outcome. Rate Ratio: Compares the incidence rate of an outcome in two groups, one exposed to factor under study and other not exposed. It is only measure that takes into account the person-time risk in each exposure group. Relative risk. For rare outcomes there are few people entering and leaving different exposure groups, the risk ratio and rate ratio are numerically similar. Both ratios in these circumstances are called as relative risk. However, it is better to specify which measure of effect we are using. Odds ratio is defined as the ratio of the odds of development of disease in exposed persons to the odds of development of disease in non-exposed persons.

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Prevalence ratio is used to compare the burden if disease in different group. It is neither an estimate of the magnitude of effect of exposure nor a measure of strength of association between an exposure and outcome. An alternative way to compare the occurrence of an outcome in a group that has been exposed to a particular factor with the occurrence in group that has not been exposed is to use a difference measure. Absolute difference is calculated by subtracting the occurrence in the unexposed group from the occurrence in the exposed group. Risk difference compares the incidence risk of an outcome in two populations. Rate difference compares the incidence rate of an outcome in two populations. When there is a causal relationship between an exposure and an outcome, the difference measure is sometimes called as the attributable risk or attributable rate. The attributable risk is defined as the amount or proportion of disease incidence (or disease risk) that can be attributed to a specific exposure. The attributable risk in the total population also called the population attributable risk – or the PAR “population attributable risk” or “population attributable fraction” as the reduction in incidence that would be achieved if the population had been entirely unexposed, compared with its current (actual) exposure pattern.

and the ones who do not as the ‘unexposed’ group. Both these groups would then be followed for about 6 months and the rates of occurrence of vitamin D deficiency in both these groups would be compared. The design thus seeks to establish a relationship between a risk factor (calcium supplementation) and the subsequent development of a disease (vitamin D deficiency). Cohort studies can be conducted in clinical or community settings. In clinical settings, these studies may be employed to study the mechanisms of disease causation or the treatment effects. In community settings, these studies are usually employed to study the population health impact of exposures. This study form may also be used to study occupational and environmental exposures responsible for disease causation. The cohort studies are referred to as longitudinal studies, implying that the studies involve a prospective follow-up from purported cause to the effect. Cohort studies are best suited for studying common diseases or where a sufficient number of cases will accumulate at the end of the follow-up period. As discussed in the vitamin D example in the earlier section, this design draws its conclusions after a lengthy period of time. The loss of patients to follow-up (due to death, migration etc.) thus presents serious challenges to this study design. All cohort studies incorporate a detailed follow-up plan to meet with such contingencies. These studies can also be undertaken to study multiple common outcomes in the general populations. Special cohorts may also be constituted to study rare exposures, for example, cohorts constructed after the Bhopal gas tragedy (rare exposure) attempt to document the effects of exposure to methyl iso-cynate.

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Box 1.5 Basic steps in conducting cohort studies ● ● ● ● ●

● ● ●

Defining the study question Defining and identifying appropriate cohort Selecting the study population, selection and enrolment of participants Defining and measuring the exposure Developing the study tools and Standard Operating Procedures for data collection Follow-up of participants Ascertaining outcome Analysing data and interpreting results

Cohort studies are classified according to the follow-up schedules for the study participants. If the follow-up is done entirely in the future, the study is referred to as a prospective cohort study. If a part of the study is conducted in the past and part in the future, it is referred to as an ambispective cohort study. A cohort study wherein the follow-up was conducted entirely in the past is referred to as a retrospective cohort study. Although prospective cohort studies are the classical form of the study, they may involve excessively long-waiting periods. This is because once the cohort is established and the cohort members are segregated as exposed and non-exposed, we have to essentially wait for the development of the outcome in both these groups. This duration varies between situations and may be relatively short in the development of food allergies, but may be as long as 5 years as in the case of vitamin B12 deficiency. The latter situation will warrant a follow-up of at least about an equal duration in all the study participants. After the identification of an appropriate cohort, the success of the study depends upon the nature of the cohort. Cohorts may be classified as ‘open’ cohorts or ‘closed’ cohorts. A cohort is labeled as ‘open’ or ‘dynamic’ when it permits new entrants into the follow-up group provided they fulfill specific criteria. For example, an open cohort of school children would permit new entrants/admissions into the school to be a part of the subsequent follow-up. The school drop-outs would be likewise omitted from the analysis. A ‘closed’ cohort of the same school children, in contrast to open or dynamic cohorts would not permit any changes to the original participant list of the study. Both forms of cohorts have specific advantages and disadvantages and are used in very different situations. The choice of the group to be selected for a cohort study is chiefly influenced by the ease and the practicality of the follow-up procedure. This is because for the accrual of sufficient outcomes/cases at the end of the follow-up period, it is essential to ensure a high follow-up rate among the study participants. Successful cohort studies like the Framingham heart study enrolled population from a relatively stable community near Boston which agreed to the study. The Nurses’ health study has studied the relationship between

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diet, physical activity, weight gain and the risk of chronic diseases. The success of this cohort lay in the ready accessibility of this group to the investigators and the provision of a high follow-up rate. The cohort may thus be chosen from the general population or from a specific population group. After the selection and enrollment of the study participants, the next step in a cohort study is to determine the exposure status of the participants. It may be noted that the cohort study bases its analysis on the determination of the outcomes in two groups: exposed and the unexposed. The determination of the exposure status at the commencement of the study is useful for the segregation of the participants into the two groups. It is mandatory to have a good operational definition of the exposure for the purpose of the study. The investigators must formulate a detailed, accurate, objective and unambiguous definition for the exposure. The criteria for the establishment of the exposure status should also be uniform across all the study subjects. For example, if the nutritional status of a group of under-5 children is to be studied, the investigators must clearly state the classification being used to assign children as under-nourished. It must also state the cut-off between normal and under-nourishment. The measurement of weight must be done according to uniform criteria, for example on the same brand of weighing scale. The methods to determine the exposure status should be similar for all the participants of the study. The exposed group should ideally be similar to the unexposed group in all factors except the exposure under study. After classifying the study participants into the two groups, the investigators proceed with the collection of the base-line information about the study participants. For example, in order to study the relationship between diet in antenatal women (exposure) and birth-weight (outcome), a cohort of women attending antenatal clinic in a district hospital may be formulated. In addition to the exposure we aim to study, there are several additional factors that may influence the causation of low birth weight among the newborns. These could vary from cultural habits in the household, socioeconomic status, cooking practices and so on. All these factors could also independently influence the occurrence of the outcome. Data-collection methods employed must therefore also collect information about these factors. This information may be collected formally as a part of the study or it may be collected from pre-existing records. For example, the information about the health status of the individual mother in a cohort may be collected from the previous antenatal health records. Hospitalization records may be collected from the hospitals within the geographic limits of the cohort. However, this information must be accurate and more importantly, should be easily linked to the specific mother/child in the survey. The commonly used methods for procuring information involve the conduction of personal

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Public health nutrition in developing countries

interviews, questionnaires dispatched by post and telephonic interviews. These methods have varying rates of response with the highest response rates achieved on personal interview. Medical examinations may be necessary to obtain information of which the subject cannot be expected to be aware. For example, no participant can be assumed to be aware about the serum level of vitamin D. A study on such substrates may necessitate the collection of biological specimens. Direct examinations can also be used to validate information obtained from interviews. However, use of all such techniques contributes towards increasing the cost of the study. Investigator time may also need to be devoted towards the training and the standardization of the biological measurements as well as the quality-check processes. The follow-up schedule for the study participants must be chalked out well in advance. Follow-up must be identical for all members in both the groups of the cohort. A differential plan of follow-up may inadvertently introduce a bias in the study. It is usually recommended to ensure the highest possible follow-up rates in both the groups. This may be facilitated by designing a comprehensive follow-up plan that may utilize several strategies. Chief among them include periodic re-examination of the subjects, postal or telephonic reviews and indirect surveillance of hospital records and death certificates. The duration of follow-up usually depends on the natural history of disease and length of latent period. Cohort studies basically provide estimates of incidence. Incidence, in contrast to prevalence, is a measure of new cases that occur in a population. The burden of disease in a community is composed of ‘old’ (already existent) and ‘new’ (newly developed, during the course of the study) cases. A cohort study aims to determine whether there are differential incidence rates between the exposed and the unexposed groups. The rates thus calculated are referred as cumulative incidence rate and incidence density (Refer to Box 1.3). Incidence density measures the exposure in terms of person-time or person-years to keep the contribution of each individual commensurate with their follow-up period. For example, an individual followed for 10 years without outcome event contribute 10 person-years, where as an individual followed for 1 year contributes one person-year to the denominator (Number of incident cases/ total person year follow-up). Cohort studies permit study progression in the same direction as would occur in nature. This study design allows a complete description of the individuals’ experiences subsequent to exposure, including the natural history of disease. As a result, they can convincingly state the temporal sequence and help add this information to the causal chain. Cohorts once set up and adequately followed-up, are a wealth of information. They may investigate the causation of multiple outcomes. For example, a cohort of obese men may yield information not just on the incidence of myocardial infarction in obese men, but may also yield information on the incidence

Principles of epidemiology and epidemiologic methods

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of colonic carcinoma. A cohort study is ideally suited for an investigation into rare exposures. A specially constructed cohort of individuals subjected to a rare exposure may help unravel the health effects of the exposure on the population at large. In general, cohort studies are usually for a long duration, mandating the set-up of a detailed follow-up plan for the study participants. The loss to follow up can be a significant deterrent to the drawing of valid conclusions and must be specifically observed as a part of the study. Thus the chief limitations of this study design are operational and administrative. In addition, ethical considerations also assume great significance in cohort studies. Table 1.3 Effect measures in cohort studies [4]

Exposure + Exposure Total

Disease +

Disease –

Total

a c n1

b d n0

m1 m0 t

Cumulative incidence rate/ incidence density Incidence ratio IR E = (I E / I0 ) Where I0 = incidence rate in standard non-exposed group; IE = incidence rate in exposed group Relative risk (risk ratio) RR E = (R E / R 0 ) Cumulative incidence relative risk (a/n1) / (b/n0) Disease + Cases Person time

a n1

Disease – b n0

Total m1 t

Incidence density relative risk Incidence difference

(a/n1) / (b/n0) IDE = IE – I 0 IDE = I0 (IR E –1) Attributable risk (risk difference) RD E = RE – R 0 RD E = R0 (RR E –1) Etiological fraction AF = (IT – I0 )/ IT I T = incidence rate in total population; I0 = incidence rate in group without exposure

Case-control study A case-control study is an efficient analytical study design. The study population in a case-control study consists of groups who either have (cases) or do not have a particular health problem or outcome (controls). Case-control studies, in contrast to cohort studies, proceed from the effect to the cause. In other words, the disease has already occurred when this study is conducted. This is a highly efficient study design for examining rare diseases and diseases with long incubation periods. This is unlike a classical cohort study which would have to either recruit a magnanimous number of participants (for yielding sufficient outcomes) or would have

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to undertake extremely long follow-ups for the long latent periods. This is deemed unnecessary by the proponents of a case-control design which overcomes these shortcomings and successfully identifies the differences in the presumed causal factors between the cases and controls. A case-control study can be conducted over a variety of settings. They are commonly employed in clinical as well as community research. Additionally, this design is often used to study occupational and environmental diseases. The choice of the case-control study design, like all other study designs, is strongly guided by the factors common for other designs. These include the current state of knowledge on the study problem, the availability of an institutional framework and the resources to conduct the study. They may be employed in clinical settings to outline the mechanism of disease causation or in community settings to identify the population health impact of exposure. Box 1.6 Basic steps in conduction of case-control study ● ● ● ● ● ●

Defining the study question Developing criteria for identification and selection of the cases Selecting appropriate controls and matching for efficiency Measuring exposure Analysing data Interpreting the results, and assessing the potential sources of error

The case-control study proceeds with the investigator attempting to determine the presence or absence of the putative risk-factor(s) in either group and then comparing them. The intention of this comparison is to determine whether the exposure is responsible for the given disease. The case-control study commences with the identification of the cases and the controls for the purpose of the study. A ‘case’ is defined as a specific outcome. It may be the presence of the disease or condition of interest, a complication etc. This case selection must be done using the standard definitions for diseases and must follow uniform criteria as outlined under cohort studies. A set of operational definitions must be set-up. Diagnostic methods employed for the purpose of the study must also be defined and included in the study protocol. It is usually recommended that case-control studies should recruit newly diagnosed cases or incident cases as a ‘case’ for these studies. The reason for such a recommendation stems from the knowledge that prevalent cases, in contrast to the incident cases, are a product of factors that cause a disease and also factors that govern the duration of illness. For example, consider the relationship between cases of colorectal cancer and sex. The occurrence of cases of colorectal cancer is higher among males than among females. But the survival is better in females than in males. Consequently, at any given point in time, if the prevalence of colorectal cancer is assessed in a community, it would yield a higher proportion of the disease in the females. This can result in a systematic error in the study. It can be however

Principles of epidemiology and epidemiologic methods

17

minimized by considering incident cases rather than prevalent cases. So the inclusion of incident cases as ‘case’ in a case-control study is backed by sound reasoning. Additionally, the incident cases being relatively recent, the cases can be expected to easily recall the influencing factors in a questionnaire. The cases may be registered from hospital admission or registry records, physician records, pathology records, clinic notes/ casefile or from clinics with a good follow-up or recording system. The selection of controls is a critical issue in case-control studies and it depends on the setting in which the study is being conducted. The controls must be free of the disease. Specific inclusion and exclusion criteria are framed to identify controls. The criteria used to select controls should be comparable in all ways with the criteria used to select cases, except disease status. In hospital-based studies, the controls are usually selected from the hospital attendees. Controls may also be selected from the same neighbourhood as the cases or from the relatives of the cases. Such controls will possibly have similar environmental exposures as the cases and may be suited for the study of certain exposure–effect relationships. Alternately, controls may also be selected from the general population; random digit dialing on the telephone can help in identifying potential study participants. Comparison of cases with specific controls contributes towards the study efficiency. In studies with small sample sizes, selection of more than one control per case helps to improve the statistical power of the study. This increase in statistical power is observed up to a 1:4 ratio between cases and controls. Beyond this number, there is hardly any gain in statistical power per new control. Case-control studies may employ matching between cases and control as another unique feature. Matching is performed for certain characteristics or variables of interest. For example, cases and controls may be matched for age and sex, socio-economic variables, literacy and so on. It is usually employed only for the known risk-factors for the outcome. Matching must be performed for only those variables which improve the statistical efficiency of the study. An overzealous attempt at matching for all possible variables must be avoided. This is important because an overmatched study may under-estimate the true odds associated with the outcome. Also, once matching has been accomplished, it is not possible to separate the effect of the matched variables. The subsequent step in the study is exposure assessment. It is done using a variety of methods. This can be accomplished through interviews or by utilizing medical or occupational records/histories. Biological markers may also be used whenever feasible. The study proceeds by a calculation of the odds ratio. This statistic, also referred to as a cross-product ratio, is an estimate of the relative risk obtained in cohort studies. The interpretation of this measure is relatively simple. For example, if the odds ratio for sepsis in low birth weight babies is 3, it means that the low birth weight babies are 3 times more likely to suffer from sepsis than normal weight babies.

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The study quality may be compromised by the presence of unique biases. Case-control studies are conducted after the disease or event of interest has occurred. As a result, the in-depth interview and examination for the exposure having occurred may be followed up with differing vigor in cases and controls. For example, the history of immunization with vitamin A may be queried and checked with great detail in a known case of malnutrition than in a normal weight child. Such biases can be controlled by blinding the data collecting team of the specific objective of the study. Alternatively, the study instrument may be so prepared and the questions may be so objectively included that there is no variability in the questioning style among the cases and the controls. This measure will ensure a uniform method of data collection regarding exposure status in both the groups. Biases can be minimized by the careful planning, design and appropriate analysis in the study. These biases are classified as selection bias, misclassification (information) bias and confounding bias. Box 1.7 Biases that may occur in case-control design [5] Selection bias refers to error due to systematic differences in characteristic between who take part in study and those who do not, such that the people selected to participate in a study are not representative of the reference population or the comparison groups are not comparable. Mis-classification bias refers to error in the measurement of exposure or outcome that results in systematic difference in the accuracy of information collected between comparison groups. Confounding bias is about alternative explanations for an association between an exposure and an outcome. It is the situation where an association between an exposure and an outcome is entirely or partially due to another exposure (called confounder). In order to be a confounder, the variable must be associated with exposure of interest, must be a risk factor for outcome of interest, and must not be on casual pathway between exposure and outcome.

Minimizing such biases is an important challenge in the conduction of case-control studies. However, in-spite of these limitations, the case-control study offers significant methodological advantages to the researcher. Newer hybrid designs, like nested case-control studies combine the advantages of cohort and case-control studies for investigating into exposure–outcome associations (Table 1.4).

1.5.2

Experimental studies – controlled and uncontrolled trials

Experimental studies are characterized by the prerogative of the investigator in assigning the participants to a particular intervention. This distinguishing feature characterizes experimental studies from the other types of epidemiologic studies. The investigator allocates the participants

Principles of epidemiology and epidemiologic methods

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Table 1.4 Effect measures in case-control studies Disease (+) Exposure (+) Exposure (–) Total

a c a+c

Exposure rates Odds ratio Attributable risk proportion Population attributable risk proportion

Disease (–)

Total

b d b+d

a+b c+d a+b+c+d

(a/a+b) and (c/c+d) [a / c] / [b / d] = ad / bc (OR-1)/OR 1-[b(c+d) /d(a+b)]

into groups and also determines which study participants receive the intervention. These studies progress forward in time, in a sense; they are longitudinal or prospective like the cohort studies. In the causal chain, experimental studies are said to provide the strongest evidence of disease causation. Although rated high on the causal chain, their inherently complex nature makes them a difficult proposition for researchers. Experimental studies may be carried out in several settings. They are often carried out in hospital settings as clinical trials to evaluate therapeutic regimes. Equally common are community-based study designs which may or may not employ control subjects. In communities they may be used to examine populationlevel interventions. Box 1.8 Following basic steps are critical for experimental studies ● ● ● ● ● ● ●

Formulating the hypothesis / Defining the study question Developing the study protocol Selecting the study population Randomization and allocation of the intervention Follow-up of participants Measuring outcome Analysing data and Interpreting results

The first step in the conduction of an experimental study is the formulation of a hypothesis. The hypothesis is the very basic premise on which the study is based. Experimental studies are an operational, financial and ethical challenge. Consequently, they are conducted in situations where there is an uncertainty which can be addressed by the conduction of this study. An experimental design is then constructed to study the hypothesis. The methodology and the steps to be followed in the study are enumerated and described in the study protocol. This protocol is implemented subject to ethical clearance by the institutional review board or ethics committee. Using specific inclusion and exclusion criteria, the investigators seek to recruit participants for this study. These criteria ensure the participation of individuals who would be capable of

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withstanding the intervention as well as the subsequent assessment of the outcome. The participants who meet the eligibility criteria must then consent to their participation in the experimental study. Consider an experimental design constructed to study the effect of a dietary intervention on anemia in pregnant women. The inclusion criteria for such a study would include the mothers registering in antenatal clinics over the study area. After determination of their hemoglobin status, the women with hemoglobin levels below 11 g% would be classified as anemic and therefore eligible to participate in the interventional study. Women with normal hemoglobin levels would be excluded from such a study. The informed consent procedure must be strictly monitored and non-consent for participation must not adversely affect the treatment of the individual. The informed consent must not be blanket consent for participation into the study but must clearly mention the interventions to which the participant will be subjected. The consenting participants may then be allocated into the study arms using random or non-random allocation depending on the design of the study. Randomization is a method to allocate individual subjects who have been accepted for a study into one of the groups (arms) of a study. The process of randomization is akin to tossing a coin for allocating the participants into groups. It may be pre-decided that all participants who toss a heads may be allocated to one group and all the participants who toss tails may be allocated to the other group. Alternatively, randomization may also be carried out using random-number tables. The usage of such tables is easy and ensures random distribution of the participants into the groups. Many studies employ computer-generated random allocation sequences which may be used for classifying the study participants into groups. Essentially, all these procedures ensure that every individual has an equal chance of being a participant in either of the two groups: the study or the control group. Consequent to randomization, the basic explanatory factors get divided evenly among the two groups. This similarity between the two groups is what makes randomization so crucial in experimental studies. Out of a total of 100 children, after randomization it may be expected that there will be near equal number of boys and girls in either group. Similarly, there would be a near equal number of underweight children in both these groups. Such a balance between the two groups extends not only between the known etiological factors or causal factors, but also between the unknown causes or contributors of a disease. For example, it may be known that the nutritional status of a child is influenced by the total daily caloric intake of the child. Randomization of participating children will achieve a near equivalence in the caloric status between the two groups. It also ensures that if there is any other confounder that is present, it too will get

Principles of epidemiology and epidemiologic methods

21

equally distributed between the experimental and the control groups. This division of measured/non-measured, visible/invisible, known/unknown variables will be approximately equal between the two arms in the presence of a big sample. The procedure of randomization helps to minimize selection bias in the study. It does so by ensuring allocation of the study participants into the groups using a pre-defined method. Thus, a conscious or subconscious bias on part of the investigator can be minimized. In the evaluation of two dietary supplementation plans for mal-nourished children, randomization assures that the investigator does not show a conscious or sub-conscious preference for any dietary plan by allotting the healthier children to that group. Additionally randomization meets the assumption of statistical tests used to compare the two groups. The group to which a particular participant is allocated may alternatively be concealed from the study investigator whenever possible. Once registered the patient remains irrevocably in the study. Such a process in which the group assignment of the next patient remains undisclosed (or concealed) from the recruiting physician is termed, ‘concealed randomization’ or ‘allocation concealment’. There are several issues that must be considered when undertaking randomization. This procedure yields the intended results only when the randomizing method is strictly followed and is adhered for each and every participant. There must be no break in the sequence or the technique for any participant. The randomization is employed only when the subject is a part of the study and must not be employed prior to the participation of the study subject. Another procedure frequently encountered in experimental studies is blinding. Blinding is done so that the prejudices or enthusiasms of the subjects don’t result in behaviour that promotes or inhibits the recognition of disease outcomes. It can be performed in three ways: single blind (The trial is so planned that the participant is not aware whether he/she belongs to the study group or control group); double blind (The trial is so planned that neither the doctor/investigator nor the participant is aware of the group allocation and the treatment received); or triple blind (The participant, the investigator and the person analyzing the data are all blind as far as group allocation is concerned). Triple blinding is considered as ideal but can be infrequently employed. It is necessary to understand that ‘concealed randomization’ is not ‘blinding’. Concealed randomization is to take place before initiation of treatment whereas blinding involves steps at and after initiation of treatment. It must be attempted to reduce or minimize a contamination in a clinical trial. This occurs when the control group receives part or all of the intervention. When the comparison is between two active treatments,

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contamination occurs when patients in one arm receive the treatment of the other arm. Such contamination tends to blur the difference between the treatments. A genuine effect may be completely obscured or may be underestimated. Controlled trials may proceed in several ways. In the parallel design, they begin with the participants of the trial being classified into the two groups (group A receiving intervention, i.e. experimental group and group B not receiving intervention, i.e. control group) according to randomization sequence. Subsequently, the two groups are followed up for the occurrence of the outcome which is compared between the groups. Outcome ascertainment is carried out in the follow up period. This outcome is defined according to the study objectives and is preferably done using objective and specific criteria. Alternatively in cross-over studies, the two groups would proceed as mentioned earlier and after ascertaining outcomes, the groups are exchanged. That is, the exposed group now participates as the control group and the original control group as the experimental group. This cross-over is permissible after a washout period that guarantees that the original intervention group is now free of the effects of the intervention. However, not all experimental studies are randomized or employ controls. Non-randomized trials are also frequently encountered in scientific literature. Due to several logistic and operational issues, it may not always be possible to randomize participants into groups. For example, when evaluating impact of national initiatives like implementation of Integrated Child Development Services (ICDS) on nutritional status at district level since all districts, it is not possible to employ a control district group. This is not possible because the intervention is administered across the country in all districts where only some blocks may not be covered. In such circumstances, epidemiologists conduct a type of experimental study referred to as a before–after study. This means that a study is conducted where in data on the nutritional status of the children is compared before and after the intervention is applied within the community. After allowing sufficient time for the intervention to cause an effect, we evaluate the population for any change in the nutritional status of the children. Any change in the nutritional status between these two time intervals is carefully examined for the possible causes. Another variety of non-randomized studies are studies of natural phenomena and their descriptions. For example the famous experiment by John Snow to identify the etiology of cholera was a natural experiment. This form of study makes use of the naturally occurring phenomena and making a careful record of the observation to arrive upon justified conclusions. Follow-up is also an integral part of any

Principles of epidemiology and epidemiologic methods

23

experimental study. It implies examination of the experimental and control group subjects at defined intervals of time, in a standard manner, with equal intensity, under the same given circumstances. The outcome of the study may include positive as well as negative events. These must preferably be objective and determined for all participants in the study. Investigators pay special attention towards ensuring a high degree of compliance among the study participants in order to facilitate assessment of the outcome. Experimental studies when conducted in this fashion provide an estimate of the efficacy of an intervention. They attempt to determine whether the intervention works under ideal, highly controlled and optimal conditions. Ideally, the determination of efficacy is based on the results of an RCT. But eventually, all interventions are employed in the larger population or community. The extent to which a specific intervention when deployed in the field does what it is intended to do for a defined population is distinct from validity and is referred to as the effectiveness of an intervention (Box 1.9).

1.5.3

Hybrid study designs

There has been recent attention towards the development of study designs that employ the advantages of more than one study design. Such designs are either combinations of study designs or modifications in the study methods. Such observational hybrid designs include nested case-control studies, follow-up prevalence study, selective prevalence study, casecrossover studies and so on. In nested case-control studies for example, a cohort is constructed and duly followed up for the occurrence of the outcome. Those participants of the cohort who experience the outcome are designated as cases while the participants who do not experience the outcome constitute the controls. Such studies are being increasingly conducted in the nutritional field. Box 1.9 Efficacy is the effect of the intervention under trial conditions, the maximum benefit under ideal conditions. Effectiveness is the effect of the intervention under operational conditions, such as would be the effect of intervention into routine practice. For example, the effect of nutritional supplementation for HIV-infected individuals may have positive impact (weight gain) in trial conditions, but when translated in clinical practice, we would expect it to be less effective because the population is less carefully selected; adherence would be low, resulting in reduced benefits.

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Table 1.5 Effect measures in experimental studies Risk difference (absolute risk reduction)

=

Rt – R c

= =

Rt / R c 100 – RR (in decimals) 1/ Risk difference

where R t is the risk/probability of outcome in the treatment group and Rc is the risk/probability of outcome in the control group Risk ratio (Relative risk) Relative risk reduction percent) or 1 – RR (in Number needed to treat

=

References 1.

STOLLY PD, LILIENFELD DE

(1994). Foundations of Epidemiology. Oxford University

Press. 2. 3. 4. 5. 6. 7.

MCEWEN, BEAGLEHOLE , TANAKA , DETELS ,

(eds). Oxford Textbook of Public Health. Oxford University Press, 2002. ABRAHAMSON JH . Survey Methods in Community Medicine. Churchill Livingstone, 1999. HENNEKENS CH , BURING JE . Epidemiology in Medicine. Williams and Wilkins, 1987. GORDIS L . Epidemiology. Elsevier Saunders, 2004. ASCHENGRAU A , GEORGE R . SEAGE III . Essentials of epidemiology in Public Health. Jones and Bartlett Publishers, 2003. BONITA R, BEAGLEHOLE R, and KJELLSTRÖM T . Basic Epidemiology. World Health Organization, 2007.

Nutrition epidemiology for developing countries

2 Nutrition epidemiology for developing countries Usha Ramakrishnan and Ines G. Casanova

Usha Ramakrishnan, MSc, PhD, is Associate Professor at the Hubert Department of Global Health, and Director of the Doctoral Program in Nutrition and Health Sciences (NHS) at Emory University. Dr. Ramakrishnan is internationally known for her expertise in maternal and child nutrition and for her research is focused on the functional consequences of micronutrient malnutrition during pregnancy and early childhood in developing countries. Ines G. Casanova, MS (Nutrition), worked at the Department of Community Nutrition at the Mexican National Institute of Public Health (INSP) for 3 years. She is currently a doctoral student in the NHS Program at Emory University.

2.1

Introduction

Epidemiology is defined as “the study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to control health problems” [1]. Meanwhile, nutrition is “the process by which substances in food are transformed into body tissues and provide energy for the full range of physical and mental activities that make up human life”. Nutritional sciences primarily involve the study of biological processes, but also integrate fields like anthropology and psychology that play an important role in the determining patterns of dietary intake and health in large groups or people, i.e. populations [2]. The application of epidemiological principles to human nutrition has resulted in the unique field of “Nutritional Epidemiology” which provides the necessary tools to generate scientifically valid information that advances our understanding of the role of nutrition in human health and/or disease [3]. Nutritional epidemiology is defined as “all the studies between diet and health in human populations” [4].

25

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Public health nutrition in developing countries

The purpose of this chapter is to provide a general understanding of “Nutritional Epidemiology” by describing the main concepts and features that define this discipline, and to focus on the application of the science of nutritional epidemiology to the nutritional and health problems that the less developed countries face. The first section is a review of different types of epidemiologic studies and their application to the methods used to assess nutritional status at a population level. This is followed by a discussion of the issues related to measurement error and the assessment of validity and precision at a population level. Finally, the last two sections focus on the role of nutrition epidemiology in a) addressing the determinants and dynamics of nutrition in developing countries and b) in public health nutrition towards the goal of improving the health and wellbeing of populations.

2.2

Epidemiological studies

Epidemiology as a science has five major objectives: (i) to identify risk factors for disease; (ii) to determine the extent of disease in a community; (iii) to study the natural history and prognosis of disease; (iv) to evaluate preventive and therapeutic methods of health care delivery; and (v) to provide the foundation for developing public policy. The two key constructs in epidemiological research are “exposure” and “outcome”. Exposure is typically defined as the variable believed to be associated with the presence or absence of the disease. In the case of nutritional epidemiology the main exposure of interest is dietary intake (including nutritional supplements), while the outcome is its effect on human health [1, 5]. The relation between dietary intake and child health is illustrated well in the UNICEF conceptual framework; inadequate food intake is directly related to disease, and both are direct causes of children malnutrition, disability and death (Figure 2.1). Nutritional epidemiology allows us to examine the nature of these associations [6]. For example, dietary fat intake or frequency of consumption of animal foods could serve as exposures of interest whereas the outcome is the disease itself (or the absence of it); such as presence/absence of stunting and/or anemia. The dynamics between exposure and outcome are central to epidemiologic studies which can be conducted using different kinds of study design. The most common classification of studies based on their design is either “observational” or “experimental”. A description of the different types of study design under the above two categories is provided in the following section with examples of their application to nutritional epidemiology.

Nutrition epidemiology for developing countries

Nutritional status

Outcome

Immediate determinants

Underlying determinants Poverty constrains the level of these determinants for individual jpiseholds

NUTRITIONAL EPIDEMIOLOGY

Health status

Dietary intake

Exposure

27

Outcome

Household food security

Ovality of care

Healthy environment, health services

Food Security Resources „ Quantity food produced „ quality food produced, diet diversity „ cash income „ food transfers

Careglver resources

Resources for health availebility of public health services sanitation, access to clean water

„  

„

Institutions

Basic determinants The impact that the resources potentially available to the household have on nutritional status is mediated and constrained by overarching economic, political, and institutional structures

Knowledge and access to education „ health status „ control of resources „  

Political and Ideological Framework

Economic Structure

Potential resources Human, agre ecological technological

2.1 UNICEF Malnutrition Framework – an example of dietary intake as an exposure.

2.2.1

Observational studies

Cross-sectional studies This study design is mainly used to estimate prevalence. Typically both exposure and disease are assessed at the same point (or period) of time in all subjects or a representative sample [7]. Examples of cross-sectional studies in nutritional epidemiology are the national health and nutrition surveys that many countries periodically implement to describe the nutritional and health status at a specific point of time. These include the Demographic Health Surveys (DHS) in many developing countries including the National Health and Family Survey (NFHS) in India, that obtain anthropometric and hemoglobin measurements in women of reproductive age and young children, the National Nutrition Surveys in Mexico, and the Nutrition and Health Examination Surveys (NHANES) in the United States of America. These

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surveys are very useful to identify population needs and can be used as the basis for health interventions [5]. When repeated over time, they also provide a basis of estimating trends and/or changes over time. For example, the DHS and NFHS surveys have been useful to examine if the nutritional status of young children has improved over time by measuring the prevalence of malnutrition at various time points (Box 2.1). Nevertheless, these studies have important limitations. The most important concern is related to “timing”; often it is impossible to determine the order of the events and thereby infer causality. Associations between diet and disease may be confounded by other variables such as socioeconomic status which is associated with both the exposure and outcome. Another problem is the “length-biased sample”, this makes reference to the fact that cross-sectional studies tend to under-represent cases or exposures with short duration, and over-represent long duration cases or exposures [7]. For example, in the case of diet, the contribution of seasonal foods might be overlooked depending on the time of the study. It is important to consider these limitations when making inferences out of cross-sectional studies. Box 2.1 Important definitions: incidence and prevalence Incidence – It is defined as all new cases of a disease that occur during a specified period of time in a population at risk for developing the disease. ●

Example: In a 6-month period 66 patients developed anemia in “town X”. Then the incidence of anemia for “town X” in 6 months is 66.

Mortality – It is a type of incidence. All new deaths that occur during a specified period of time in a population at risk for developing a disease is defined as mortality. Prevalence – It is defined as the number of persons with a certain disease present in a population at a specific time divided by the number of persons in the population at that time. ●

Example: A survey conducted on 26th of February in “town X” determined that 3000 persons had anemia at that time. The city has 30000 habitants; then the prevalence of anemia in “town X” is 0.10 or 10%.

Ecologic studies This design differs from all other epidemiologic studies in the unit of observation. Ecologic studies focus on groups of people instead of on individuals. The most common use of this type of studies is to compare between countries; sometimes they have been used to compare other defined groups like schools, workplaces, organizations, cities, etc. Both exposure and outcome are measured at a population level. Food consumption or availability is an example of the data that is often used. The data are typically from cross-sectional and obtained from national

Nutrition epidemiology for developing countries

29

nutrition surveys or food production statistics. The information is expressed per capita, where the amount of total food available is divided by the number of people and does not necessarily reflect individual intake [1, 5, 7]. Food balance sheets that describe all food and nutrient availability at the national level [8] are often used; for example, the grams of fat consumed per capita in China, India and Japan can be related to the prevalence of obesity in each of these countries. Cohort studies In a cohort study the researcher classifies the participants in two groups based on exposure status and then follows both groups to compare the incidence of disease. A positive association between exposure and disease is represented by a greater incidence in the exposed group compared to the unexposed [1]. The main strength of this design is the ability to make inferences about etiology [3]. It is possible to determine timing and directionality because exposure is assessed before the onset of the disease. These studies are useful to determine the relation between diet and disease [5]. The main limitation however is that they may be time consuming and expensive especially when you are examining conditions that may take a long time to develop such as cancers and/or are rare in which case you need a very large sample size. A well known example of cohort studies in the field of nutrition is the Nurses Health Study in the United States. Other examples of cohort studies include the INCAP longitudinal study from Guatemala [9, 10], the Pelotas Birth Cohort in Brazil that followed children born in 1982 in the city of Pelotas up to adulthood [11], and the Japan Collaborative Cohort Study for Evaluation of Cancer (JACC) [12]. Many of these studies have followed up their subjects for several decades either from early childhood to adulthood, young adulthood to later adulthood which have allowed them to examine the role of early nutrition in the etiology of chronic disease and other health outcomes. Case-control studies In case-control studies, the investigators first identify a group of individuals with a specific disease/condition (cases), following which they randomly select a group of individuals with similar characteristics but are disease free (controls). This is followed by the assessment of one or more exposures of interest which are then compared in both groups. For example, dietary exposures are established using surveys or medical records. Diet can be assessed at four different levels: individual, household, institutions and national. These studies, particularly in the case of dietary intakes, often suffer from recall problems and/or low quality data because of the retrospective design. Another concern in case control studies is the

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appropriate selection of the control group. These potential sources of bias, referred to as systematic error often result in incorrect conclusions about the nature of the associations being examined. It is therefore important to consider these limitations and interpret the results of these studies cautiously. However, these studies are logistically more feasible than prospective studies (i.e. cohort studies) and can provide relevant information to assess the diet-disease interactions [1, 3, 5, 7, 13].

2.2.2

Experimental studies

An experiment is understood as a trial where the investigator(s) manipulates the exposure of interest. Experimental studies are typically preferred in a scientific setting but often difficult and expensive to carry out. Nevertheless, studying human beings involves many factors that the researcher is unable to control; this is true particularly for nutritional epidemiology [5]. Experimental epidemiology is also limited ethically to studies in which exposures are expected to cause no harm. The other important ethical consideration is the appropriate use of a placebo and need to ensure that all participants are assured “the standard of care” in the specific setting where the study is being conducted. For example, iron supplementation is routine during pregnancy in many developing countries and denying this could be regarded as “unethical” [7]. Randomized controlled trials (RCTs) – Randomized controlled trials are considered the gold standard in assessing the effect of an intervention. In these trials, subjects are randomly assigned either to an exposed (treatment) or unexposed (control or placebo) group. Clinical trials in nutrition typically include a baseline and a follow up measurement of nutrition or health related exposures and outcomes. The greatest advantage of these studies is their effectiveness in assessing causality. Box 2.2 Reporting clinical trials – the Consolidated Standards of Reporting Trials (CONSORT) Statement CONSORT was designed by a group of clinical trial researchers, statisticians, epidemiologists, and biomedical editors and has been supported by a growing number of medical and health care journals. CONSORT encourages transparency with reporting of the methods and results, so that reports of RCTs can be better interpreted. The use of CONSORT also reduces inadequate reporting. Most importantly, evidence suggests that the use of CONSORT could positively influence the way in which RCTs are conducted, by setting standards that should be considered during the design stage. [14–16]. The CONSORT checklist comprises 22 items that include information on reporting the design, analysis and interpretation of the trial. This includes specific details on the objectives, nature of the intervention, randomization and blinding, data collection and analysis. The flow diagram provides information on how to report the changes in sampling and the study population (Figure 2.2).

Nutrition epidemiology for developing countries

31

Randomization is the assignment by chance to the treatment or to the control group. This tool helps reduce the chances of selection bias, and also helps to control for confounding factors that otherwise could be overlooked by the researcher [1]. Details on the ideal ways to randomize and allocate treatments are described in The CONSORT (Consolidating Standards of Reporting Trials) statement that was developed and published in the mid 1990s with the aim of improving the quality of the reports of clinical trials [14–16] (Box 2.2). Assessed for eligibility (n= )

E n ro llm e n t

Exclud ed (n=

)

N ot m eeting inclusio n criteria (n = ) R efu sed to participa te (n= ) O ther reasons (n = )

A n alys is

F o llo w -U p

A lloc a tio n

R an dom ize d (n= )

Allo cated to inte rvention (n= ) R eceived allocated inte rvention (n= ) D id not receive allocated inte rvention (n= ) G ive reasons

Los t to follow –u p (n= G ive reasons

)

Allo cated to inte rvention (n= ) R eceived allocated inte rvention (n= ) D id not receive allocated inte rvention (n= ) G ive reasons

Los t to follow –u p (n= G ive reasons

)

D iscontinued interven tion (n = ) G ive reasons

D iscontinued interven tion (n = ) G ive reasons

An alyzed (n= )

An alyzed (n= )

Exclud ed from analysis (n= G ive reasons

)

Exclud ed from analysis (n= G ive reasons

)

2.2 CONSORT Statement 2001 flow diagram.

Another advantage of RCTs is the usage of a placebo (indistinguishable from the treatment), which allows blinding to the treatment. In a single

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blinded study the subjects are unable to distinguish if they are taking the treatment or the placebo; while in a double blinded study, neither the subjects or the researchers know the assignation to the groups. Blinding eliminates the possibility of bias induced by modification of the behavior of subjects or researchers related to the grouping [5, 13]. The chances for differential bias in the measurement of outcomes are reduced which increases the validity of the findings. It may however be difficult to conduct placebo-controlled RCTs when food based interventions are being evaluated. Although the participants cannot be blinded to the treatment, the inclusion of a control group and blinding of the personnel who collect and analyze the data are recommended to minimize bias. The inclusion of a control group allows one to compare changes over time in a group that did not receive the treatment and determine if the treatment group fared better. For example, if the prevalence of anemia did not decline in women who received multiplemicronutrient supplements but increased in the control group over the same time period, it would be easier to interpret that the treatment group still benefited as the supplements prevented the increase in anemia that would have otherwise occurred. Another major advantage of including control groups is to minimize the effect of confounding variables that may be associated with the outcome of interest. Another element of clinical trials is the utilization of “intention to treat’ principle in the analysis of outcomes. This concept is related to adherence to the treatment and is used in efficacy trials; “Intention to treat” means that groups are analyzed as initially assigned, independent of adherence [1]. For example, in a study of comparing the effects of consuming multiple micronutrients to iron only supplement in women of reproductive age, if 600 women were originally randomized to treatment but only 550 actually received the treatment and 400 consumed at least 80% of the intended dose, intention to treat analysis will compare the outcome of interest for e.g. prevalence of anemia in all 600 women who were originally randomized to either the treatment or control groups irrespective of how many doses they consumed. Comparing the benefits of the intervention only among those who consumed at least 80% of the intended dose would be treated as a sub-analysis. Community interventions Community intervention trials are an important tool in nutrition epidemiology. They are similar to clinical trials, except that the interventions are targeted to groups of individuals, for e.g. villages or organizations such as schools etc (as opposed to individuals). An exposure is introduced to a whole community or group of people, and a similar community is used as a control. When more than two communities or large groups of people are intervened, the assignment to the groups should be

Nutrition epidemiology for developing countries

33

by randomization. Examples of community interventions are environmental changes like water fluoridation, increasing fruit and vegetable availability by building a market, etc. Dietary interventions may be more convenient at a family, household or community level [7].

2.3

Nutritional epidemiology – measurement

Careful consideration of the methods selected to assess nutritional status in terms of their suitability (see Box 2.3) as well as accuracy and precision are important for nutrition epidemiologic studies. This is especially critical in the case of the exposure and outcome variables. Today, nutritional assessment in many low income countries emphasizes new simple, noninvasive approaches. These methods are used to assess nutritional deficiencies or excesses, as well as to monitor or evaluate the effect of interventions aimed to improving nutrition and health outcomes [17]. Inadequate measurement however can lead to inappropriate conclusions, and waste valuable resources [3]. Nutritional assessment is defined as “the interpretation of information from dietary, laboratory, anthropometric and clinical studies”, where this information is used to determine the nutritional status of individuals or populations [18]. These procedures were typically use to describe the nutritional status of populations since the 1960s but more recently have been used to examine the relationship between diet (or nutritional supplements) and disease. Box 2.3 Nutritional assessment in developing countries At a population level, nutritional assessment systems are classified in surveys, surveillance systems, screening and interventions. ● Nutrition surveys are cross sectional studies, mainly used to identify groups at risk of nutritional deficiencies. ● Nutritional surveillance is a continuous monitoring of the nutritional status of selected groups (usually high-risk groups). ● Nutritional screening is the identification of malnourished individuals or groups that require an intervention. ● Nutrition interventions are evaluated by nutritional assessment methods [3].

2.3.1

Methods to assess nutritional status

The selection of appropriate nutritional assessment methods is one of the most important elements in nutrition epidemiology. These methods have been traditionally used to characterize deficiency stages; and lately, to establish associations between health maintenance and risk factors for chronic diseases. The most common methods, as stated above, of nutrition assessment include (a) Dietary assessment in which information about food intakes is obtained and often used to calculate intake of nutrients

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Public health nutrition in developing countries

(b) Biochemical measures of blood or other body tissues that provide indications of nutritional status and diet composition. (c) Anthropometric assessment that includes measures of body dimensions that reflect long-term effects of diet including growth and body composition. (d) Clinical assessment that includes clinical signs of severe deficiency. A description of nutritional assessment methods and its applications to nutritional epidemiology is presented in the following sections [18]. Dietary methods As mentioned before, the main exposure in nutritional epidemiology is diet. However, diet is not a single exposure but a complex set of exposures that vary over time and in different places. Measurement of dietary intakes is complicated and requires well trained personnel and validated methods. Estimation of continuous levels of exposure to specific dietary variables, like food patterns, is complicated by the daily variation of food intake. Also, the inter-correlation of dietary variables complicates the study of effects associated to independent factors. Individuals are usually unaware of the composition of the foods they consume; hence nutrient composition is usually determined indirectly [5, 7, 13]. In general, in nutritional epidemiology, diet has been studied in terms of nutrient intakes; diet however can also be described in terms of foods, food groups or dietary patterns. Several dietary methods are available; the choice should be guided by the objectives of the study and the characteristics of the study group [5, 7, 13]. The main tools used to assess dietary intakes are short-term recall methods and food frequency questionnaires. ●

Short time recalls and diet records – The most widely used dietary assessment method is the 24 hours recall. It is the basis of several national nutrition surveys and many cohort studies. This method consists of an interview by a nutritionist or trained personnel. The interviewer, generally with the help of food models or standard quantities, collects information on the participant intake in the last 24 hours. The interview lasts approximately 20 minutes and has the advantage that minimum effort is required on the part of the participant [7]. The validity of 24 hours recalls have been assessed by observation in a controlled environment, and application of the questionnaire next day. The results yield that subjects both reported foods that they had not consumed and forgot foods that they had actually eaten [19]. The main limitation of the 24 hours recall method is that food consumption is high variability from day to

Nutrition epidemiology for developing countries

●

35

day. An alternative to address this problem are food diaries. Dietary records or food diaries are detailed meal by meal registers of types and quantities of food consumed during an specific time, generally 3–7 days. Subjects weight each portion before eating, or alternatively household measures can be used. These methods however are time-consuming and typically require literacy compared to 24 hour recalls. The application of short time and diet recall methods to epidemiologic studies is also inappropriate for case control studies, because the exposure of interest might have occurred earlier or later, and the recall might not register it. Multiple 24 hours recalls can be useful for cohort studies; however the costs may be a limitation, particularly in developing countries. These methods can be used for validation or calibration of other methods of dietary assessment more practical for nutritional epidemiology in developing countries [17,18]. Food frequency questionnaires – The food frequency questionnaire (FFQ) approach was developed as a means to measure long term dietary intake. A FFQ has two main components: a list of foods and beverages and a time scheme for the subject to indicate how often he/she consumes each food. A comprehensive assessment of the diet is desirable whenever possible. This is because it is generally impossible to anticipate all the information regarding diet that will be important at the end of data collection. A limited list of foods may leave out items that in retrospect result important. Additionally, sometimes total diet composition is necessary to prevent confounding by other dietary factors (i.e. total energy). Food frequency questionnaires are classified as quantitative and semi-quantitative. The difference between the two is that quantitative questionnaires provide additional information on serving sizes; whereas semi-quantitative questionnaires only assess the type of food and frequency of intake. Evidence suggests that including serving sizes does not represent a significant improvement in assessing diet. Food frequency questionnaires are widely used in nutritional epidemiology. They have great advantages for assessing diet at a population level: they are easy from subjects to complete, often self-administered, and processing is relatively inexpensive [7, 20, 21].

Biochemical methods Gibson [18] classifies biochemical tests as (a) static and (b) functional tests. Static biochemical tests measure a nutrient or a metabolite in fluids or tissues and are useful in identifying intermediate stages of nutrition

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deficiencies when the body stores become depleted. These methods can also be used to assess excess of nutrients (i.e. cholesterol) or reactions to the intake of a specific nutrient (allergic reactions). Static biochemical tests are useful at a population level and have been used in national nutrition surveys. Functional tests assess specific nutrient dependent functions, for example activity of a nutrient dependent enzyme such as Flavin Adenine Dehyrdogenase (FAD) that requires riboflavin [5, 18]. These tests however are not suitable for large-scale nutrition surveys especially in resource poor environments. Anthropometric methods Anthropometric methods involve measurement of physical dimensions of the body and gross composition of the body [18]. These methods are used to assess moderate to severe malnutrition; nevertheless it is impossible to identify specific nutrition deficiencies. The main advantage of anthropometric methods is that they can detect chronic malnutrition. Body composition reflects very accurately nutritional history. Another advantage is that these methods can be performed relatively quickly and inexpensively. Examples of these measures are height, weight, body circumferences, etc. The measurement then are interpreted using indexes like the Body Mass Index (BMI), height to weight circumference or height for age, amongst others [5, 18]. Clinical methods The aim of these methods is to detect signs (manifestations that can be observed) and symptoms (reported by the patients). The assessment is done by physical examination or medical history. Clinical manifestations appear at advanced stages of nutritional deficiencies and often are not very specific. These signs however have become less common with improvements in nutritional status and often require screening large samples. It is recommended to use these methods in combination with laboratory, clinical and/or anthropometric methods [5].

2.3.2

Indices and indicators

Construction of indices is often necessary for the interpretation and the grouping of the four methods previously described. Indices are continuous variables, formed by the combination of two or more measurements, which can be related to characteristics like age, sex or race. Indices are often evaluated at a population level by comparison with predetermined cutoff points. When used to assess the nutrition

Nutrition epidemiology for developing countries

37

status at a population level indices become indicators. Nutritional indicators are widely used in public health or for decision making at a population level. For example, iodine deficiency at the population level is defined as a total goiter rate over 5% in school age children. The proportion of the population with nutrient intakes below the Estimated Average Requirement can also be an indicator of dietary inadequacy. For nutritional epidemiology the selection of indicators is a key issue in the design of studies and evaluations [18, 22, 23]. Inappropriate conclusions may be made if the correct indicator is not selected. For example, body mass index (BMI) which is widely used as an indicator of body composition and overweight (BMI>25) may not be appropriate in pregnant women and/or special populations like athletes. Similarly, certain biochemical indicators of micronutrient status such as serum ferritin and retinol may not work well in populations where infections are common.

2.3.3

Study design

Study design is a critical in nutritional epidemiology and is influenced by a variety of factors. The first element to consider is the purpose or the reason to conduct the research which will determine the type of design (cross-sectional, cohort, case-controls, experimental, etc) and choice of measurements, indices and indicators. The next and equally important consideration is the availability of resources that include time, money and expertise available [3]. Typically, logistic and economic limitations make it impossible to include the entire population in the study. Consequently, as part of the study design, it is important to develop a sampling protocol to select a group of individuals. This sample of individuals ideally should be an accurate representation of the source population and of an adequate size to respond to the objectives of the study. The information obtained in the study will depend on the way these individuals are selected. Hence, it is important to carefully develop a sampling system. The first element to consider in developing a sampling protocol is the availability of a sample frame, or a list of all the individual parts of the population (persons, schools, hospitals, etc). If this information is not available, it is necessary to select the sample using non-probabilistic methods; on the other hand if the sample frame is available it is possible to use probability based sampling protocols. These procedures are usually conducted by people trained in sampling techniques. Several statistical packages (for e.g. EPI-INFO, SAS, STATA) and specialized software packages (e.g. PASS) are available to calculate sample sizes. The World Health

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Organization (WHO) also has a useful resource for calculating a sample size on their website (Box 2.4). Finally, an adequate study design provides the researcher elements of validity, precision and accuracy which are important to minimize bias. A brief description of these constructs is presented in the following sections. Box 2.4 A tool to calculate sample size The STEP-wise approach to surveillance is a program of the WHO to collect standardized information in different countries. This program provides two useful tools to calculate sample size and to determine a sampling frame: the “Sample Size Calculator” and the “Sampling Spreadsheet” which are available online. (http://www.who.int/chp/steps/resources/sampling/en/). The sample size calculator describes the application of the formula that requires information on the level of confidence (for e.g. 95 % confidence), the margin of error (< 0.05) and expected baseline level of the indicators which is assumed to be 0.5 if no information is available. This is followed by adjusting for other factors such as the design effect in case a complex sample design is used, age-sex strata and expected response rate. The sampling spreadsheet provides additional information that is useful for using the following different approaches to obtaining the sample. ● Probability proportional to size sampling ● Simple random sampling ● Weighing your data

Validity is defined as the capacity of reflecting the true situation of the population that is being studied. For a study to have high validity it must measure the exposure, for example diet, at a relevant time, in a relevant population or sample using methods that reflects adequately the exposure and outcome. Validity also assumes that there is no error in the way the information is collected, analyzed and interpreted. Validity can be classified as internal or external. Internal validity refers to the quality of the measurements and procedures inside the study. External validity is the generalizability of the study. In order to have external validity is necessary to first have internal validity. However, a study that is internally valid may have limited external validity which means that the results cannot be applied to the general population [1, 3, 13, 18]. Validity is also used to describe the methods used to assess the exposure or the disease. A valid test is able to distinguish accurately between who has the disease and who does not, or who is exposed and who is not. When validating a test there are two elements to consider: sensitivity and specificity. Sensitivity is defined as the ability of a test to identify correctly those who have the disease (or exposure); while specificity refers to the ability to identify correctly those who do not have the disease (or exposure) (see Box 2.5).

Nutrition epidemiology for developing countries

31

Randomization is the assignment by chance to the treatment or to the control group. This tool helps reduce the chances of selection bias, and also helps to control for confounding factors that otherwise could be overlooked by the researcher [1]. Details on the ideal ways to randomize and allocate treatments are described in The CONSORT (Consolidating Standards of Reporting Trials) statement that was developed and published in the mid 1990s with the aim of improving the quality of the reports of clinical trials [14–16] (Box 2.2). Assessed for eligibility (n= )

E n ro llm e n t

Exclud ed (n=

)

N ot m eeting inclusio n criteria (n = ) R efu sed to participa te (n= ) O ther reasons (n = )

A n alys is

F o llo w -U p

A lloc a tio n

R an dom ize d (n= )

Allo cated to inte rvention (n= ) R eceived allocated inte rvention (n= ) D id not receive allocated inte rvention (n= ) G ive reasons

Los t to follow –u p (n= G ive reasons

)

Allo cated to inte rvention (n= ) R eceived allocated inte rvention (n= ) D id not receive allocated inte rvention (n= ) G ive reasons

Los t to follow –u p (n= G ive reasons

)

D iscontinued interven tion (n = ) G ive reasons

D iscontinued interven tion (n = ) G ive reasons

An alyzed (n= )

An alyzed (n= )

Exclud ed from analysis (n= G ive reasons

)

Exclud ed from analysis (n= G ive reasons

)

2.2 CONSORT Statement 2001 flow diagram.

Another advantage of RCTs is the usage of a placebo (indistinguishable from the treatment), which allows blinding to the treatment. In a single

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Public health nutrition in developing countries

A test can also be evaluated by considering its predictive value; this is described as the proportion of individuals classified by the test as diseased that actually have the disease (positive predictive value), or the proportion of individuals classified by the test as not having the disease that are truly disease free (negative predictive value). These two values depend also on the prevalence of the disease: when prevalence is high it is more probable to correctly identify subjects as diseased [1, 3, 13, 18]. Precision is defined as the degree to which repeated measures of the same variable yield the same value. This is also known as reproducibility or reliability. For a study to achieve internal validity it is necessary to consider the assessment of precision during the study design. Typically, replicate observations are recommended. A way to determine the reproducibility of the measures is by using the coefficient of variation (CV = standard deviation*100%/mean). Precision is a function of two elements: the random measurement error and the actual change in the measurement induced by time. Both factors should be considered by the study design. Some strategies have been proposed to increase the precision of measurements related to nutrition: ●

●

●

● ●

Compiling an operations manual with clear guidelines for taking each measurement. Training all the examiners to use the standardized techniques consistently. The measurements should be consistent between different examiners. Selecting and standardizing all the instruments used by data collection. Testing, refining and validating questionnaires. Reducing the effect of random errors by repeating all the measurements (when possible) [24, 25].

Accuracy is used to describe the extent to which the measurement is close to the true value. An accurate measurement needs to be precise, but a precise measurement is not necessarily accurate; it might be that the procedure always yields the same result (precise) but the result might not be the correct (inaccurate). This type of error is defined as systematic error or bias. To achieve accuracy is important to consider the following strategies: ● ● ● ●

Making unobtrusive measurements, Blinding, Adequate calibration of the instruments, and Training of the personnel that conduct the measurements.

Because an accurate result requires precision the recommendations described earlier also apply to this section.

Nutrition epidemiology for developing countries

41

Sources of measurement error – Error in nutritional epidemiology is classified as “random” or “systematic”. Random error is the one that generates a deviation from the correct result only by chance and can result from (a) individual biological variation, (b) an inadequate sampling procedure or (c) a non systematic measurement error. Random error is very common in diet assessment; the high individual variations during time may lead to inaccurate conclusions, by showing associations with outcomes that are only product of chance. Random error can be minimized by increasing precision and accuracy; nevertheless, it can never be completely eliminated [1, 3, 13, 18]. As mentioned before, bias is defined as a systematic error. The most common biases are selection and information bias. Selection bias happens when the subjects included in the study are systematically different than those that were not included; this makes it impossible to generalize the results to the entire population. An example is when people that have an inadequate dietary intake consistently refuse to participate in the study; in that case, the results can only be applied to the sector of the population that has adequate dietary intakes. Information or misclassification bias can be introduced on a variety of ways: not calibrated instruments, inaccurate tests, observer bias, untrained personnel, etc. An example is a 24 hours recall that consistently underestimates fat intake [18]. Confounding is a type of bias that masks the true relationship between an exposure and an outcome. A confounder is a variable that is distributed differently in the exposed and unexposed groups, and that affects the outcome being assessed. For example, in a study looking at the relationship between alcohol consumption and colon cancer, the association might be confounded by smoking: smoking increases the risk of colon cancer and people than drink are more likely to smoke. In this case alcohol consumption might appear to cause colon cancer, but the actual factor increasing the risk among the exposed is smoking. For a variable to be a confounder it must be related to the outcome, related to the disease but not be an intermediate in the causation pathway. For example, HDL cholesterol is not a confounder in the relationship between physical activity and cardiovascular diseases: physical activity prevents cardiovascular diseases by increasing HDL cholesterol. Typical confounders are age, gender and race/ethnicity. It is important to consider all possible confounders since the design stage to be able to account for them during the analysis and interpretation of the results. A statistical term that also influences the relationships between exposure and outcome is the interaction or effect modification. Interaction happens when the outcome in the presence of two or more risk factors differs from the outcome expected from the individual

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effects. There are many methods to control for confounding or address effect modification during the analysis; nevertheless none of these methods can be used if confounding and interaction are not considered in the stage of design of the study [1, 3, 13, 18].

2.3.4 Interpretation of findings The presentation of findings from epidemiological studies varies widely; it typically includes measures of variability and statistical significance of the associations. For example, inclusion of 95% confidence intervals for estimates is highly recommended rather than just ‘p’ values. The measures of variability can be calculated for either measures of central tendency such as group means, or for measures of association such as an odds ratio or relative risk as shown in Box 2.7. Box 2.7 Important definitions: measures of association Risk- it is defined as the incidence of disease in a population and is primarily used in cohort studies, where it is possible to estimate the incidence in the total population. For example if 10 patients experience a heart-attack in a cohort of 100 patients, the risk is 10/100=0.1. Relative risk (RR) – this measure of association is defined as the risk in the exposed divided by the risk in the unexposed. For example if the incidence of heart attacks in the exposed group was 20/50=0.4 and the incidence in the unexposed group was 10/50 = 0.2 resulting in a RR = 0.4/0.2 = 2. The exposed have twice the risk of the unexposed of suffering a heart attack. Odds – it is the probability of an event happening divided by the probability of the event not happening. For example, the probability of having a heart attack of 50-year-old man is 0.1. Then the odds of having a heart attack are 0.1/(1 0.9)=0.11. Odds ratio (OR) – this measure of association is primarily used in case control studies, where the risk cannot be determined. It is obtained by dividing the odds of being exposed of the cases by the odds of being exposed of the controls. For example, the odds of being a high fat consumer (or being exposed) for persons that suffered a heart attack (cases) is 0.33; while the odds of being a high fat consumer in persons that did not suffer a heart attack is 0.11, then the OR=0.33/ 0.11= 3. When the sample is big, the OR approximates the relative risk.

Since there is considerable variability in how studies are conducted both in terms of the study design and study population, tools such as metaanalyses that combine the results of several studies have become popular. They are particularly useful to guide policy and reduce problems associated with inadequate power due to limited sample size and contradictory findings. Typically meta-analyses have been done primarily using data from well designed RCTs. Estimates from each study are included and weighted to generate weighted mean difference or risk ratio. The Cochrane Group is known for conducting this kind of analysis and provides stringent criteria for the inclusion of well designed intervention trials in the

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calculation of the weighted estimates. Several methodological issues including the role of publication bias need to be considered while interpreting results from systematic review and meta-analysis [26]. There are several examples of meta-analyses in public health nutrition that have important policy implications. Of note is the meta-analysis that evaluated several large community-based trials of vitamin A supplementation on child mortality and found a protective effect [27]. In contrast, a recent metaanalysis evaluated the impact of micronutrient interventions on child growth and found that only multiple micronutrient interventions were beneficial but the effect size was small indicating the need for other strategies [28].

2.4

Importance of nutrition epidemiology in developing countries

Nutritional epidemiology in developing countries faces greater and more demanding challenges. The health status of developing countries has historically been characterized by predominant infectious diseases. In this context, undernutrition and micronutrient deficiencies are the main focus of nutritional epidemiology, since they aggravate the severity and duration of infectious diseases. Malnutrition also slows economic growth and perpetuates poverty; recent work has shown the direct and indirect effects on productivity that are mediated via poor physical status and/or poor cognitive function as well as increased health care costs [29]. More recently, however, chronic diseases that were considered characteristic of industrialized countries [30] have dramatically increased in the less developed countries (LDC). Cardiovascular disease (CVD) is the leading cause of death worldwide and LDC account for ~80% of all these deaths [31]. The traditional approach to understanding nutrition related problems is therefore no longer adequate in the developing world that is facing the dual burden of undernutrition and overnutrition. “Transitional societies” who were previously low-income societies now face significant improvements in income that affect disease and dietary patterns [32–34]. Epidemiologic transition is defined as the shift in morbidity and mortality causes, from mainly communicable infectious diseases to non communicable chronic diseases. This transition is intimately related to the nutrition transition, defined as the rapid changes in dietary patterns, characterized by an increase in fat intake and a decrease in the consumption of traditional foods; that changes modify the epidemiology of overweight and undernutrition. In low income countries these changes are occurring in an accelerated and polarized way. Communities with both under and overweight individuals are common in many developing countries like India, Brazil, China and the Russian Federation. This phenomenon may

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Public health nutrition in developing countries

be explained by dramatic changes in dietary patterns and physical activity. Rapid shifts in income, educational levels, urbanization, globalization, and major sources of energy are some of the explanations for the rapid changes in dietary patterns. Technological resources, less activity at work and at school, insecurity and unplanned urbanization decrease physical activity, contributing also to nutritional and epidemiologic transitions [35, 36]. Another important factor in the rapid onset of obesity and nutrition related chronic diseases are demographic changes. An increase in life expectancy and a decrease in birth rates have changed the age distribution of transitional societies. The proportion of the population over 60 years of age is growing in these countries. This sector of the population is at a higher risk to suffer chronic diseases and impose a higher burden to the health system [30]. Nutritional epidemiology thus plays a key role in addressing the challenges faced by developing countries. Three main challenges have been identified: addressing the pending burden of undernutrition and micronutrient deficiencies; prevention of diet related chronic diseases with a life-course perspective; and achieving nutrition for optimal health and well-being across the lifespan or healthy aging. Nutrition status of the population is determined by complex interactions of socioeconomic and environmental factors, along with genetic determinants. It is impossible to address the current challenges without knowledge and understanding of nutrition and epidemiologic determinants. Nutritional epidemiology provides scientific tools to better understand these determinants and implement cost-effective approaches; evidence based interventions and policies that will be more effective in improving nutritional status of the population [29] which calls for the timely and appropriate application of nutritional epidemiology in developing countries that are undergoing nutritional and epidemiologic transitions.

2.5

Nutrition epidemiology and public health nutrition

Nutritional epidemiology is the basis for public health nutrition. Studies conducted at a population level relating diet and nutrition with health outcomes provide scientific information to develop interventions and policies which in turn can improve the nutritional and health status of the population. In light of the nutritional and epidemiologic panorama and the limited resources available to address these situations, nutritional epidemiology is an important tool in designing, evaluating and renewing interventions and policies. The information obtained by this discipline can be use to improve the design and implementation of programs. For developing countries the application of nutritional epidemiology in the form of public health nutrition is especially relevant considering all the challenges that were previously described. For these countries it is

Nutrition epidemiology for developing countries

45

important to find cost effective interventions; that is, interventions that provide greater benefits than the economic, human and material resources invested in their implementation. The high cost benefit of several nutrition interventions (like promoting breastfeeding) has been estimated using well designed epidemiological studies [29]. Currently, programs that can prevent or reduce malnutrition are not being effectively implemented or scaled up in most regions of the world; particularly in developing countries where service delivery mechanism is inadequate and utilization of identified solution is low. The development and implementation of health and nutrition programs depends on policy makers, program planners and implementers, markets and civil society, along with the behaviours of households and individuals. Research focused on delivery, utilization and evaluation of nutrition programs and services helps to build evidence base information to guide decisions and select the best options for delivering interventions [13, 29, 37]. The crucial element in the development of effective interventions is the translation from scientific research, discussion and assessment, to government, industry and civil society. It has been proposed that the main challenges for public health nutrition are to agree on a suitable evidence based approach, develop a conceptual framework (Box 2.8) for decision making, and act professionally. Decisions in public health nutrition should be rational and evidence based. Nevertheless, this raises the concern of the quality and quantity of the information available for decision-makers. The scientific arena is filled with contradictions, and judgments are usually cautious with lack of adequate convincing information to policy makers. Also, it is hard to define the amount of information needed to undertake an action. A way around these limitations is designing research that can be applied to develop nutrition interventions [38–40]. Box 2.8 Definition of conceptual framework A conceptual or logical framework is used in research to define a problem, outline an approach to an idea, or to define a course of action. All the components of the research, the approach to the problem or hypothesis and the potential course should be represented in the conceptual framework. It can be used as a planning and guiding tool throughout all the research process: before research, during research and after research. A well designed framework is important for nutritional epidemiology to analyze the results from epidemiological trials; and for public health nutrition in the translation of these results into programs and interventions. The WHO in its “Progress newsletter”, 2005 states that “in using a conceptual framework it is advisable to see it not as a prescriptive model but rather as a framework for stimulating thinking about the potential options and opportunities for enhancing the chances for research utilization”. It also proposes six guiding principles to develop a framework with practical applications:

46

Public health nutrition in developing countries

1. The different models presented in the literature share common underlying concepts and elements. It is possible to take that elements and use their essence for practical application. 2. Models created for research utilization are often complex and thus hard to use for research application. A practical model simplifies the pathways to facilitate implementation. 3. It is possible to identify common factors that facilitate or impede research utilization. 4. It is useful to classify the different factors and elements influencing research in three phases: pre-research, during research and after research. Although, it is important to consider that in the practicum they represent a continuous. 5. A conceptual framework can be utilized to assess research utilization along different application of research results for example “initiation of further research; advocacy or a new program, policy or practice”. 6. A conceptual framework should be able to capture broader contextual factors that can influence research and research implementation and “should refrain from imposing a false sense of order on what is often a chaotic and seemingly non-rational process” [41]. An example of a well designed conceptual framework in nutrition is the UNICEF malnutrition framework presented on Figure 2.1.

There are many examples of the application of nutritional epidemiology to public health. The most well known is the development of nutritional guidelines. The constant improvement and reassessment of nutritional guidelines is based in epidemiologic studies that assess the relationship between diet and health. An extensive discussion on the influence of nutritional epidemiology on the development of dietary guidelines in the United States was published by Byers in 1999 [4]. Examples of the applications of nutritional epidemiology to public health also exist in developing countries. A compilation of science based nutrition and physical activity interventions can be found in the report of the Pan-American Health Organization (PAHO), “Nutrition and an Active Life: from Knowledge to Action” [41]. Some of the conclusions of this compendium are the following: ●

●

●

●

●

There is sufficient evidence on the impact of malnutrition on the health of individuals and populations to confirm the need for effective, low-cost programs to reduce its prevalence. The successful experiences described on the book are flexible enough to adapt to a wide variety of circumstances. These models hold great potential for successful adoption in other parts of the world. To achieve the expected results, technical expertise and support of diverse disciplines are required. All the experiences required the collaboration of a broad segment of interests in the design and implementation of the interventions. One of the essential elements to success is the full empowerment of all the institutions involved and the civil society in terms of project objectives and their active participation.

Nutrition epidemiology for developing countries ●

47

To demonstrate their achievements, programs should conduct impact evaluations [42].

In conclusion, a good understanding and appropriate application of the principles of nutritional epidemiology is crucial for developing countries to improve the health status and well-being of their populations. This chapter provides an overview of the main elements and uses of nutritional epidemiology in developing countries and shows how it can be used in many aspects of nutritional sciences: from improvements in nutritional assessment to the application of research to public health nutrition that are urgently needed.

References 1. GORDIS L (2008). Epidemiology, 4th edition, Saunders (ed), Philadelphia. 2. Encyclopaedia Britannica. 3. M A R G E T T S B M and N E L S O N M (1997). Design Concepts in Nutritional Epidemiology, 2nd edition, Oxford: Oxford University Press. 4. B Y E R S T (1999). The role of epidemiology in developing nutritional recommendations: past, present, and future. Am J Clin Nutr 69, no. 6, pp. 1304S– 1308S. 5. ZIEGLER EE and LJ FILER (1996). Present Knowledge in Nutrition, 7th edition, Washington: ILSI Press. 6. VENEMAN AM (2007). UNICEF report on state of the world children 2007: the double advantage of gender equality. Assist Inferm Ric 26, no. 1, pp. 46–50. 7. ROTHMAN KJ, GREENLAND S, and LASH TL (2008). Modern Epidemiology, 3rd edition, Philadelphia: Lippincot Williams and Wilkins. 8. FAO, Food Balance Sheets. 2009. 9. RAMAKRISHNAN U, BARNHART H, SCHROEDER DG, STEIN AD, MARTORELL R (1999). EARLY CHILDHOOD NUTRITION , education and fertility milestones in GUATEMALA . J NUTR 129, no. 12, pp. 2196–2202. 10. STEIN AD, MELGAR P , HODDINOTT J, MARTORELL R (2008). Cohort Profile: the Institute of Nutrition of Central America and Panama (INCAP) Nutrition Trial Cohort Study. Int J Epidemiol 37, no. 4, pp. 716–720. 11. BARROS FC, VICTORA CG and VAUGHAN JP (1990). The Pelotas (Brazil) birth cohort study 1982-1987: strategies for following up 6,000 children in a developing country. Paediatr Perinat Epidemiol 4, no. 2, pp. 205–220. 12. TAMAKOSHI A, YOSHIMURA T, INABA Y, ITO Y, WATANABE Y, FUKUDA K, ISO H; JACC Study Group (2005). Profile of the JACC study. J Epidemiol 15, no. 1, pp. S4–8. 13. LANGSETH L (1996). Nutritional Epidemiology: Possibilities and Limitations, Belgium: ILSI Europe. 14. HOPEWEL S , CLARKE M , MOHER D, WAGER E, MIDDLETON P , ALTMAN DG, SCHULZ KF, The CG (2008). [CONSORT for reporting randomized controlled trials in journal and conference abstracts: explanation and elaboration]. Zhong Xi Yi Jie He Xue Bao 6, no. 3, pp. 221–232. 15. KNOBLOCH K , GOHRITZ A and VOGT PM (2008). CONSORT and QUOROM statements revisited: standards of reporting of randomized controlled trials in general surgery. Ann Surg 248, no. 6, pp. 1106–1107; discussion 1107–1108.

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and ALTMAN DG (2001). The CONSORT statement: revised recommendations for improving the quality of reports of parallel group randomized trials. BMC Med Res Methodol 1, p. 2. SOLOMONS NW and VALDES - RAMOS R (2002). Dietary assessment tools for developing countries for use in multi-centric, collaborative protocols. Public Health Nutr 5, no. 6A, p. 955–968. GIBSON R (2005). Principles of Nutritional Assessment, 2nd edition, Oxford: Oxford University Press. KARVETTI RL and KNUTS LR (1992). Validity of the estimated food diary: comparison of 2-day recorded and observed food and nutrient intakes. J Am Diet Assoc 92, no. 5, pp. 580–584. WILLETT WC and HU FB (2007). The food frequency questionnaire. Cancer Epidemiol Biomarkers Prev 16, no. 1, pp. 182–183. DELCOURT C, CUBEAU J , BALKAU B , PAPOZ L (1994). Limitations of the correlation coefficient in the validation of diet assessment methods. CODIAB-INSERMZENECA Pharma Study Group. Epidemiology 5, no. 5, pp. 518–524. HABICHT JP (2000). Comparing the quality of indicators of nutritional status by receiver operating characteristic analysis or by standardized differences. Am J Clin Nutr 71, no. 3, pp. 672–673. HABICHT JP and STOLTZFUS RJ (1997). What do indicators indicate? Am J Clin Nutr 66, no. 1, pp. 190–191. CUMMINGS GS and CROWELL RD (1998). Source of error in clinical assessment of innominate rotation. A special communication. Phys Ther 68, no. 1, p. 77–78. CUMMINGS KM , KIRSCHT JP , BECKER MH and LEVIN NW (1984). Construct validity comparisons of three methods for measuring patient compliance. Health Serv Res 19, no. 1, pp. 103–116. STERNE JAC and EGGER M (2005). Regression methods to detect publication and other bias in meta-analysis. In: ROTHSTEIN HR, SUTTON AJ , BORENSTEIN M (eds.) Publication Bias in Meta-Analysis: Prevention, Assessment and Adjustment. New York: John Wiley & Sons, pp. 99–110. FAW Z I WW , C H A L M E R S T C , H E R R E R A M G , M O S T E L L E R F (1993). vitamin a supplementation and child mortality. A meta-analysis. JAMA 269, no. 7, pp. 898–903. RAMAKRISHNAN U , NGUYEN P and MARTORELL R (2009). Effects of micronutrients on growth of children under 5 years of age: meta-analyses of single and multiple micronutrient interventions. Am J Clin Nutr 89, pp. 191–203. Repositioning nutrition as central to development. A strategy for large-scale action (2006). The World Bank. UAUY R and KAIN J (2002). The epidemiological transition: need to incorporate obesity prevention into nutrition programmes. Public Health Nutr 5, no. 1A, pp. 223–229. REDDY KS and YUSUF S (1998). Emerging epidemic of cardiovascular disease in developing countries. Circulation 97, pp. 596–601. POPKIN BM and DU S (2003). Dynamics of the nutrition transition toward the animal foods sector in China and its implications: a worried perspective. J Nutr 133, Suppl. 2, pp. 3898S–3906S. POPKIN BM and GORDON -LARSEN P (2004). The nutrition transition: worldwide obesity dynamics and their determinants. Int J Obes Relat Metab Disord 28, Suppl 3, pp. S2–S9.

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35. 36. 37. 38. 39.

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and ZHAI F (2002). Understanding the nutrition transition: measuring rapid dietary changes in transitional countries. Public Health Nutr 5, no. 6A, pp. 947–953. POPKIN BM (2003). Dynamics of the nutrition transition and its implications for the developing world. Forum Nutr 56, pp. 262–264. POPKIN BM (2004). The nutrition transition: an overview of world patterns of change. Nutr Rev 62, no. 7 Pt 2, pp. S140–S143. LABARTHE MC (2008). [1/10. Nutrition, a public health priority]. Soins 722, pp. 59–60. Unknown. Nutrition and health transition in the developing world: the time to act. Public Health Nutr 5, no. 1A, pp. 279–280. MADANAT HN , TROUTMAN KP and AL -MADI B (2008). The nutrition transition in Jordan: the political, economic and food consumption contexts. Promot Educ 15, no. 1, pp. 6–10. VERHEIJDEN MW and KOK FJ (2005). Public health impact of community-based nutrition and lifestyle interventions. Eur J Clin Nutr 59, Suppl 1, pp. S66–S75; discussion S76. WHO (2005). The challenge of putting research to use. Progress in Reproductive Health Research, p. 70. FREIRE W (2005). Nutrition and Active Life: From Knowledge to Action, Paho (ed), Washington DC.

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Undernutrition in children

3 Undernutrition in children Sheila C. Vir

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

3.1

Undernutrition, child survival and millennium development goals

The term ‘undernutrition’ comprises both protein energy malnutrition (PEM) and micronutrient malnutrition (MNM). “Undernutrition includes being underweight for one’s age, too short for one’s age (stunting), dangerously thin for one’s height (wasting) and deficient in vitamins and minerals (micronutrient deficiencies)” [1]. Malnutrition is commonly used as an alternative to undernutrition but technically it is a broad term which also refers to overnutrition [1]. Undernutrition, as presented in Fig. 3.1, contributes to more than one-third of child deaths and more than 10% of the global disease burden [1, 2, 3]. This implies that one in three children who die from pneumonia, diarrhea and other illness would survive if these children were not undernourished. Children with severe acute malnutrition are at the highest risk of dying – over nine times more likely to die than children who are not undernourished [3]. On the other hand, moderate and mildly undernourished children are at lower risk of dying but are large in numbers in developing countries [1]. Undernourished children who survive may suffer irreversible damage to their development. Undernutrition, an important determinant of maternal and child health, has significant adverse effect on survival and growth as well as cognitive and physical development [3]. Overcoming undernutrition is critical with

50

Undernutrition in children 3 7% N e on ata l

1 3% 2% 4% In ju rie s

N e on ata l A cute respiratory infectio n s G lo ba lly, u nd ern utrition con tribu tes to m ore tha n o n e th ird o f chid d ea ths

4% M ea sle s 7% M alaria

51

D ia rrh oe a M alaria M ea sle s In ju rie s H IV / A ID S O th er

1 6% D ia rrh oe a 1 7% A cute respiratory infectio n s

3.1 Undernutrition and mortality in children under-5 years old [1].

reference to not only the first Millennium Development Goal (MDG) to eradicate extreme poverty and hunger [4] – the specific target of the first Millennium Development Goal is to reduce the prevalence of underweight by 50 per cent among children younger than 5 years between 1990 and 2015 – but influences the achievement of the other MDG goals pertaining to child survival, maternal health, education, gender equity (Table 3.1) [5]. Undernutrition slows down national progress. “One underweight or one undernourished child is an individual tragedy. But multiplied by tens and millions, undernutrition becomes a global threat to societies, to economies and to generations to come” [6]. Table 3.1 Millennium Development Goals (MDG) and Nutrition Effect [5]

Goal 1 Goal 2 Goal 3 Goal 4 Goal 5 Goal 6

MDG Goal

Nutrition Effect (if Goal not achieved)

Eradicate extreme poverty and hunger Achieve universal primary education Promote gender equality and empower women Reduce child mortality Improves maternal health

decreased human capital, adverse impact on cognitive and physical development reduced school attendance, retention and performance reduced access to food, health and care resources – female biases increased burden of disease and death compromised maternal health – maternal stunting and iron and iodine deficiencies increased risk of HIV transmission, compromise antiretroviral therapy, and hasten the onset of full blown AIDS and premature deaths

Combat HIV/AIDS, malaria and other diseases

This chapter focuses on undernutrition with special reference to stunting, underweight and wasting. Details on micronutrient deficiencies in children are covered in other chapters of this book.

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3.2

Undernutrition in children – stunting, underweight and wasting

UNICEF Report 2009 [1] estimates that there are globally 195 million under 5 years who are stunted (low height for age) and about 129 million who are underweight (low weight for age). Weight is an indicator of acute deficiencies. Stunting reflects a chronic restriction of linear growth whereas wasting (low weight for height) reflects acute weight loss and is used for identification of children with severe acute malnutrition (SAM). Stunting is considered a better overall predictor of undernutrition than underweight [3]. It has been argued that in countries undergoing nutrition transition, with rapid economic growth which presents with a child nutrition scenario of decrease in protein energy malnutrition and an associated rise in obesity prevalence, monitoring stunting and wasting in young children is more appropriate than monitoring underweight, a composite measure of both stunting and wasting [7]. Stunting is considered an appropriate measure since in a developing country situation, the environment is often not conducive for children who are stunted early in life to gain optimum height. On the other hand, underweight can be overcome with appropriate nutrition and health improvements. An underweight child at the age of 4–5 years may present with normal weight for age despite slow growth and development that may have occurred due to deficiencies during pregnancy or infancy [1]. A child who is underweight can also be stunted or wasted or both. It has been observed that severe wasting is not accompanied by stunting in 80–100% of younger children and 40–50% of older children [2]. Moreover, countries with similar stunting rates can have vast difference in prevalence rates of severe wasting [8].

3.3

Undernutrition and age trend

Earlier analysis of growth faltering in children, using the National Centre for Health Statistics (NCHS) reference with primary focus only on assessment of weight for age, had indicated that faltering starts at about three months of life in developing country settings [9–12]. Pattern of growth faltering with age was studied in 2001 by Shrimpton et al [13] by analyzing data of 39 national surveys. It was observed that at birth the average weight for age, length for age and weight for length were quite close to NCHS reference (Figure 3.2). However, these three growth indices presented a different growth pattern in the first three months of life. As indicated in Fig. 3.2, mean weight for age (underweight) was noted to start faltering at about three months of age and there was continuous and rapid decline until about 12 months. The

Undernutrition in children

53

Z -sc ore (N C H S )

G lobal M ean W /A, L/A and W /L 1 0,7 5 0,5 0,2 5 0 -0,25 -0,5 -0,75 -1 -1,25 -1,5 -1,75 -2

W a sting (W eig ht for L ength ) U nd erw eig ht (W eig ht for a ge) Stun ting (Leng th for ag e) 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 A g e (m on ths) W eight for Leng th

W eight for A g e

Len gth fo r A g e

3.2 Mean anthropometric z scores by age for all 39 studies (children 0–59 months), relative to the NCHS reference [13].

decline was observed to continue but was slower until about 18–19 months of age. On the other hand, the process of stunting began at birth and continued during the first 3 years of life. After the first three months, fall in stunting and underweight was noted to be very similar upto 12 months. Stunting continued to decrease upto 40 months of age. Stunting that occurred in the first 3 years was reported to be irreversible. On the other hand, weight for length (wasting) decrease was concentrated in the period 3–15 months followed by rapid improvement. The age-wise prevalence of undernutrition in developing countries at the national or regional level, using NCHS reference, has traditionally been reported for six monthly or 12 monthly intervals and not monthwise. In India, the analysis of national data of child undernutrition revealed that undernutrition (weight for age) prevalence in children was highest in the age group 12–24 months as compared to 6–12 months or > 24–36 months, >36–48 months or >48–60 months. Based on this interpretation, a shift in the national programme focus to children under 2 years instead of those under 5 years has been recommended. In 2001, an analysis of month-wise data (Figure 3.3) of underweight children between 3 and 24 months was reported from Uttar Pradesh, India [14]. The analysis, using NCHS standards, z scores classification (median, –2 SD, –3 SD), revealed that the highest proportion of underweight children were in the age group of 8–11 months [14]. This problematic age of late infancy was observed to coincide with a significant increase in nutritional requirement of infants during this period which are often not met due to poor complementary feeding practices, limited capacity for mastication and stomach volume as well as increased activity, exposure to environment and susceptibility to diarrhea. It was emphasized that actions for preventing undernutrition in children should concentrate efforts primarily on under ones [15].

Public health nutrition in developing countries

54 80

PE R C EN TA G E

70 60 50 40 30 20 10 0 3

4

5

6

7

8

9

10 11 12 13 14 15 16 17 18 19 20 21 22 23 A GE (M O NTH S)

3.3 Month-wise undernutrition prevalence in children 3–23 months [14].

Using the revised WHO Child Growth Standards, it is now evident that undernutrition in the first six months of life itself is a serious problem [16]. It was emphasized in 2008 that such a growth trend in the first half of pregnancy was not apparent earlier with the limitation of using the National Centre for Health Statistics (NCHS) reference which incorrectly made it appear that growth was protected during the first months of life [16]. This is possibly due to the fact that NCHS reference used measured length at birth and 3 months, while a curve fitting method was used for intermediate ages [17, 18]. The WHO standard (Box 3.1), on the other hand, provides a better description of physiological, growth since the standard is based on empirical data at birth, weeks 2, 4 and 6 and monthly thereafter in the first year [17, 18]. Using the WHO standards, it is now observed (Figure 3.5) that stunting prevalence increases progressively and reaches a plateau at around 24 months of age while the prevalence of severe wasting is higher at younger age and then declines and reaches a plateau at 24 months [8]. The worldwide growth faltering pattern study, based on analysis of data of 54 countries using WHO standards show “that growth faltering in early childhood is even more pronounced than suggested by previous analysis based on the National centre for Health Statistics reference” [17]. Analysis of India’s third National Health and Family Survey (NFHS3) data on month-wise prevalence of undernutrition in Indian children below 5 years, using WHO standards, for the period 2005–2006 presents a similar trend as noted in the global analysis [21] – Fig. 3.4. The NFHS 3 data was also analysed to study the month-wise trend of severely wasted, severely stunted and severely underweight children [22]. The findings are presented in Figs. 3.4 and 3.5. As indicated in Fig. 3.4, the proportion of children with stunting and underweight continued to increase and was highest by 24 months of age while the trend in

Undernutrition in children

55

Box 3.1 WHO growth standards National Centre for Health Statistics (NCHS) reference, also known as NCHS/ WHO International Growth Reference, was recommended three decades ago by WHO [19]. The NCHS reference was based on data on longitudinal study of children of European ancestry from a single community in the United States which was collected between 1929 and 1975 [20]. These children were measured every three months. Majority of these infants were fed artificial milk. The limitation of NCHS was that the measurement was not adequate to describe the rapid and changing rate of growth in early infancy. Additionally, there were shortcomings inherent in the statistical methods available and used. In 1990, following an in-depth analysis of growth data from breastfed infants, a review group recommended that a new growth standard be constructed. The emphasis was on standard rather than a reference to be constructed. A reference is simply applied for comparison whereas a standard serves for both comparison as well as a basis for assessing the adequacy of growth. The standard could therefore be used as a tool for value judgement. Between July 1997 and December 2003, a WHO Multicentric Growth Reference Study (MGRS) was thus conducted [20]. The study involved exclusive breastfed children in six sites of different regions of the world – Brazil, Ghana, India, Norway, Oman and the USA. In Ghana, India and Oman, children from effluent economic groups whose growth was not environmentally constrained were selected. Term low birth weight (<2500 grams) were not excluded. The MGRS comprised information from a longitudinal follow-up from birth to 24 months with a cross-sectoral component of children 18–71 months. The study showed that children everywhere grow in similar pattern when their nutrition, health and care needs are met. In 2006, new World Health Organisation standards (WHO standard) were introduced on the basis of the MGRS. The new WHO growth standard identifies breastfed child as the normative model for growth and development standards, depicts normal early childhood growth under optimal environmental conditions, and can be used to assess children regardless of ethnicity, socioeconomic status and type of feeding. The WHO standard describes how children should grow when not only free of disease but also when reared following healthy practices such as breastfeeding and non-smoking environment. Differences of WHO standard compared to previously recommended NCHS/WHO international reference are particularly important in infancy. According to WHO Multicentric Growth Reference Study Group [20], the following differences are considered noteworthy – stunting will be greater throughout childhood, substantial increase in underweight rates during 0–6 months and a decrease thereafter, wasting rates will be substantially higher during infancy (i.e. up to 70 cm length).

severe wasting showed a decreasing trend in the first 12 months. Severe undernutrition prevalence, as measured by all the three indicators, is about 10 percent in the first six months of life [22]. Severe wasting shows a decreasing trend upto 16 months of age while in the first 22–24 months, severe stunting and severe underweight show an increasing trend. The analysis clearly reveals that undernutrition sets in the first two months of life itself. The findings reveal that undernutrition during the first six months of life is a much greater problem and needs attention. It is evident from these analysis using WHO standards that low birth rate (LBW) (Box 3.2) and its association with neonatal deaths (Fig. 3.6) and undernutrition in the first six months of life cannot be ignored. For preventing growth failure in children, prenatal and early life interventions are critical.

Public health nutrition in developing countries

P erce n ta ge (% )

56 100 90 80 70 60 50 40 30 20 10 0

U nd erw e igh t Stun ting

W a sting S e verely w asted

2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52 54 56 58 A g e in m on ths

P ercen ta ge (% )

3.4 Prevalence of underweight by age in children below 5 years [21, 22]. 100 90 80 70 60 50 40 30 20 10 0

Se ve rely Underweight Se ve rely Stunte d Se ve rely Wasted

2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 3840 42 44 46 48 50 52 54 56 58 Ag e in m on ths

3.5 Month-wise prevalence of severe undernutrition in children in India [22].

A total of 19 million newborns per year are born LBW. India accounts for 7.8 millions LBW babies born per year in developing world (Figure 3.7). India and Pakistan together contribute to almost half of the world’s LBW each year. India contributes to 39% while Pakistan contributes to 9%. The estimations on LBW incidence rate reported have limitations since almost 60% of newborns in developing countries are not weighed at birth [1].

3.4

Stunting, underweight and wasting – an overview of the global situation

UNICEF report 2009 on undernutrition [1] indicates that of the 195 million stunted children under 5 years of age in developing world, 90% live in Asia and Africa. Eighty percent of the world’s stunted children live in 24 countries. Five countries together (four of these 5 countries being from Asia) contribute to almost 50% of the global under 5 years stunted children – India (31.2%), China (6.5%), Nigeria (5.2%), Pakistan (5.1%) and Indonesia (3.9%) – Table 3.3.

Undernutrition in children

57

Box 3.2 Low birth weight (LBW) Low birth weight has been defined by the World Health Organisation [23] as weight at birth, irrespective of gestation age, of less than 2500 g (upto and including 2499 g). Birth weight is governed by two major processes: duration of gestation and intrauterine growth rate. LBW is either the result of preterm birth (before 37 weeks of gestation) or due to restricted foetal (intrauterine) growth or intrauterine growth restriction (IUGR). In developed countries, IUGR (birth weight <2500 g and gestation age >37weeks) is far less prevalent. Most LBW babies in developed world are premature rather than growth retarded. In contrast in developing countries, IUGR accounts for the majority of LBW [24]. Small for gestational age (SGA) is often used as a proxy for IUGR. WHO defines SGA as birth weight below the tenth percentile for gestational age based on sex-specific reference. Some SGA infants may be constitutionally small and not truly growth restricted. The determinants of IUGR are low energy intake, poor weight gain during pregnancy, low pre-pregnancy BMI, short stature, malaria, cigarette smoking, pregnancy induced hypertension, ethnic origin and other genetic factors. LBW contributes to a range of poor health outcomes. Infants born at term weighing 1500–1999 grams are 8.1 times more likely to die and those weighing 2000–2099 who are 2.8 times more likely to die from all causes during the neonatal period than are those weighing 2499 g at birth [3]. LBW, which is related to maternal malnutrition, is a causal factor in 60–80% neonatal deaths (Figure 3.6) [25]. LBW who survive have a higher chance of facing compromised health care and entering a vicious cycle of ill health and undernutrition. The level of LBW in developing countries is 16.5% – almost the double in the developed regions with 7% LBW [26]. There is significant variation in LBW incidence across six main geographical regions [26]. LBW rate is estimated to be 18% in Asia, 14 % in Africa and 6.4% in Europe (Table 3.2). Direct causes of neonatal deaths, 200*

Low birth weight, which is related to maternal malnutrition, is a causal factor in 60-80 per cent of neonatal deaths. C on ge nita l (7% ) Teta nus (7 % ) D ia rrho ea (3% ) Pre terrn (27 % ) As ph yx ia (23 % Se p sis/p ne um on ia (26 % ) O the r (7 % )

0

20

40

60

80

10 0

* Percentages may not total 100% because of rounding. 3.6 Direct causes of neonatal deaths [25].

The proportion of children who are moderately underweight or moderately stunted is higher in LBW babies. Figure 3.9 presents an association of LBW with nutritional status of children below 2 years. In nine countries, every second child is reported to be stunted with prevalence rates higher than 50% – Afghanistan (59%), Yemen (58%), Guatemala and Timor-Leste (54%), Burundi, Madagascar, Malawi (53%) and Ethiopia and Rwanda (51%). India has a lower stunting prevalence rate of 48.1% but has the largest number of stunted children – 61 million Indian children are estimated to be stunted and contribute to almost a third

58

Public health nutrition in developing countries

Table 3.2 Global and regional estimate of LBW [26]

% Low birth weight infants World More developed Less developed Least developed countries Africa Asia Europe Latin America and Caribbean North America Oceania

15.5 7.0 16.5 18.6 14.3 18.3 6.4 10.0 7.7 10.5

Number of low birth weight infants (1000s) 20, 629 916 19, 713 4, 968 4, 320 14, 195 460 1, 171 343 27

5.3 m illion O ther A sia 7.8 m illion India

1.1 m illion China 1.2 m illion Latin A m erica & Caribbean 4.3 m illion Africa

3.7 Low birth weight infants (millions) in developing countries [26].

of the stunted children in the developing world (Box 3.3 presents an overview of undernutrition in India). Figure 3.8 presents the percentage of infants weighing less than 2,500 g at birth in six countries which are reported to have the highest incidence rate of LBW [1]. In developing countries, on the whole, stunting prevalence rate in under-5 children is estimated to be 34 percent. The stunting prevalence rate is 40 percent in Africa and 36 percent in Asia (Figure 3.10). In developing world, underweight prevalence rate in children under 5 years is 21 percent. Unlike stunting, the underweight rate is higher in Asia than in Africa (Figure 3.10). Underweight prevalence rates of over 30% are reported from 17 countries which includes three countries from Asia – India, Nepal and Bangladesh [1]. The four following countries have underweight prevalence rates higher than 40% – Timor-Leste (49%), India and Yemen (43%) and Bangladesh (41%). In the global context, India contributes to 42 percent of the total estimated 129 million underweight children in developing

Undernutrition in children

M au rita nia

59

34

P a kista n

32

Ye m en

32

S u da n

31

In dia

28 27

N ige r 0%

3 0%

2 0%

1 0%

4 0%

3.8 Percentage of infants weighing less than 2,500 g at birth in countries with highest rates [1]. Note: Estimates are based on data collected in 2003 and later with the exception of the Sudan (1999) and Yeman (1997). Table 3.3 Details of five countries that together contribute to half of world’s stunted under-5-year children [1] Country

Rank

Stunting prevalence (%)

India China Nigeria Pakistan Indonesia Total

1 2 3 4 5

48 15 41 42 37

% of developing world total (195.1 million) 31.2 6.5 5.2 5.1 3.9 51.9

p <0 .00 0 30

60, 788 12, 685 10, 158 9, 868 7, 688 101187

p <0 .00 0

p <0 .00 0

2 6.3 23

25 P e rce nta ge

Number of children who are stunted (Thousands, 2008)

20 1 5.3

1 7.2

1 3.3

15

1 0.6 10 5

L B W ba bies w h o are n ot w a sted

L B W ba bie s w h o a re m od era te ly w a sted

L B W ba bie s w h o a re no t stun te d

L B W ba bie s w h o a re m od era te ly stun te d

LB W b ab ie s w h o a re no rm al w e ig ht

L B W ba b ies w ho are m o de rately u n de rw eigh t

0

3.9 Association of Low Birth Weight (LBW) and nutritional status of children < 2 years [22].

Public health nutrition in developing countries

P ercentag e

60

45 40 35 30 25 20 15 10 5 0

40 36

A frica A sia D e ve lo ping cou ntrie s

34 27 23

21

17 13

10

U n de rw eigh t

Stun ting

W a stin g

3.10 Percentage prevalence of undernutrition in children under-5 years, based on WHO Growth Standard, in Africa, Asia and developing countries [1].

world under fives while Pakistan, Bangladesh and Nigeria each contribute to 5 percent (combined 15 percent) and the remaining 43 percent underweight children are from other developing countries. As presented in Figure 3.10, 13% of children under 5 years in developing world are wasted while the wasting prevalence rate is 17 percent in Asia and 10 percent in Africa [1]. Ten countries account for 60% of under 5 year children who suffer from wasting and eight of these countries have moderate wasting prevalence rates higher than 10 percent while 2–7 percent children in these countries are severely wasted (Figure 3.11). These estimated 26 million severely wasted children from developing world are nine times at higher risk of dying compared to normal children [1]. 22

M od era te w a stin g

20

P e rce n ta ge

20 18

S e ve re w asting

17

16 14 12 10 8

16

14

14

14 12 10

7

6

6 4 2

7

6

6

4

3

4

6

7 3

2

3.11 Ten countries which contribute to sixty percent of the global under 5 years of wasted children [1].

P h ilipp in es

E g yp t

S ud a n

D em o cra tic R ep ub lic of the C o ng o

E th op ia

Ind on esia

B an glad esh

P a kista n

N ig eria

Ind ia

0

Undernutrition in children

61

The greatest reduction in underweight prevalence in children under 5 years, between the period 1990 and 2008, has been reported in five countries – Bangladesh, Mauritania, Viet Nam, Indonesia and Malaysia. During this period, three countries (Bangladesh, Mauritania and Viet Nam) are reported to have not only the highest decline in underweight in under-5-year children but also over 20 percentage points decline in stunting prevalence rates (Figure 3.12). Unlike Bangladesh and Mauritania, the percentage prevalence rate of stunting in children in Vietnam continues to be higher than underweight prevalence rate. Box 3.5 at the end of the chapter presents the factors contributing to higher rate of decline in underweight or stunting noted in selected countries in the last two decades. 80 70

Stun ting

63 67

P erce nta ge

57

57

60 46

50 40

U n de rw eigh t

48

45 36

36

27

30

31

20

20 10 0 1 99 2

2 00 7

B a ng la de s h

1 98 7

2 00 6

V ie tna m

1 99 0

2 00 8

M aurita nia

3.12 Stunting and underweight (percentage of children ) under 5 years – declining trends in stunting and underweight [1].

3.5

Determinants of undernutrition

The cause of undernutrition is not limited to inadequate access to food. UNICEF conceptual framework of malnutrition in children and women (Figure 3.14) presents a number of varied factors which influence the maternal and child nutrition status [29]. Undernutrition is a result of multiple, complex, interactive causes which influences food, care and health of an individual and the nutritional status. Immediate causes of undernutrition in children are lack of proper infant and young child feeding resulting in low intake of nutrients and loss of nutrients due to frequent infections such as diarrhea, acute respiratory infections, measles, sepsis, etc. Nutrition status of children resulting from immediate causes is aggravated by underlying factors operating at households and community levels such as household food insecurity, inadequate care of women and children combined with unhealthy environment with lack of ready access to safe drinking water and environmental sanitation. The underlying

62

Public health nutrition in developing countries

Table 3.4 Undernutrition in India [21, 28] States Sikkim Mizoram Manipur Kerala Punjab Goa Nagaland Jammu & Kashmir Delhi Tamil Nadu Andhra Pradesh Arunachal Pradesh Assam Himachal Pradesh Maharashtra Karnataka Uttaranchal West Bengal Haryana Tripura Rajasthan Orissa Uttar Pradesh Gujarat Chhattisgarh Meghalaya Bihar Jharkhand Madhya Pradesh India

Underweight (%) 19.7 19.9 22.1 22.9 24.9 25.0 25.2 25.6 26.1 29.8 32.5 32.5 36.4 36.5 37.0 37.6 38.0 38.7 39.6 39.6 39.9 40.7 42.4 44.6 47.1 48.8 55.9 56.5 60.0 42.5

IMR

U5MR

33 37 14 12 41 10 26 49 35 31 52 32 64 44 33 45 44 35 54 34 63 69 67 50 57 58 56 46 70 53

40.1 52.9 41.9 16.3 52.0 20.3 64.7 51.2 46.7 35.5 63.2 87.7 85.0 41.5 46.7 54.7 56.8 59.6 52.3 59.2 85.4 90.6 96.4 60.9 90.3 70.5 84.8 93.0 94.2 74.3

causes of undernutrition in children are linked to basic causes such as poverty and lack of education which are influenced by larger political, economic, social and cultural environment. Poor access to safe source of water increases transmission of water borne diseases and contributes in setting up a cycle of infection and undernutrition (Figure 3.15). Eighty-eight percent cases of diarrhea worldwide are attributed to unsafe water, inadequate sanitation and poor hygiene [30]. The practice of hand washing after defecation is critical. In northern states of India, with over 50 percent undernutrition, less than 30 percent mothers washed hands after defecation [15, 31]. In such situations, diarrhea and other infections in children are common and result in increased loss of nutrients from the body as well as lower the immune defences. Moreover, children who are sick often have low appetite which aggravates poor intake of food. A vicious cycle of undernutrition and infection is set up (Figure 3.15).

Undernutrition in children

63

Box 3.3 Undernutrition in children in India In India, in 2005–2006, 40 percent children below 3 years of age and 42.5 percent children below 5 years of age are reported to be underweight [21]. The percentage of stunted children under 3 years is 44.9 percent while 48 percent children under 5 years are stunted. The proportion of underweight children below 3 years has decreased from 42.7 percent in 1998–1999 [27] to 42 percent in 2005–2006. On the other hand stunting in the same period has decreased by a larger margin from 51 percent to 44.9 percent in under 3 years children (Figure 3.13). Severe wasting has increased from 6.7 percent to 7.9 percent in this decade indicating possibly a better survival of wasted children under the ongoing health programmes.

60

N FH S 2 (1998-99)

N FH S 3 (2005-06)

Percentag e

50 40 30 20 10 0 U nderw iegh t

Severe U nderw eigh t

Stunting

Severe stunting

Wasting

Severe w asting

3.13 Trends (1998-2006) in nutritional status in children < 3 years [21, 27]. Child undernutrition is a problem throughout India, but the situation is considerably better in some states than in others. Table 3.4 shows that underweight percentage is higher than 40 percent in eight states – Madhya Pradesh, Bihar, Gujarat, Chhattisgarh, Jharkhand, Orissa, Uttar Pradesh and Meghalaya. These eight states have a high under-5 mortality rate (U5MR) ranging from 60.9 to 94.2 and infant mortality rate (IMR) between 46 and 70 (Table 3.4). The proportion of children under 3 years with stunting rate of over 50% are from five states – Gujarat, Chhattisgarh, Meghalaya, Bihar, Uttar Pradesh while underweight of over 50% is reported from three states – Madhya Pradesh, Bihar and Jharkhand. Children in states of Mizoram, Sikkim, Manipur and Kerala have comparatively better nutritional status.

Besides unsafe drinking water and poor sanitation, the other important underlying causes of undernutrition are inadequate availability of food through the year, poor maternal health and nutrition as well as inadequate and timely access to health services. Agriculture productivity, food policy and food prices influence food availability. It is well established that environmental factors and not genetic endowment are the principal determinants in disparities in child growth [32]. Poor stature, low pre-pregnancy weight or low body mass index combined with conception at young age below 18 years, poor care during pregnancy with inadequate weight gain, poor spacing between pregnancies, high level

64

Public health nutrition in developing countries

M alnu tritio n in C h ildre n & W o m e n

In ad eq u ate d ieta ry in take

Im m ed ia te cau se s

D ise ase

In ad eq u ate care o f child ren & w om en

In ad eq u ate a ccess to fo od

o utco m e

In su fficie n t h ea lth service s & un he althy e nviro nm e nt

U n de rlyin g cau se s

In ad eq u ate E d uca tion R e so urce s & C o ntrol H u m a n, E con o m ic & O rg an isatio na l

B a sic cau se s

P o litical & Ide o lo gical facto rs E con o m ic Structu re

P o te ntial R e so urce s

3.14 Conceptual framework of malnutrition [29]. W eigh t L o ss, G row th Fa ltering , Im m u nity L ow e red , M u cosa ID a m ag e

D is e a se : H igh er in cad e nce, S e ve rity, D ura tion

In ad eq u ate d ie ta ry in take A p pe tite lo ss, N utrie nt lo ss, M alab so rp tio n, A ltered m eta bo lism

3.15 Undernutrition and infection cycle [29].

of energy expenditure by women in undertaking physical stressful chores such as carrying water, cooking fuel etc contributes to undernutrition and sets up an inter-generational cycle of low birth weight, growth failure and undernutrition – a cycle of undernutrition to be repeated over generations (Figure 3.16).

Undernutrition in children

65

Child growth failure

Low birth weight baby

Early pregnancy

Low w eight and height in teenagers

Short adult women 3.16 Intergenerational cycle of undernutrition [29].

Incidence of LBW is 3–4 times higher in mothers who are adolescents or below 18 years as compared to those over 18 years [33]. Undernourished mothers who gain less than 8–10 kg of weight during pregnancy or start pregnancy with low body mass index are more likely to give birth to preterm or low birth babies [34]. Evidence suggests that low birth children are disadvantaged even before they are born and rarely catch up in growth [35, 36]. Undernourished children are more likely to grow up to be short adults who often fail to attain optimum height resulting in being stunted in adulthood. Stunted mothers have a higher chance of giving birth to small babies or low birth weight babies resulting in second generation adverse effect on child growth. Analysis of data of high-income countries indicates that for every 100 g increase in maternal birth weight, a child’s birth weight increases by 10–20 g [37]. Such evidence from low-income and middle-income countries is limited. However, it is well established that stunting in young children adversely influences cognitive development, school performance, educational achievement as well as economic productivity in adulthood and hinders economic development of future generation[38]. Mother’s education is an important underlying factor contributing to undernutrition. There is evidence that stunting rates in children decline as levels of education of women increase [39]. As indicated in Fig. 3.17 higher level of education which can be considered a proxy indicator of the decision making power with women, is associated with a reduction in percentage of adolescence marriage, low BMI and underweight prevalence in children [21]. Empowered women, who have control over their incomes, are more likely than men to invest in food, nutrition, health and education of children and self care. The social context in which women reside

Public health nutrition in developing countries

66

P ercentage (% )

80 75 70

M alnutrition (underweight) M others m arried by age 18

65 60 55 50 45 40 35 30 25 20 15 10 5 0

M edian age of 1st conception (years) W om en with B M I below normal

No education <8 years

<8-9 years 10 years and above

3.17 Women’s education and trend in BMI and underweight in children – Rajasthan, India [21].

influence their power to take decisions regarding health and other careseeking behaviours. An analysis of India data reveals that the risk of underweight in children has a significant association with domestic violence experienced by women [22]. The low status of women in many developing countries is considered to be one of the primary reasons for undernutrition across the life cycle. A regression analysis of risk factors of undernutrition in children indicates that the primary risk factors associated with underweight in developing regions, such as India, in order of magnitude of risk, are body mass index (BMI) of mothers, occurrence of childhood diseases, child’s age 12–35 months and illiteracy of mothers (Table 3.5). As presented in Table 3.5, poor hygiene practices are observed to be important contributory factors of stunting in children. Occurrence of child diseases contributes to highest risk to wasting in children [14, 40]. Poverty is a basic cause of undernutrition in children. Poverty and low income contributes to undernutrition by adversely influencing food and nutrition security, housing and living environment with increased risk of infections. Poor population have a lower access to health and family planning services and are often involved in hard physical labour which also contributes to poor nutrition. The vicious cycle of poverty and undernutrition (Figure 3.18) adversely influence the nutritional status of children and economic development of future generation [41].

Undernutrition in children

67

Table 3.5 Risk factors for underweight, stunting and wasting in children – an analysis of situation in Uttar Pradesh, India [40] Underweight Risk factor BMI Disease Child’s age Literacy

Stunting

Wasting

Factor loading 1.63 1.58 1.41

Risk factor

Factor loading

Risk factor

BMI Literacy Child’s age

1.30 1.27 1.26

Disease BMI Child’s age

Factor loading 1.64 1.29 1.19

1.28

Hygiene

1.19

Literacy

1.17

Incom e poverty

Low food intake

Fre quent in fe ctions

H ard phys ica l la bou r

Fre quent preq nancie s

Larg e fam ilies

M alnutritio n D irect loss in prod uctivity fro m p oor physic al labo ur

Indirect loss in produ ctivity fro m p oor cognitiv e developm en t and scho oling

Loss in reso urces fro m increa sed health care costs of ill health

3.18 Vicious cycle of poverty and malnutrition [41].

However, poverty resulting in poor purchasing power of the family and poor access to food by family is not the sole cause of undernutrition in children. Data from nine states of India (Table 3.6) indicates that 59.2–93.1 percentage of adult women in these states consume over 70% recommended dietary allowances (RDA) of energy and protein as compared to only 19.4–52.3% of children 1–3 years of age in those families consuming over 70% RDA [42]. The data highlights the fact that young children below 3 years of age who need much less food as compared to adults are often deprived of food in the crucial stage of growth not necessarily due to lack of access of food by family but very often due to inadequate knowledge regarding appropriate feeding and care practices to be followed for young children, i.e. exclusive breastfeeding in the first six months followed by complementing breastfeed with right quantity of food of right composition with adequate energy density as well as right consistency and right frequency of feeding.

Public health nutrition in developing countries

68

Table 3.6 Undernutrition and percentage of adults and children with protein–calorie adequacy [42]

States

Prevalence of undernutrition (%) in children

Andhra Pradesh Gujarat Karnataka Kerala Madhya Pradesh Maharashtra Orissa Tamil Nadu West Bengal Pooled (a)

36.5 47.4 41.1 28.8 60.3 39.7 44.0 33.2 43.5 41.6

Distribution (%) protein calorie adequacy – sedentary adult women(a)

Distribution (%) protein calorie adequacy – 1–3 year children

87.7 69.8 80.2 78.6 77.6 59.2 93.1 80.6 84.8 80.0

52.3 24.2 25.5 19.4 33.7 30.8 24.9 23.2 37.1 30.1

70% requirement defined as energy protein adequacy

Undernourished children in the developing world are reported not only in the low wealth quintile but also the top quintile – though the gap is wide. As presented in Table 3.7, 56.6 percent children in India in the lowest socio-economic group are reported to be undernourished compared to 19.7 percent in the wealthiest group [21]. The data highlights the fact that it is not only food insecurity or hunger per se which is contributing to the high percentage of undernourished children in developing countries. Table 3.7 Prevalence of underweight by location, wealth quintile, gender and caste Underweight Prevalence 2005–06 Total Urban Rural Female Male Scheduled caste Scheduled tribe Other castes Quintile 1 (Poorest) Quintile 2 Quintile 3 Quintile 4 Quintile 5 (Wealthiest)

3.6

42.5 32.7 45.6 43.1 41.9 47.9 54.5 33.7 56.6 49.2 41.4 33.6 19.7

Severe underweight Prevalence 2005–06 15.8 10.8 17.5 16.4 15.3 18.5 24.9 11.1 24.9 19.4 14.1 9.5 4.9

Maternal and child undernutrition – evidence for actions

“Too early, too close, too many and too late pregnancies adversely affect nutrition and health status of mother child dyad” [42]. Poor nutritional

Undernutrition in children

69

status of mother, including chronic energy deficiency and micronutrient deficiencies, before and during pregnancy is critical to successful outcome of pregnancy. Birth weight is influenced by the nutrition and health status of mother. Mother’s weight and height at conception influences birth weight to a great extent. A number of studies have demonstrated a good correlation between birth weight and maternal weight as well as poor pre-pregnancy weight gain. Maternal body size is strongly associated with size of newborn children [24]. Risk of intrauterine growth restriction (IUGR) is associated with short stature of mother and poor maternal nutrition stores [3, 43]. Data from India reports an association between mother’s weight and birth weight as well as an association of birth weight with economic situation – the latter in turn is observed to be associated with lower height and weight of mothers (Tables 3.8 and 3.9). Table 3.8 Effect of maternal body weight on birth weight [44] Mother weight (kgs)

No.

Mean birth weight (gm)

<45 45-54 >=55 Total

128 251 96 475

2639.6 2779.1 3009.41 2788.0

Table 3.9 Birth weight and socio-economic status [45] Poor income Age (years) Parity Height (cm) Weight (kg) Hb (g/dl) Birth weight (kg)

24.1 2.41 151.5 45.7 10.9 2.70

Middle Income 24.3 1.96 154.2 49.9 11.1 2.90

High income 27.8 1.61 156.3 56.2 12.4 3.13

In a developing country, such as India, maternal situation such as adolescence marriage (a proxy for adolescence conception), height, level of education, access and use of health services (such as consumption of full dose of iron–folic acid supplement, antenatal care and institutional delivery) have been observed to have a significant association with underweight prevalence rates in children below 2 years of age (Table 3.10). LBW children in a developing country, as stated earlier, are often full term newborns with intrauterine growth retardation. The survival chance of these children is much better than pre-term newborns. However, these surviving children are at higher risk of poor nutritional and health. Full term LBW children have been reported to have a low trajectory for growth in infancy and childhood (Figure 3.19) – resulting in increasing the chances of prevalence of undernutrition in young children [46]. Figure 3.9

Public health nutrition in developing countries

70

Table 3.10 Maternal factors significantly associated (a) with underweight in children in Uttar Pradesh, India [22]

Maternal situation ■

■

■

■

■

■

■

Age of marriage <18 >18 Height of mother <145 cm > 145 cm No education 10 years and above education Emotional violence No emotional violence Consumption of IFA tablets for <90 days Consumption of IFA tablets for >90 days <3 ANC check-ups >3 ANC check-ups No institutional delivery Institutional delivery

Level of significance(a) 0.000

43.1 35.1 50.0 38.5 46.2 23.8 47.5 41.5 39.8 22.0 44.6 28.8 43.3 29.1

0.000 0.000 0.035 0.000 0.000 0.000

Level of significance < 0.05 indicates significant association

W e ig h t (k g )

(a)

% of underweight children

B irth weight >3 500 g 3000-3 500 g 2500-3 500 g 2500 g <2 250 g

9 8 7 6 5 4 3 2 1 0 3

6 A ge (m on ths)

9

12

3.19 Growth in relation to birth weight [46].

(presented earlier in Box 3.2) highlights the association of LBW with nutritional status of young children. Birkin et al [47] in a study of association between birth weight and growth concluded that infants with lower birth weights are likely to remain shorter and lighter throughout childhood, especially those who are intrauterine growth retarded rather than premature. Conversely, those infants with higher birth weights are likely to remain taller and heavier and have a higher risk of obesity. The study indicates birth weight is a strong predictor of weight and height in early childhood, not only for low birth weight children but also for those of normal and high birth weight.

Undernutrition in children

71

Undernutrition in children begins with the mother [2]. Mother’s own foetal growth and her diet from birth to pregnancy affect birth weight. Studies from India and other developing countries indicate that reduction in dietary intake below habitual levels or increase in work load above habitual levels as well as adolescent pregnancy is associated with worsening in maternal nutrition status and low birth weight. Deterioration in maternal nutritional status has been reported with reduction in normal habitual diet during drought or pre-harvest season, increase in work with induction of new manual labour and adolescent pregnancy [41]. An analysis of 36, 555 birth records from North India revealed seasonal variations in birth weights. The incidence of LBW was reported to be minimal in post winter births. It was observed that these mothers in the third trimester not only had a better appetite in the winter season but also consumed much higher quantities of fresh vegetables and fruits which were easily accessible in the winter season [48]. Women’s nutrition and health status through out the life cycle from childhood through adolescence and into adulthood is critical in determining maternal and neonatal health outcomes. Intrauterine growth restriction is associated with low BMI of mothers, mothers conceiving prior to 18 years of age, poor food availability during pregnancy, suboptimal energy intake along with continued high manual physical activity, high parity, inadequate rest and absence of maternity leave before delivery [3, 49, 50, 51, 52]. Maternal undernutrition, low maternal body mass index (BMI <18.5 kg/m2) is prevalent in many regions of developing countries. The proportion of women with low BMI is higher in South Asia – 14.3% in Nepal, 20.4% in Pakistan, 28.5% in Bangladesh and 35.6% in India (13, 21, 53, 54). The social practice of early marriage and high rates of teenage pregnancy is a major factor contributing to poor height and low BMI. Amongst girls living in disadvantaged situations, the velocity of growth during adolescence is slower and is extended for a longer period. Early conception during the growing adolescent period in these girls often results in arresting growth of adolescent mothers [36]. Undernourished girls in developing countries who become pregnant in the growing adolescent phase are at much higher risk of LBW. Children born to teenage mothers are 40% more likely to die in their first year than those born to women in their twenties [36]. The proportion of such women who begin child bearing below 18 years is high in developing countries – 16 % in India [21], 20% in Nepal [53] and 37% in Bangladesh [54]. Several studies indicate adult height is positively associated with birth weight and length. Many countries in south-central Asia have more than 10% women with short stature [16]. The percentage of women with short stature, height below 145 cm is 11.4% in India and 14.2% in Nepal and

72

Public health nutrition in developing countries

15.7% in Bangladesh [16, 53, 54]. Short stature of mother and poor maternal nutrition stores are associated with increased risk of intrauterine growth restriction. An increase in adult height of 0.7–1.0 cm is associated with 1 cm increase in birth length [38]. Improving nutritional status of mother before and during pregnancy is critical for reducing undernutrition in children [24, 55, 56]. A study from Gambia demonstrated that prenatal dietary supplementation reduced retardation in intrauterine growth when effectively targeted at risk mothers. Gambia study was a 5-year controlled trial of all pregnant women in 28 villages who were provided with daily supplement of high energy groundnut biscuits (4.3 MJ/day) for about 20 weeks before delivery. Food supplement to mothers increased weight gain in pregnancy. The birth weight increased significantly during the nutrition deprived season of June to October – weight gain increased by 201 grams in the hungry season, 94 grams in the harvest season and by 136 g for the whole year. Birth length and gestation were not affected [57]. In India, a variation in mean birth weight of babies born during different time periods has been reported. Highest mean birth weight was observed in March (post-winter) and lowest in August (post-summer and dry season) and an association with availability of fresh fruits rich in minerals and vitamins was indicated [48]. In 13 trials (4665 women), modest increase in maternal weight gain and mean birth weight was observed with balance energy–protein supplement. A substantial reduction in risk of small for gestational age (SGA) birth was also observed. High protein or balance protein supplement alone was not beneficial [58]. Kusin et al [59] in a controlled randomised trial in Madura, East Java studied the impact of high energy (1950 kJ/465 kcal) and lowenergy supplement (218 kJ/52 kcal) to pregnant women in the last trimester of pregnancy. The effect of this intervention on the children’s growth was assessed longitudinally for the first 5 years of life in the mothers who had consumed the supplement for at least 90 days. Infants entered the study at birth and their growth was measured at 4-week intervals until 12 months old; thereafter they were measured every 3 months. The birth weight in such cases is increased by nearly 100 g [59]. It was observed that up to the age of 24 months, children of mothers receiving high energy supplement were significantly heavier than the other group with low-energy supplement. The high-energy group children were also taller throughout the first 5 years. There was a 20% reduction in stunting at 5 years of age. Weight-for-height was similar in both groups, but stunting (height-for-age) was less prevalent in high energy supplement group. The study concluded that in a community characterized by chronic energy deficiency among women

Undernutrition in children

73

2 80 0

50

2 70 0

40

2 60 0

30

2 50 0

20

2 40 0

10

2 30 0

% Ibw

m ea n bw t. (g )

of reproductive age, energy supplementation of women for the last 90 days of pregnancy, was effective in the promotion of postnatal growth and reduction in undernutrition in preschool children. A study in Guatemala also demonstrated that children born to women who had received high protein-moderate energy supplement were taller than those receiving non-protein–low-energy supplement [60]. Besides inadequate consumption of energy and protein, deficiency of micronutrient is common in women in developing countries. Globally almost half of pregnant women, about 56.4 million are estimated to be anemic [61]. Iron deficiency is often the primary cause of anemia. Anemia accounts for 20% maternal mortality and contributes to lowering birth weight. Low birth weight can be attributed to anemia per se or combined effect of poor nutritional status of mother or poor access to antenatal services. It has been reported that the incidence of LBW doubles when haemoglobin level is <8 g/dl (Figure 3.20) [62].

0 <8

8 to 11 H a em og lo b ing (a/d I)

>= 11

b irth w e ig ht (g) L B W (% )

3.20 Effect of maternal Hb on birth weight [62].

Intervention measures are important prior to onset of pregnancy for building iron stores and preventing severe anemia. Building iron stores right from adolescence age itself has been recommended [63]. Iron supplementation study from Vietnam has demonstrated that weekly iron– folic acid prior to and during pregnancy is associated with better iron stores in the first and second trimester of pregnancy and with reduced prevalence of low birth weight compared with pregnant women who receive daily iron-folic acid supplementation during pregnancy [64]. Iron supplementation has been demonstrated to improve birth weight, even in non-anemic women [65]. Deworming in the second trimester of pregnancy in Nepal has been reported to lowering the rate of severe anemia during the third trimester and improving birth weight [66].

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Public health nutrition in developing countries

Besides iron, pregnant women are often deficient in several other micronutrients such as iodine, zinc, calcium, vitamin A. These deficiencies are often “not visible” but can result in health problems in mothers and intra-uterine growth restriction [2, 67, 68]. Addressing micronutrient deficiencies during pregnancy in mother increases birth weight [67]. Fall et al [69] in a meta-analysis on impact of multiple micronutrient supplementation during pregnancy in low income countries on birth size and length of gestation observed a mean increase in birth weight of 22 g with a range in birth weight increase across studies from 4.9 to 75.5 g. The study concluded that “the effect on birth weight is greater in women with higher BMI and is very small in energy deficient mothers”. This increase was in comparison to what was achieved by iron-folic acid supplement. Shrimpton et al [67] observed that the increase in birth weight achieved by the multiple micronutrient supplements is of similar order of magnitude as that reported to be achieved with food supplementation during pregnancy. A hospital-based trial in pregnant women enrolled at 24–32 weeks of gestation with low BMI (less than 18.5) and anemia (haemoglobin level of 7–9 g/dl) showed that a supplement containing 29 vitamins and minerals taken in addition to the regular iron–folic acid supplementation increased birth weight by 98 g, increased birth length by 0.80 cm, reduced early neo-natal mortality by 50% as compared to placebo and resulted in decline in incidence of LBW from 43.1% to 16.2% [70]. The impact of multiple micronutrient supplementation on growth and development later in childhood has been reported from follow up studies in Nepal, Bangladesh and Vietnam [71, 72, 73]. Vietnam effectiveness trial reported not only reduction in LBW rate but on stunting rate at 2 years of age [72]. The Nepal study [73] reported no impact on height but influence on weight, head and mid-arm circumference while the Bangladesh study reported positive impact on motor skills [71]. A systematic review of 12 efficacy and 6 effectiveness trials covering 12 countries from three continents (Asia, Latin America and Sub-Saharan Africa) concludes “multiple micronutrient supplement during pregnancy in developing countries contribute significantly to a body of evidence which shows that supplementing women in pregnancy can improve outcomes beyond anemia, including deficiencies of other minerals and vitamins and birth weights” [74]. Based on the review of the meta-analysis results of comparing multiple micronutrients with daily iron folic acid supplementation during pregnancy, it has been proposed to replace iron folic acid supplements with multiple micronutrient supplement in the package of nutrition and health interventions during antenatal care [67]. Box 3.4 presents details of micronutrient supplements used in the various trials that were covered under the meta-analysis. The findings stress the need to improve nutritional

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Box 3.4 Micronutrient supplements used in efficacy and effectiveness trials In 1999 UNICEF, the World Health Organization (WHO) and the United Nations University (UNU) jointly proposed a standard composition of multi-micronutrient supplement for pregnant women comprising 15 vitamins and minerals. The supplement was proposed to be used in efficacy and effectiveness trials to assess its impact on pregnancy and birth outcome. This supplement is referred to as United Nations International Multiple Micronutrient Preparation (UNIMMAP). Nine trials in eight countries (Bangladesh; Burkino Faso; China; Guinea-Bissau; Indonesia (Lombok and Indramayu); Nepal (Janakpur); Niger; Pakistan) used UNIMMAP as antenatal supplements. The other three trials conducted in Mexico, Nepal (Sarlahi) and Zimbabwe used other multiple micronutrient supplement formulation as presented below (Table 3.11) [75]. Table 3.11 Micronutrient composition of supplements used in 12 trials Micronutrient Iron (mg) Zinc (mg) Copper (mg) Selenium (ug) Magnesium (mg) Iodine(ug) Vitamin A (ug RE) p-Carotene (mg) Vitamin B. (mg) Vitamin B, (mg) Folic acid (ug) Niacin (mg) Vitamin B6 (mg) Vitamin B,2 (ug) Vitamin C (mg) Vitamin D (ug) Vitamin E (mg) Vitamin K (ug)

*

UNIMMAP"

—

30 15 2.0 65 — iso 800 — 1.4 1.4 400 18 1.9 2.6 70 5 10

Mexico 62.4 12.9 — — 252 — 2,150 (1U) — 0.93 1.S7 215 15.5 1.94 2.04 66.5 7.7 5.7 (IU) —

Sarlahi, Nepal 60 30 2.0 — 10 — 1,000 — 1.6 1.8 400 20 2.2 2.6 100 10 10 6S

Zimbabwe 0" 15 1.2 65 — — 3,000 3.5 1.5 1.6 0 17 2.2 4.0 80 10 10 —

RE, retinol equivalent; UNIMMAP, United Nations International Multiple Micronutrient Preparation

status before as well as during pregnancy. Besides supplementing with multiple micronutrients in situations with a high number of undernourished women, supplementary feeding is considered an important intervention.

3.7

Addressing undernutrition in children – a life cycle approach

World-wide growth faltering analysis using WHO standards stress the significance of prenatal and early life interventions to prevent the growth failure that mainly happens during the first 2 years of life [17]. The need to concentrate on the “critical window from conception to 24 months of

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age” for targeting interventions is recommended [2, 5]. Successful implementation of intervention measures during pregnancy and lactation, together with appropriate infant and young child feeding as well as care of infants, young children and adolescent girls is essential for reduction in the level of stunting in young children. It has been proposed that intensive timely actions concentrate on population group “at risk” of undernutrition such as pregnant mothers and children below 12 months [14]. Reaching this “risk” group is feasible through the primary health care system. Contacts during antenatal care (ANC) services and routine immunisation provide opportunity for promoting and monitoring appropriate feeding practices and adoption of health and hygiene practices (Table 3.12). ANC services need to systematically include interventions such active promotion of minimum weight gain of 10–12 kg through adoption of practices such as intake of additional diet (additional food equal to one pre-pregnancy major meal) during pregnancy, ensuring minimum 2 hours day rest and regular consumption of iron or multiple micronutrient supplements. It has been emphasized that any delay beyond infancy, may be too late for effective prevention of undernutrition in children [14]. As presented in Table 3.13, the Lancet series on maternal and child undernutrition has identified the following evidence-based direct interventions with demonstrated effectiveness [77]. These interventions are included in the recent strategies at the global level [78]. Interventions to improve nutritional status (Figure 3.21) need to stress on a package of selected actions, through the life cycle, to be effectively implemented in the entire region or a country [1]. Registering and reaching newly married women is critical for introducing intervention measures for preventing adolescent pregnancy as well as for improving health and nutritional status prior to onset of pregnancy. All these efforts for reduction of undernutrition need to be complemented with access to safe drinking water since evidence shows that hygiene interventions can reduce stunting at 36 months by 2–4% [78]. In addition to the above referred package of intervention, basic causes at societal level such as improved women’s status are critical [22, 79]. It is well established that women who have control over income are more likely than men to invest in their children’s education, health and nutrition [80, 81, 82, 83]. Conditional Cash Transfer (CCT) programme of Mexico is an example of an effort to reduce poverty and food insecurity along with an emphasis for poor women to invest in betterment of the children [84]. Efforts for accelerated and sustainable reduction in undernutrition in children requires long-term investments for improving women’s education, empowering women and implementing measures for reducing poverty and ensuring food and nutrition security [22, 80].

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Table 3.12 Linking promotion of appropriate infant and young child feeding with immunization contact points [76] Pregnant women Immunization contacts Tetanus toxoid 1st dose Tetanus toxoid 2nd dose

Counselling and monitoring Antenatal care Promote and monitor • Increase in energy dense food • Regular intake of iron folic acid (or multiple micronutrient) • Minimum 2 hours day rest • Weight gain 10–12 kg Preparing for breastfeeding • Initiate breastfeeding within 1 h of birth • Significance of colostrum feeding • Promote exclusive breastfeeding (EBF) for 6 months • No water in first 6 months Institutional delivery • Preparing for institutional delivery

Infants Immunization Contacts

Age

BCG

At birth or along with DPT 1

OPV (O dose)

OPV 1, DPT 1 OPV 2, DPT 2

OPV 3, DPT 3

At birth or within 28 days of birth

6 weeks (1.5 months) 10 weeks (2.5 months)

14 weeks (14.5 months)

Measles + 1st dose 9 months of vitamin A

Counselling and monitoring Newborn and infant care Promote and monitor • Ensure newborn care intervention package being followed • Record birth weight • Initiate BF within 1 hour of birth – ensure appropriate position / breast attachment • Ensure colostrum feeding Advice • EBF continued for 6 months • No introduction of water with EBF • Hygiene and hand washing • Introduce family spacing measures Promote and monitor • EBF continued (no water) • Check growth – height / weight of child Advice • Continue EBF during illness / diarrhoea • Advice hygiene / hand washing Promote and monitor • EBF to be continued up to 6 months Advice • Continue EBF during illness • Sensitize on introduction of appropriate complementary feeding (CF) and continued Breastfeeding (BF) at 6 months • Hygiene / hand-washing practices • Diarrhoea prevention and management Promote and monitor • Complementary feeding (Amount, type, frequency) • Continued BF Advice • Continue BF up to 2 years or beyond • Record child’s height / weight

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Table 3.13 Direct interventions with demonstrated effectiveness on maternal and child undernutrition [77] Evidence

Maternal and birth outcomes

Newborn babies

Infants and young children

Evidence sufficient for implementation in all developing countries

Iron–folate supplementation

Promotion of breastfeeding (individual and group counselling)

Promotion of breastfeeding (individual and group counselling)

Maternal supplements of multiple micronutrients Maternal iodine through iodization of salt

Behaviour change communication for improved complementary feeding for infants Zinc supplementation Zinc in management of diarrhoea

Maternal calcium supplementation

Vitamin A fortification or supplementation

Interventions to reduce tobacco consumption or indoor air pollution

Universal salt iodization Hand washing or hygiene interventions Treatment of severe acute malnutrition

Evidence for implementation in specific situational context

Maternal supplements of balanced energy and protein Maternal iodine supplements Maternal deworming in pregnancy Intermittent preventive treatment for malaria

Neonatal vitamin A supplementation Delayed cord clamping

Conditional cash transfer programmes (with nutritional education) Deworming Iron fortification and supplementation programmes Insecticide treated bednets

Insecticide treated bednets

Addressing undernutrition is complex and involves a diversity of approaches for achieving success (Box 3.5). A strong government action at various levels, leadership at the highest level, mobilization and information sharing with vulnerable groups, appropriate monitoring and evaluation system with timely corrective actions and significant allocation of resources and public spending is critical for addressing undernutrition in children.

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Adolescen ce / Pre-Preg nancy De lay ag e o f m arriage / first pregn an cy >18 yea rs ■ Pro m ote healthy we ight ■ W eekly iron fo lic acid sup plem e ntation ■ Co nsum ptio n of iron / m u ltiple m icro nutrien t fortifie d fo od ■ Ed uca tio n, fam ily life e du cation and em powe rm en t o f w om en ■

Children 6-23 m onths

Interventio ns for Interven tio ns for the young children m other ■ Co m plem e ntary ■ En erg y d en se fortified feedin g fo od s and ■ Co ntinued bre ast■ Ha nd wa sh ing with soa p. fe ed ing Food h yg iene ■ Iron fo lic acid sup plem e nt ■ Vitam in A supp le me ntation ■ Da ily inta ke of i o dized salt ■ Zinc trea tm en t an d fee ding d uring diarrhea ■ De worm ing ■ Ha nd wa sh ing with soa p ■ Use of sa fe drinking w ater ■ Full im m uniza tion

Pregn ancy En erg y d en se food/ ta rgete d energ y fo od supple m ent (u nd e rnourish ed and de prived w om en) and ad eq ua te p rotein ■ Iron fo lic acid / m icro nutrien t supp le me nt ■ Da ily intake o f io dized sa lt ■ De worm ing (if re quired) ■ Tre atme n t o f n ight blin dness in p re gn ancy ■ M alaria pro ph yla xis an d in te rmitte nt therap y ■ Re du ce work loa d and energy expend iture ■ Ha nd wa sh ing an d hyg iene ■ Re du ce sm oke lad en hom e environm en t / to ba cco ■ A dequate day rest ■

Infants <6 m onths Intervention s for infants Exclu sive b rea st fee din g (no wa ter) ■ Ap pro priate fe ed ing of HIV expo sed in fa nts ■

Interven tio ns for the m other ■ En erg y d en se food ■ Increa se quality protein s ■ IFA su pp lem en ts / m ultim icron utrient supplem entation ■ Da ily use o f io dised sa lt ■ Use of fortifie d food such as iron fo rtified flou r ■ Space preg na ncies (>2 years) fa mily pla nn ing se rvices

Birth ■

Initiate breast fee ding w ithing 1 ho ur (includ in g colo strum feed ing)

3.21 Prevention of undernutrition – a life cycle approach (Adapted from [1]).

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Box 3.5 Reduction of undernutrition – success factors – interventions – country case studies The success factors for reduction of child undernutrition are primarily adequate and defined comprehensive policies which are not limited to provision of food supplements alone. Effective implementation of policies through well defined service delivery systems and effective management as well as availability of sufficient resources are critical. Analysis of factors contributing to accelerated progress in nutrition situation of children in Thailand, China, Brazil and Vietnam is presented below [80]. In Thailand, child malnutrition reduced from 50% in 1982 to 25% in 1986. The 2nd National and Health Policy (1982–86) focused on targeted nutrition interventions to eliminate severe malnutrition and effective implementation of behaviour change and communication to prevent mild to moderate malnutrition. The focus of the intervention was on social mobilization – one community volunteer for 20 households – through community-based primary health care delivery system. One of the major factors contributing to the success was high political priority, a large investment of 20% of total government expenditure and integrating nutrition within the National Economic and Social Development Plan. In China, malnutrition reduced from 25% to 8% between 1990 and 2002. The success is attributed to successful poverty alleviation strategy as well as rapid economic growth along with implementation of nutrition, health and family planning programmes at large scale. Additionally, focusing on important interventions such as sanitation and mother’s education. This combined with central leadership, local government ownership and effective monitoring and feed back mechanism were the primary success factors. In Brazil, 60% reduction in malnutrition was reported between 1975 and 1989. Following sharpest economic growth and poverty alleviation, substantial national resource was invested in food distribution and nutrition programmes as well as water, sanitation and health .Social sector input for education increased significantly. Since 2004, nutrition policy efforts have been intensified with high resource investment. In Viet Nam, the prevalence of underweight has decreased from 51.5% in 1985 to 24.6% in 2006 – a reduction of 1.3% per year. The prevalence of stunting decreased at the rate of 1.5% per year during this period – from 59.7% in 1985 to 27.9% in 2006 [85]. In the early phase, risk factors were analysed and special attention was accorded to maternal health and nutritional status and child health and family planning services. Family planning programme resulted in creating opportunities to families for better investment in child nutrition and health care. Additionally, poverty alleviation programmes combined with high investment in PEM control programme since 1999 contributed in reducing undernutrition. Reducing child malnutrition was a goal in the 10th Party Conference’s document with a revised strategy for Child Malnutrition Control Programme for the period 2006–2010. Stunting Reduction Plan of 2008–2013 gives special focus to prepregnant and pregnant women and reducing LBW to under 6%.

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84. 85.

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review of methods and characteristics of studies included in the meta-analyses. Food and Nutrition Bulletin vol. 30, no. 4, pp. S517–S526. VIR S (1990). Women’s nutrition – convergence of programmes, a critical issue. Indian Journal of Maternal and Child Health vol. 1, no. 3, p. 74. ZULFI QAR A BHUTTA , TAHMEED AHMED , ROBERT E BLACK , SIMON COUSENS , KATHRYN DEWEY , ELSA GIUGLIANI, BATOOL A HAIDER , BETTY KIRKWOOD , SAUL S MORRIS, H P S SACHDEV , MEERA SHEKAR , for the Maternal and Child Undernutrition Study Group. DFID (2010). The neglected crisis of undernutrition: DFID’s strategy. DE ONIS (2003). WHO Global database on child growth and malnutrition, methodology and applications. Int J Epidemiology vol. 32, pp. 518–526. RUEL MT (2008). Addressing the underlying determinants of undernutrition: examples of successful integration of nutrition in poverty reduction and agriculture strategies. SCN News vol. 36, pp. 21–29. HODDINOT J and HADDAD L (1994). Woman’s income and boy girl anthropometric status in the Coto d’voire. World Development vol. 22, no. 4, pp. 543–553. KATZ E (1994). The impact of non-traditional export agriculture on income and food availability in Guatemala: an intrahousehold perspective. FNB vol. 15, no. 4. QUISUMBING A (2003). Household decisions, gender and development. A synthesis of recent research. IFPRI: Washington DC / Johns Hopkins University Press: Baltimore, MD. LEV S (2006). Progress against poverty. Sustaining Mexico’s PROGRESSA – opportunities program. Booking Institution Press: Washington DC. KHAN NC , HOP LH , TUYEN LD , KHOI HH , SON TH , DUONG PH (2008). A national action plan to stunting reduction in Vietnam. SCN News vol. 36, pp. 31–37.

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Dual nutrition burden in women: causes, consequences...

4

Dual nutrition burden in women: causes, consequences, and control measures Prema Ramachandran

Prema Ramachandran, MD in Obstetrics and Gynaecology, is currently the Director of Nutrition Foundation of India. She was an advisor with the Planning Commission (Health, Nutrition and Family Welfare) for nine years and gave the lead to prepare the drafts for the Ninth and Tenth Plan chapters on these sectors. Prior to joining the Planning Commission. Dr Ramachandran was with the Indian Council of Medical Research (ICMR) for 25 years, carrying out clinical and operational research studies on health and nutrition services.

4.1

Introduction

Women especially pregnant and lactating women, form one of the most vulnerable segments of the population from nutritional point of view. Numerous studies in India and elsewhere have shown that in chronically undernourished women, subsisting on unchanged low dietary intake, pregnancy and lactation have an adverse effect on maternal nutritional status. Maternal undernutrition is associated with low birth weight and all its attendant adverse consequences. Epidemiological studies from India during seventies and eighties documented the magnitude and adverse consequences of chronic energy deficiency (CED) on the mother–child dyad and paved way for intervention programmes to address undernutrition during pregnancy and lactation. “Too early, too close, too many and too late” pregnancies adversely affect nutrition and health status of the mother–child dyad. Timely contraceptive care has become an indirect effective intervention to prevent deterioration in maternal and child nutrition. Yet another important indirect cause of undernutrition continues to be infections. Undernutrition increases the susceptibility to infections – infections aggravate undernutrition. While undernutrition continues to be a major problem as in the earlier decades, the current decade has witnessed the progressive rise in overnutrition in women during reproductive age especially among the affluent segments of population both in urban and rural areas and associated increase in the prevalence of non-communicable diseases. A review of the available data on the quantum of under and overnutrition in women, the factors

86

Dual nutrition burden in women: causes, consequences...

87

responsible for the emerging problem of dual burden of malnutrition, health hazards associated with it, prevention, early detection and effective management of dual nutrition burden in women is presented. Su rveys [1] 100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0% 1975-7 9

1988-9 0 <1 8.5

1996-9 7

18.5-25.0

2000-0 1

> 25.0

4.1 Time trends in nutritional status of women [1].

4.2

Emergence of dual nutrition burden in India

Data from the National Nutrition Monitoring Bureau (NNMB) on nutritional status of rural women as assessed by BMI over the last three decades is shown in Fig. 4.1. It is obvious that over this period there has been a reduction in undernutrition and increase in the prevalence of overnutrition. Data NNMB rural surveys on time trends in weight, height and triceps fat fold thickness in all age groups in females is shown in Figs. 4.2, 4.3, and 4.4, respectively. In rural population there is an increase of about three cms in adult height while the increase in body weight over the period is much greater. This increase in body weight is mainly due to fat deposition as apparent from the progressive increase in the fat fold thickness over this period. The increase in fat fold thickness begins in childhood. 60

Weigh t (kg)

50 40 30 20 10

1996-9 7

1975-7 9 2000-0 1

45-54

18-24

Age (years) NC HS

15+

12+

9+

6+

3+

0+

0

1988-9 0

4.2 Time Trends in mean weights in rural women [1].

Public health nutrition in developing countries

5 5-6 0

1 9 8 8-9 0

1 9 7 5-7 9 2 0 0 0-0 1

1 9 9 6-9 7

3 5-4 4

Age (y ears) NCHS

1 8-2 4

16+

14+

12+

8+

10+

6+

4+

2+

190 170 150 130 11 0 90 70 50 0+

H eight (cm s)

88

20 15 10 5

NCHS 1 9 9 6-9 7

Age (yea rs) 1 9 7 5-7 9 2 0 0 0-0 1

5 5 -6 0

1 8-+ 24

1 6+

1 2+

8+

6+

2+

0 0+

Tric ep Sk infold (m m )

4.3 Time Trends in mean heights in rural women [1].

1 9 8 8-9 0

4.4 Time Trends in mean tricep fatfold in rural women [1].

Data from NNMB surveys in urban slums on time trends in weight and fat fold thickness at triceps are shown in Figs. 4.5 and 4.6. Mean body 60 W eight (kg)

50 40 30 20

1 9 7 5 -8 0

1 9 9 3 -9 4

4.5 Time Trends in mean weights in Urban women [1].

4 5 -5 4

Age (Years) NCHS

1 8-2 4

15+

9+

3+

0+

0

12+

10

Dual nutrition burden in women: causes, consequences...

89

N C HS

1 97 5-8 0

45 +5 4

18 +2 4

A ge (Yea rs)

1 5+

12 +

9+

6+

3+

18 16 14 12 10 8 6 4 2 0 0+

Tric ep Skinfold (m m )

weight, mid upper arm circumference and fat fold thickness at triceps were higher in all age groups in 1993–94. The increase in body weight is mainly due to increase fat as shown by rising fat fold thickness. .

1 99 3-9 4

4.6 Time Trends in mean triceps fatfold thickness in Urban women [1].

Data from National Family Health Survey-2 [2] indicates that the prevalence of undernutrition in urban areas is half of the prevalence of undernutrition in rural areas in 1998–1999 (Table 4.1). Prevalence of overnutrition is four-folds higher in urban as compared to rural areas. There is a progressive decline in the prevalence of undernutrition and progressive increase in the prevalence of overnutrition in adult women with increase in age. Data from NFHS-3 show that prevalence of both under and overnutrition in women is higher than men [3]. Table 4.1 Prevalence of undernutrition and overnutrition among women [5, 5–45] Characteristic

Rural Urban Age 15–19 20–24 25–29 30–34 35–49 All

Mean BMI

BMI < 18.5

BMI ? 25

1998–99

1998–99

1998–99

19.6 21.1

40.6 22.6

5.9 23.5

19.3 19.3 19.8 20.4 21.1 20.3

38.8 41.8 39.1 35.0 31.1 35.8

1.7 3.6 7.3 11.7 16.8 10.6

Interstate differences in dual nutrition burden

Public health nutrition in developing countries

90 50 40

%

30 20 10 S ikkim D elhi K e ra la P u nja b M e gh alaya M a nipu r M izo ra m A ru na ch a l P rad esh N ag a la nd G oa Ja m m u & K ashm ir Ta m iln ad u H im a ch a l P rad esh U ttra nch al H arya na A n dh ra prad esh K a m a taka G u ju rat M ah rash tra Ind ia R a ja stha n U tta r P rad esh Tripu ra A ssa m W est B en g al M a dh ya P rad esh O rissa C h ha tish ga rh Jah rkh a nd B iha r

0

% < 1 8 .5 kg /m 2

% >2 5.0 kg /m 2

4.7 Interstate differences in nutritional status of women NFHS-3 [6].

Data from India Nutrition Profile and NNMB surveys as well as NFHS data [2, 3, 4] show that all the states in India have entered the dual nutrition burden era but there are substantial interstate differences in prevalence of under and overnutrition (Figure 4.7). Populous states like Uttar Pradesh, Bihar, Madhya Pradesh, Rajasthan and Orissa have high undernutrition and low overnutrition rates. States like Delhi, Punjab has low undernutrition and high overnutrition rates. However, states like Goa, Tamil Nadu and Himachal Pradesh have relatively high undernutrition and overnutrition rates.

4.3

Nutritional status of pregnant and lactating women

4.3.1

Dietary intake in pregnant and lactating women

Data between 1975 and 2006 from NNMB and Indian Nutrition Profile (INP) surveys [5] (using 24-hour dietary recall method) show that between 1975 and 1995 there has been some increase in dietary intake. By the mid-nineties average intake of cereals almost met the RDA. However, data of early 2000 indicates a reduction in cereal intake inspite of the fact that cereals are available, accessible and affordable. There has been a progressive reduction in the pulse intake, which might be related to the rise in the cost of pulses. Intake of vegetables and fruits continue to be low (Table 4.2). Dietary intake of pregnant and lactating women is not different from that of the non-pregnant and nonlactating women (NPNL).

Dual nutrition burden in women: causes, consequences...

91

Table 4.2 Time trends in dietary intake (g/day) in pregnant and lactating women [1] Groups

Year

Non-pregnant and non-lactating women Pregnant women

Lactating women

1975–79 1996–97 2000–01 2005–06 1975–79 1996–97 2000–01 2005–06 1975–79 1996–97 2000–01 2005–06

Cereals Pulses Milk and and and millets legumes milk products 386 434 389 365 359 463 408 362 436 518 442 406

31 29 26 27 34 29 28 27 30 34 28 30

56 72 67 80 75 70 77 87 58 67 65 80

GLV’s

11 16 18 18 12 17 15 16 15 11 18 17

Roots Other and vegetubers tables

51 53 69 63 58 34 69 55 48 43 69 63

47 49 50 52 44 42 44 49 45 42 54 56

Fruits

11 24 20 26 11 26 21 25 13 34 24 24

Fats Sugar and oil and jaggery

9 13 12 13 12 12 12 14 10 13 13 14

16 21 16 14 19 15 17 14 16 19 13 13

Nutrient intake in pregnant and lactating women over the last three decades is presented in Table 4.3. Between 1975 and 1996 there was an increase in the total energy, protein and fat intake. However, over the last decade there has been a reduction in the energy intake. This might be due to the increasingly sedentary lifestyle in majority of the population and consequent reduction in energy requirement. In each of the four periods of time there is no difference in nutrient intake of pregnant and lactating women and non-pregnant, non-lactating (NPNL). All these data clearly indicate that in India women do not consume more food during pregnancy and lactation. Table 4.3 Time trends in nutrient intake in non-pregnant non-lactating (NPNL) and pregnant and lactating women (NNMB) [1] Groups

Years

1975–79 women 1996–97 2000–01 2005–06 Pregnant 1975–79 Women 1996–97 2000–01 2005–06 Lactating 1975–79 Women 1996–97 2000–01 2005–06 NPNL

Protein Total Energy Calcium Iron Vitamin Thiamin Riboflavin Niacin (g) fat (g) (kcal) (mg) (mg) A (µg) (mg) (mg) (mg) 45.4 49.9 48.2 46.5 40.8 47.2 49.7 46.8 47.6 56.5 50.3 49.6

17.1 24.5 27.6 21.8 18.8 21.5 25.9 22.5 18.3 24.6 25.9 22.1

1698 1983 1878 1738 1597 1994 1933 1726 1797 2243 2028 1878

330 382 445 443 390 339 463 456 358 373 408 447

21.0 22.0 14.1 13.8 20.0 23.0 14.0 14.0 23.0 23.0 14.6 14.7

118.0 148.0 219.8 254.0 160.0 142.0 227.0 261.0 133.0 162.0 212.0 249.0

1.00 0.90 1.20 1.10 1.00 0.90 1.20 1.10 1.10 1.10 1.30 1.20

0.70 0.80 0.60 0.60 0.60 0.80 0.70 0.60 0.70 0.90 0.60 0.60

11.0 12.0 14.9 14.2 10.0 11.0 15.1 13.7 12.0 14.0 16.3 15.5

Vitamin C (mg) 24 32 45 47 21 28 45 42 23 29 48 46

Studies carried out at National Institute of Nutrition, Hyderabad, in late seventies [6] showed that there was a socio-economic gradient in dietary intake in majority of women. In all the three groups, dietary intake

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Public health nutrition in developing countries

was not higher in pregnant women as compared to non-pregnant women from the same income group. The low income group women weighed 10 kg less than high income group of women and the birth weight of the offspring was only 2.7 kg (Table 4.4). Women from the upper income group consumed 2000 to 2500 kcal per day during pregnancy. In middle and high income groups, pregnant women do not perform hard physical labour during pregnancy and there was reduction in physical activity during pregnancy. The pre-pregnancy weight in this population group ranged between 45-55 kg and pregnancy weight gain was 11 kg. The mean birth weight of infants was 3.1 kg (Table 4.4).These data suggest that among habitually well-nourished women who eat to appetite, there is no increase in dietary intake during pregnancy; unchanged dietary intake did not have any adverse effect either on their own nutritional status or on the course and outcome of pregnancy. Table 4.4 Effect of socio-economic status on maternal nutrition [63]

Low income Middle income High income

No. (N)

Age (years)

Parity

1468 108 63

24.1 24.3 27.8

2.41 1.61 1.61

Height (cm)

Weight (kg)

151.5 156.3 156.3

45.7 49.9 56.2

Hb (g/dl)

Birth weight (kg)

10.9 11.1 12.4

2.7 2.9 3.13

Studies carried out by National Institute of Nutrition (NIN) during the seventies and early eighties [6] confirmed that among urban and rural lowincome group population in Hyderabad, there was no increase in dietary intake during pregnancy and lactation. Dietary intake ranged from 1200 to 1800 kcal per day. Pregnant women continued to look after the household and Table 4.5 Changes in anthropometric indices during pregnancy [6] Weight (kg) NPNL 1st trimester 2nd trimester 3rd trimester

42.3 41.5 44.6 46

Arm circumference (cm) 22.5 22.2 22.1 21.7

FFT (Fat fold thickness) (mm) 10.5 9.6 9.7 9.2

other activities and remained moderately active throughout pregnancy. These women weighed an average 43 kg prior to pregnancy and gained 6 kg during pregnancy. There was however a reduction in fat fold thickness (FFT) during pregnancy suggesting that the fat was getting mobilised to meet the gap in energy requirement (Table 4.5). There was no obvious deterioration in the maternal nutritional status during pregnancy or following repeated pregnancies provided the inter birth interval is longer

Dual nutrition burden in women: causes, consequences...

93

than 24 months.

4.3.2

Factor associated with deterioration of maternal nutritional status

Studies from India and other developing countries have shown that reduction in dietary intake below habitual levels or increased workload above the habitual levels were associated with deterioration in maternal nutritional status and reduction in birth weight. Some readily identifiable situations associated with deterioration in maternal nutritional status and reduction in birth weight are ●

● ●

● ● ● ●

reduction in habitual dietary intake (during drought and the preharvest season), increase in work (e.g., newly inducted manual laborers), combination of both the above (food for work programmes) during drought, adolescent pregnancy, pregnancy in lactating women, short inter-pregnancy interval and infections during pregnancy.

Effect of work status There is a progressive increase in women’s participation in labor force partly due to economic reasons. The economic returns are sometimes essential for improving the dietary intake of the family but the dual burden of work at home and at the work place has resulted in some deterioration in maternal nutrition status as indicated by body weight (Figure 4.8). 46

W eig ht (kg)

44 42 40 38 W orking W orking W orking women women women Nonpregnant Lactating Pregnant 4.8 Nutritional Status of Rural Women (Low Income) [6].

Public health nutrition in developing countries

94

52

B ody w eight (kg)

50 48 46 44 42 40 38 Not lactating

<=12

13-24

>24

Duration of lactation in m onths

4.9 Weight of pregnant women who concieved during lactation [6].

2.85 birth w eig ht (kg)

2.8 2.75 2.7 2.65 2.6 2.55 2.5 2.45 13-24 <1 2 Interpregnan cy in terv als (mo nth s) pregnant

>2 4

pregnant w om a n w ho we re lactating

4.10 Effect of conception during lactation on birth weight of infants.

Effect of conception during lactation on mother-child dyad Data from NFHS 1, 2 and 3 [2, 3, 4] indicate that the mean duration of lactation in India is about 24 months. Conception during the first year of lactation is relatively uncommon. This usually occurs in women who introduce supplements to the infant early, i.e. prior to six months. Most conceptions in lactating women occur during the second and third year of lactation. Studies on dietary intake of women who had conceived during lactation have shown that their dietary intake is essentially similar to the dietary intake of non-pregnant women from similar income groups.

Dual nutrition burden in women: causes, consequences...

95

The average calorie intake is no more than 1200–1800 kcal/day, and is inadequate with respect to all the nutrients. The dual stress of pregnancy and lactation widens the already existing gap between dietary intakes and nutrient requirements. Investigations undertaken by the National Institute of Nutrition, Hyderabad, has reported irrespective of the duration of lactation, women who conceived during lactation weighed less in all the trimesters of pregnancy than those who conceived after lactation. The difference in body weight was more marked in the third trimester, especially in the small group of women who had conceived during the first six months of lactation (Figure 4.9). Birth weight of neonates born to women who conceived during lactation or conceived within first 12 months after delivery was also lower (Figure 4.10). Too close and too many pregnancies have adverse nutrition and health consequences on the mother–child dyad and emphasizes that contraceptive care at appropriate time is an indirect but effective intervention to prevent deterioration in maternal nutritional status. Infections and undernutrition Morbidity due to common bacterial and viral infections are higher in under nourished women and infections aggravate undernutrition. HIV infection is a relatively new addition to the already existing burden of undernutrition associated with chronic wasting infections like TB. Maternal HIV infection and mother to child transmission of HIV infection has an adverse effect on birth weight, survival and growth in infancy and childhood.

4.4

Interventions to improve dietary intake and nutritional status in women

Research studies in India and in other countries have shown that pregnant women with reduction in habitual dietary intake or excess energy expenditure or whose body weight is less than 40 kg are identified and given adequate continuous food supplementation and antenatal care and so there is substantial improvement in the outcome of pregnancy, birth weight and neonatal mortality. Encouraged by such data, India has included food supplementation for pregnant and lactating women under Integrated Child Development Services (ICDS) programme who come to anganwadis. The reported coverage is between 15% and 20% in most ICDS projects. Unfortunately, ICDS programme does not screen pregnant women for undernutrition or provide adequate, continuous supplements to those with energy gap or those with moderate/severe undernutrition. In ICDS programme, improvement in nutritional status and its impact on maternal nutrition and birth weight is very limited. Since food supplements are provided to pregnant and lactating women without screening,

96

Public health nutrition in developing countries

identifying undernourished women, and special efforts for ensuring continued supplementation and monitoring compliance. One of the major problems is to ensure that food supplements reach the undernourished women. Even when the logistics of reaching the food to women is meticulously worked out and efficiently carried out, food sharing patterns within the family results in the ‘target’ women not getting significant quantities of the supplements. Obviously this is another important factor responsible for the demonstrated lack of beneficial effect. The lack of adequate antenatal care and continued physical work during pregnancy are two other factors responsible for the lack of impact. The Tenth Five Year Plan of Government of India envisaged that efforts will be made to weigh all women as early as possible in pregnancy and monitor their weight gain. Well nourished women will be advised not to increase their dietary intake to prevent overnutrition and obesity. Pregnant women who weigh less than 40 kg will be identified and ● ● ● ●

given food supplements consistently throughout pregnancy, given adequate antenatal care, monitored for weight gain during pregnancy and If weight gain is sub-optimal, efforts have to be made to identify the causes and attempt remedial measures.

Effective inter-sectoral coordination between auxiliary nurse midwives (ANMs), ASHAs and ICDS frontline workers (anganwadi workers or AWW) will enable the identification of undernourished pregnant and lactating women and provision of appropriate care to them. The panchayti raj institutions (PRIs) can play an important role by ensuring that these women receive food supplement throughout pregnancy. During the Tenth Five Year Plan, a pilot project on food grain supplementation to under nourished, pregnant and lactating women was initiated in 51 backward districts in the country. Evaluation of this programme indicated that there was community acceptance of the idea that pregnant and lactating women should be weighed and undernourished persons identified on the basis of body weight should be given 6 kg of food grains free of cost every month until delivery or first year of lactation is completed. The AWWs were able to carry out weighing and identification of undernourished women. Families were able to have an access to grains in most cases. Inspite of food sharing most of these women gained weight. The National Rural Health Mission (NRHM) envisages that on the village health and nutrition days, the ANM and AWW will work together and provide the required health and nutrition care. They will identify pregnant women with body weight less than 45 kg and lactating women with body weight less than 40 kg and give them food supplementation on priority. Prevention, detection and management of anemia will also receive

Dual nutrition burden in women: causes, consequences...

97

the attention it deserves. It is expected that if effectively implemented, this strategy can bring about substantial improvement in maternal nutritional status in pregnancy and lactation. 1 00

8 .9

1 0.6

8 0.3

7 8.6

1 0.8

1 0.8

1 97 9

2 00 4

% of e ne rgy

75 50 25 0

P ro te in

C a rb

Fat

4.11 Contribution of nutrients to energy intake [1]. 2 50 0

K cal/ CU / day

2 00 0 1 50 0 1 00 0 5 00 0 1 97 5-7 9 1 98 8-9 0 1 99 6-9 7 2 00 0-0 1 2 00 4-0 5

R u ral

1 97 5-7 9 1 99 3-9 4

U rb an slu m

4.12 Time trends in energy intake [1].

4.5

Factors responsible for the emerging problem of overnutrition

4.5.1

Changes in dietary intake

Data on time trends in nutrient intake are available from surveys conducted by the NNMB [1] is presented in Figs. 4.11 and 4.12. There has been some decline in intake of most of the nutrients both in urban and rural

98

Public health nutrition in developing countries

areas over the last three decades. Energy intake is lower in urban areas in spite of higher intake of fats and oils because of lower cereal intake. Over the past three decades there have been a reduction in the percentage of total energy intake from carbohydrates and some increase in the percentage of dietary energy from fats (Figure 4.11). In spite of this, the proportion of dietary energy from fat remains lower than 15%. Over the last three decades, there has been a reduction in energy intake both in urban and rural areas (Figure 4.12). Data from National Sample Survey Organisation (NSSO) [7] have shown that this is not due to lack of access to food or affordability. It is possible that the perceptive population realises that with reduction of the physical activity there is a reduction in energy requirement and possibly reduction in their energy intake has to be considered. However, there are disparities between intakes of urban and rural populations, different states and different socio-economic groups. Among the affluent segments of population especially in urban and peri-urban areas, there has been an increase in the fast food and soft drink consumption and consequent increase in empty calorie intake. This coupled with increasingly sedentary life style has been responsible for the steep increase in overnutrition in this segment of population.

4.5.2

Physical activity

Physical activity is one of the major determinants of energy requirement. Physiologists recognize four domain of physical activity – work, domestic, transport and discretionary. Until two decades ago in most developing countries including India, physical activity in work, domestic and transport domains was very high. As a result majority of the population expended very little energy in discretionary physical activity. Because of the high physical activity level in daily chores, majority of the population were moderately active and hence their energy requirement was that of a moderately active population. They enjoyed the health benefits of moderate physical activity without any discretionary physical activity (Figure 4.13). The last two decades witnessed significant changes in lifestyle. The availability of transport both personal and public has improved several folds (Figure 4.14) and energy expenditure in reaching places of study/work has become a fraction of what it was two decades ago. NSSO consumption expenditure surveys have shown steep increase in expenditure on transport confirming the trend of increasing use of mechanized transport. Better access to water and fuel both in urban and rural have resulted in substantial reduction in energy spent by women on collecting water and fuel.

Dual nutrition burden in women: causes, consequences... W ork D om ains

D o m e stic d om a in

Tra nsp ort do m ain

99

D iscre tio na ry A ctivity D o m a in

Developed country

Developing country

4.13 Physical activity: domain [13]. 3 .5 3 .0 25 20 15 10 5 0

C a rs / Jee ps M otorise d 2 w he elers P o pu la tion

1 97 1-7 1

1 98 0-8 1

1 99 0-9 1

2 00 0-1

2 00 3-4

4.14 Relative increase in the production of vehicles and the population [8].

During the last decade some well-planned studies investigating physical activity pattern in urban and rural areas and in different income group have been initiated. The PURE India study documented level of mechanization for transport and domestic activities in urban and rural areas (Table 4.6). It is obvious that in urban areas, transport as well as household activity is highly mechanized. Majority of urban population are working in white or blue-collar jobs, where occupation related physical activity levels are low. As a result even though urban women spend time in domestic and occupation related activities, their energy expenditure for these activities is low (Figure 4.14). Their discretionary activities are TV viewing, computer games etc with very low energy expenditure. Unchanged dietary intake reduced physical activity and consequent energy requirement is responsible for positive energy balance and increase in overnutrition in the population.

Public health nutrition in developing countries

M inu te s/da y

100

Energy expenditure on various activities

8 00 7 00 6 00 5 00 4 00 3 00 2 00 1 00 0 U rb an m en S le e p

W o rk

U rb an W o m e n D o m e stic

R u ral m en

D isc re tio n a ry E xe rc is e

Tra ns p o rt

R u ral W om e n D isc re tio n a ry -S e d e n ta ry

4.15 Energy expenditure on various activities [9].

4.5.3

Energy balance studies in urban-affluent population

Cross-sectional studies undertaken among affluent housewives [11] in the age group of 30–70 years in Delhi showed that their dietary intake remained unaltered between 2100 and 2300 kcal/day. In each age group the energy expenditure was lower by about 70–100 kcal/day [10]. This positive energy balance was associated with a weight gain of about 5 kg per decade (Table 4.7). These women did not make any conscious effort to increase physical activity nor take up regular exercise regime until they were over 60 years of age or had health problems. It is possible that similar situation exists among men in these segments of population. Among affluent segments of population, small but persistent positive energy balance may be the most important factor responsible for the slow but steady weight gain in adults. Table 4.6 Level of mechanization in urban and rural populations (% household ownership) [9] Rural Monthly household income (Rs)

Urban

1860

12674

7.9 0.2

78.2 12.2

0.1 4.5

41.4 95.2

24.9

98.2

Transport Motorized two-wheelers Car Household appliances Washing machine Kitchen mixer/blender Leisure Television

Dual nutrition burden in women: causes, consequences...

101

Table 4.7 Energy intake and expenditure in urban affluent housewives [10] Groups

Weight BMI BF% (Kg) (kg/m2)

TDEI (kcal)

TDEE (Kcal/day)

D3 (30–39 years) [n=22]

59

24.8

32.8 2,134 2056±238.7 1724.5–2665.5)

D4 (40–49 years) [n=20]

64

26.4

36.5 2,264 2191±306.6 (1785.4–2817.3)

D5 (50–59 years) [n=20]

69

28.6

40.3 2,195 2146±173.1 (1849.4–2494.0)

D6 (60–69 years) [n=14]

66

29.3

44.0 2,065 1971±118.4 (1770.0–2144.3)

D7 (70–88 years) [n=07]

56

24.5

38.5 1562

Parrmer Energy Measured Balance RMR (kcal/day) (TDEE/ (Kcal) measured RMR) +78

+73 +49

1562+ 260 (1166–2059)

1.33±0.14 (1.12–1.59)

1779± 273 (1267–2304)

1.24±0.10 (1.10–1.49)

1752± 274 (1224–2203)

1.24±0.12 (1.06–1.51)

1457 ±154 +94

(1224–1742)

1.36+0.14 (1.16–1.69)

1736±162.8 (1553.0–2012.0) ? 174

1292± 108 (1152–1454)

1.35±0.14 (1.15–1.52)

TDEI – Total Daily Energy Intake TDEE – Total daily Energy Expenditure BF – Body Fat RMR – Resting Metabolic Rate

4.6

Undernutrition – overnutrition linkages

The seeds for obesity in adult life might be sown decades earlier. The thrifty gene hypothesis proposes that populations who had faced energy scarcity over millennia may evolve, so that majority has thrifty gene which conserves energy. If this population gets adequate or excess energy intake, they lay down fat, develop abdominal obesity, increased insulin resistance, which may progress to diabetes and incur risk of hypertension and CVD. Barker’s thrifty phenotype hypothesis shifts the evolution of thriftiness to intrauterine period. Indians with one-third low birth weight rate can be deemed to have acquired the risk of metabolic syndrome in utero. Bhargava and co-workers [11] have shown that in urban Delhi during the nineties, even low middleincome adults who were undernourished in infancy, childhood and adolescence, develop obesity, both general and abdominal. About one-sixth of this cohort suffers from impaired glucose tolerance and hypertension at the age of 30 (Table 4.8 and 4.9). Table 4.8 Time trends in nutritional status of Delhi cohort [11]. Male

Female

Age

No.

Weight (kg)

At birth 2 yrs 12 yrs 30 yrs

803 834 867 886

2.89±0.44 10.3±1.3 30.9±5.9 71.8±14.0

No.

Weight (kg)

561 609 625 640

2.79±0.38 9.8±1.2 32.2±6.7 59.2±13.4

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Table 4.9 Current status of Delhi cohort [11] Characteristic

Men

Weight (Kg.) Height (m) BMI Waist–hip ratio BMI > 25 BMI > 23 Central Obesity (percent) Impaired GTT

Women

No.

Value

No.

Value

886 886 886 886 886 886 886 849

71.8±14.0 1.70±0.06 24.9±4.3 0.92±0.06 47.4 66.0 65.5 16

640 638 638 639 638 638 639 539

59.2±13.4 1.55±0.06 24.6±5.1 0.82±0.07 45.5 61.8 31 14

The lesson to be learnt from these data is that it is never too early for Indians to start practicing healthy lifestyle and dietary habits. Early detection and correction of undernutrition until children attain appropriate weight for their height is essential to promote linear growth. Adolescents and adults should consume balanced diet with just adequate energy intake. Exercise has to become a part of daily routine to promote muscle/bone health and prevent development of adiposity in all age groups.

4.6.1 Health consequences of overnutrition It is well documented that Indians have higher body fat for the same BMI as compared to the Caucasians. Prevalence of abdominal obesity is higher in Indians. Both overnutrition and abdominal obesity are associated with increased risk of hypertension, diabetes and CVD. Nutrition Foundation of India carried out studies exploring relationship between overnutrition, hypertension and biochemical changes associated with increased risk of cardiovascular diseases in persons belonging to different income groups 30 H igh B P (% )

25 20 15 10 5 0 L ow

H ig h

>2 5 .0

1 8.5 -2 5.0

<1 8 .5

BM I

WHR M ales

Fe m ales

4.16 Overnutrition and hypertension High BP (%) [12].

Dual nutrition burden in women: causes, consequences...

103

H ig h B P p e rce nta ge

40 30 20 10 0 L ow

H ig h

< 1 8 .5

L ow

H ig h

1 8.5 -2 5 .0 M ales

H ig h

L ow

2 5.0 + F e m a le s

4.17 Abdominal adiposity and hypertension [12].

Valu e s (m g % )

working in a government institution. Prevalence of abdominal adiposity (high waist–hip ratio (WHR)) was higher in subjects (50.3%) as compared to overnutrition (BMI>25; 30.8%). The higher the BMI and WHR, the higher were the prevalence rates of hypertension both in men and women (Figure 4.16). The prevalence of high blood pressure in the normal and overweight subjects was higher when WHR was high. Overweight/obese subjects of both sexes with abdominal adiposity had higher systolic and diastolic blood pressure as compared to those without abdominal obesity (Figure 4.16). Blood glucose, serum cholesterol and triglycerides were significantly higher in subjects with BMI>25 (Figure 4.17) and higher WHR (Figure 4.18). A cluster of risk factors has been demonstrated to be associated with central obesity. These include glucose intolerance, obesity, hyperinsulinemia, hypertriglyceridemia, and hypertension, all of which are important risk factors for ischamic heart disease. Poor access to health care for non-communicable diseases among poorer segments of population (especially in women) might be associated with higher case fatality rates in all non-communicable diseases. It is therefore imperative to improve access to essential health care for noncommunicable diseases to women from all segments of population. <1 8 .5

2 40 2 00 1 60 1 20 80 40 0 M ale

Fe m ale

B loo d su ga r (m g% )

M ale

Fe m ale

C h oleste rol (m g% )

M ale

Fe m ale

Triglyceride s (m g% )

4.18 Effect of BMI on Biochemical Parameters [12].

<1 8 .5-2 5

M ale

>2 5

Fe m ale

H D L ch oleste ro l (m g% )

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104

Value (m g%)

I WHR 2 00 1 60 1 20 80 40 0

M ale

Fe m ale

B loo d su ga r (m g% )

M ale

Fe m ale

C h oleste rol (m g% )

M ale

II W H R

Fe m ale

Triglyce rid es (m g% )

M ale

III W H R

Fe m ale

H D L ch o le ste ro l (m g% )

W H R - M ales-< 0.9 3 , Fe m ales,0 .8 1; W H R II- M a le s-0.9 3 -1.00 , Fe m alse s-0 81 -0 89 ; W H R III- M a le s-> 10 0 Fe m alse s-08 9

4.19 Effect of WHR on Biochemical Parameters [12].

4.6.2

Interventions to reduce overnutrition

Currently overnutrition rate in India is relatively low. It is imperative that vigorous efforts are made to ensure that further escalation in overnutrition does not occur. Sustained increase in physical activity especially discretionary physical activity is the major intervention required to combat emerging problem of overnutrition in women. The lifestyle changes that have led to steep reduction in physical activity have occurred mainly in the last decade. The urban elite among whom overnutrition rates are the highest have become aware of the need for increasing physical activity, it is likely that further escalation in overnutrition rates might be prevented. Currently, overnutrition rates in rural areas are low. Appropriate steps will have to be taken to generate awareness about the need for sustained high physical activity so that overnutrition rates continue to remain low. Among the segments of population who are indulging in junk food eating, well directed nutrition education messages may help to bring about healthy eating habits. It is essential that these messages have to be repeated; efforts have to be made to provide to support them during the difficulties they experience in breaking the junk food habit.

4.7

Summary and conclusion

Surveys carried out by the National Nutrition Monitoring Bureau and National Family Health Survey indicates that India has entered the dual nutrition burden era. In all the states and in all strata of society both under and overnutrition coexist. The proportion of women with undernutrition is higher in states with high poverty levels. Overnutrition is more common among affluent segments of population especially those living in urban areas.

Dual nutrition burden in women: causes, consequences...

105

Over the last three decades there has been 2–4 cm increase in mean height and significant increase in the mean body weight. Increase in body weight is mostly due to increase in body fat as shown by increase fat fold thickness. Consumption expenditure surveys and diet surveys have shown that mean energy intake in women well below 2000 kcal/day and there has been a small reduction in total energy intake in both urban and rural areas. There has been some increase in dietary energy derived from fat and a reciprocal reduction in percentage of dietary energy derived from carbohydrate; however, even in 2006 energy from fat is less than 15% of over all energy intakes. Dietary intake of pregnant and lactating women is similar to dietary intake of non-pregnant and non-lactating women. There is no deterioration in maternal nutrition with pregnancy and lactation provided inter pregnancy interval is over 2 years. Reduction in dietary intake below habitual levels or increased workload above the habitual levels is associated with deterioration in maternal nutritional status and reduction in birth weight. Some readily identifiable situations associated with deterioration in maternal nutritional status and reduction in birth weight are ●

● ●

● ● ● ●

reduction in habitual dietary intake (during drought and the preharvest season), increase in work (e.g., newly inducted manual laborers), combination of both the above (food for work programmes) during drought, adolescent pregnancy, pregnancy in lactating women, short inter-pregnancy interval, and infections during pregnancy.

In all states of India undernutrition continues to be a major problem in women. Maternal undernutrition is associated with low birth weight; leading to poor growth during infancy, childhood, adolescence and small stature in adults. Identification of pregnant women below 45 kg and special effort to provide food supplements and monitor for adequate weight gain in these women under the ICDS or NRHM Programme, would contribute to reduction in incidence of low birth weight. Major factor responsible for emerging problem of overnutrition is substantial reduction in physical activity levels in all segments of population. In some segments of population junk food eating is a contributory factor. Over the last two decades there has been ● ●

reduction in the number of the persons engaged in manual work, substantial improvement in mechanical aids in agriculture, industry and allied activities,

106 ●

●

●

●

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improvement in access to water and fuel near households both in urban and rural areas, availability of mechanized transport at affordable cost has resulted in fewer people walking or cycling to work place, school or market, kitchen aids have reduced physical activity during cooking and household chores, and among urban affluent class, TV and computers contributed to steep reduction in physical activity.

As a result of these lifestyle changes, there has been a reduction in energy requirements. Unchanged energy intake and reduced energy requirement is associated with positive energy balance, fat deposition and weight gain. Overnutrition and abdominal adiposity are associated with increased risk of non-communicable diseases. Recent studies from Delhi have shown undernutrition in childhood may be a predisposing factor for overnutrition and increased risk of noncommunicable diseases in adult life. Indian women appear to have a predisposition for adiposity (especially abdominal), insulin resistance, diabetes, hyper-triglyceridaemia and cardiovascular diseases. It is essential that the dual nutrition and health burden is combated through efficient implementation of time tested, effective and inexpensive interventions to achieve significant reduction in both over and undernutrition and their adverse health consequences.

References 1. National Nutrition Monitoring Bureau (NNMB) (1979–2002).NNMB Reports. National Institute of Nutrition, Hyderabad. 2. IIPS National Family Health Survey (NFHS-2): http://www.nfhsindia.org/india2.html; last accessed on 24/09/07. 3. IIPS National Family Health Survey (NFHS-3): http://mohfw.nic.in/nfhsfactsheet.htm; last accessed on 24/09/07. 4. IIPS National Family Health Survey (NFHS-1) http://www.nfhsindia.org/anfhs1.html. 5. Department of Women and Child Development India Nutrition Profile 1 (1995–96), Government of India, New Delhi. 6. RAMACHANDRAN P (1989). Nutrition in pregnancy. In “Women and nutrition in India” GOPALAN C . and KAUR S. (eds). Nutrition Foundation of India, Special Publication (No.5), pp. 153. 7. National Sample Survey Organization: Reports of NSSO surveys 1973–2000. NSSO, New Delhi. 8. Economic Survey of India 2003–04; http://indiabudgetnic.in/es2006-07/ esmain.htm last accessed on 24/09/07. 9. PURE Prospective Urban and Rural Epidemiological Study: http:// www.ccc.mcmaster.ca/pure/index.html; last accessed on 24/09/07.

Dual nutrition burden in women: causes, consequences... 10.

WASUJA M, SIDDHU A

107

(2003). Decade wise alterations in energy expenditure and energy status of affluent women (30–88 years) – A cross-sectional study. Delhi University, New Delhi. (Ph.D. Thesis). 11. BHARGAVA SK, SACHDEV HP, FALL HD, OSMOND C , LAKSHMY R, BARKER DJP, BISWAS SKD, RAMJI S , PRABHAKARAN D , REDDY KS . Relation of serial changes in childhood Body Mass Index to impaired glucose tolerance in young adulthood. New Eng J Med vol. 350, pp. 865–875. 12. Nutrition Foundation of India (2005). Twenty Five Years Report 1980–2005. New Delhi. 13. KURPAD AV. Changing energy requirements of Indians. In: Proceedings of Nutrition Foundation of India (NFI)—WHO symposium on “Nutrition Development Transition in India”, July 2010.

5 Measuring undernutrition and overnutrition in children Dheeraj Shah and H.P.S. Sachdev

Dheeraj Shah MD, DNB, MNAMS is an Associate Professor in Pediatrics at University College of Medical Sciences, Delhi. He is also the Associate Editor of Indian Pediatrics. Dr. Shah has served as a visiting fellow at The Royal college of Pediatrics and Child Health, London, UK and was an Associate Professor at the Department of Pediatrics and Adolescent Medicine, B.P. Koirala Institute of Health Sciences, Dharan, Nepal. H.P.S. Sachdev MD, FIAP, FAMS is a senior consultant in Pediatrics and Clinical Epidemiology at Sitaram Bhartia Institute of Science and Research, New Delhi. He is also an adjunct professor at St. John’s Research Institute, Bangalore and visiting professor at MRC Epidemiology Resource Centre, Southampton. Dr. Sachdev has served as a professor in the Department of Pediatrics, Maulana Azad Medical College, National President of Indian Academy of Pediatrics, Secretary of Nutrition Society of India and Editor-in Chief of Indian Pediatrics.

5.1

Introduction

Nutritional status of the individuals and populations can be assessed by various methods such as measurement of food intake, biochemical parameters (e.g. serum proteins, lipid profile, iron studies, etc.) and nutritional anthropometry. Moreover in recent years, sophisticated methods such as magnetic resonance imaging (MRI), dual energy X-ray absorptiometry and Dexa-scan have been used to estimate various nutritional parameters. Anthropometry is the most commonly used method to assess nutritional status of individuals and populations as it is inexpensive, convenient and non-invasive. Depending on the anthropometric indicators selected, it can be used for various purposes such as screening at-risk children and measuring short-term or long-term changes in nutritional status. However, there are inherent limitations in using anthropometry as a tool for nutritional assessment [1]. One aspect of this is that changes in anthropometry may take some time after nutritional deprivation

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Measuring undernutrition and overnutrition in children

109

to set in and the deprivation may be fairly long standing for linear growth retardation. Also, simple anthropometry in the context of overnutrition may cause difficulty in distinguishing lean from adipose tissue thus failing to distinguish well-built (e.g. athletes) from obese people. Despite these limitations, anthropometry is the most practical way of measuring nutritional status of individuals or populations.

5.2

Anthropometric techniques

For anthropometry to be valid, it is necessary that the data are collected in a proper way and the recommended measurement technique is followed. The child’s accurate age is required and any error in recording or interpreting child’s age makes the whole process of anthropometry fruitless. In communities, it is common to state the age as the year of life the child has now entered. For example, if the child has completed 5 years of age in September 2007, parents might start telling his/her age as 6 years from as early as October 2007. If possible, the exact date of birth of the child should be asked or examined from a document (such as birth certificate or horoscope) and the exact age on the day of measurement should be calculated by the evaluator him/herself and measured to the nearest month. If dates cannot be recalled, use of a local calendar or recollection of important events may assist mothers in recalling the date of birth. Accurate anthropometric measurement is a skill requiring specific instruments and training. Whatever equipment is chosen, staff needs training to ensure its proper use. The training of personnel on specific measurement and recording techniques should include not only theoretical explanations and demonstrations, but also provide an opportunity for participants to practice the measurement techniques, as well as reading and recording the results. Once all personnel have adequately practiced the measurement and recording techniques, and feel comfortable with their performance, standardization exercises should be carried out to ensure that all interviewers acquire the skills necessary to collect high quality data [2].

5.2.1

Measuring length/height

Length/height boards should be designed to measure children under 2 years of age lying down (recumbent) and older children standing up. The board should be able to measure up to 0.1 cm. A measuring board should be lightweight, durable and have few moving parts. Length (for infants and children upto the age of 23 months) (Figure 5.1) Place the measuring board on a hard flat surface, i.e. ground, floor, or

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steady table. Kneel/stand on the right side of the child so that you can hold the foot piece with your right hand. With the mother’s help, lay the child on the board by supporting the back of the child’s head with one hand and the trunk of the body with the other hand. Gradually lower the child onto the board. An assistant should cup his/her hands over the child’s ears and place the child’s head against the base of the board so that the child is looking straight up. The child’s line of sight should be perpendicular to the ground. Make sure the child is lying flat and in the center of the board. Press the child’s shins and knees firmly against the board and with your right hand place the foot piece firmly against the child’s heels. When the child’s position is correct, read the measurement to the nearest 0.1 cm, release the child carefully and record the value [2, 3]. Height (for children aged 24 months and older) (Figure 5.2) Place the measuring board or stadiometer on a hard flat surface against a wall, table, tree, etc. Make sure the board/stadiometer is not moving. Ask the mother to remove the child’s shoes and unbraid any hair that would interfere with the height measurement. Make sure the child’s legs are straight and the heels and calves are against the board/wall. Tell the child to look straight ahead at the mother who should stand in front of the child. Make sure the child’s line of sight is level with the ground and the shoulders are level. The hands of the child should be at the child’s side and the head, shoulder blades and buttocks are against the board/ wall. Place your open left hand under the child’s chin and with your right hand lower the headpiece on top of the child’s head making you push through the child’s hair. When the child’s position is correct, read the measurement to the nearest 0.1 cm, remove the headpiece from the child’s head and your left hand from the child’s chin. Record the measurement immediately to avoid any recall errors [2, 3].

5.2.2

Measuring weight

Weighing scales used should be portable, durable and sensitive. Spring scales are commonly used in field-studies. There are several different attachments that can be used to help weigh children with spring scales. The size of the child will determine which attachment should be used. For weighing infants, a sling or basket is usually attached to the spring scale. For children, weighing trousers are used to suspend them. These are small pants with straps that the child steps into. The trousers are then hung from the scale by the straps. Whatever is used to suspend the child, the scale should be zeroed to ensure that the weight of the trousers, sling or basket is not added to the child’s weight.

Measuring undernutrition and overnutrition in children

5.1 Technique for measuring length (for children 0–23 months)

111

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Public health nutrition in developing countries

5.2 Technique for measuring height (for children >24 months)

Measuring undernutrition and overnutrition in children

113

Using a hanging scale (Salter-type or spring balance) (Figure 5.3) Hang the scale from a secure place like the ceiling beam. You may need a piece of rope to hang the scale at eye level. Ask the mother to undress the child as much as possible. Attach a pair of the empty weighing trousers or sling to the hook of the scale and adjust the scale to zero, then remove from the scale. Put your arms through the leg holes of the trousers and grasp the child’s feet pulling the legs through the leg holes. Attach the strap of the pants to the hook of the scale and gently lower the child to allow him/her hang freely. Hold the scale and read the weight to the nearest 0.1 kg when the child is still and the scale needle is stationary. Gently lift the child by the body, release the strap from the hook of the scale and record the measurement immediately. Using an electronic or mechanical weighing scale Remove or minimize the clothing on the child. Place the scale on a hard and flat surface. Correct any zero error in case of mechanical type of scales and ensure zero reading (by taring) in case of electronic scales. In case of older child using a standing type of scale, ask the child to stand on the middle of the scale and record the reading when the needle stops moving or when the numbers stop changing (in case of electronic scales). While weighing a young child on a lying-down type of scale, place a clean sheet of paper or warm cloth on the surface of the scale. Bring the reading to zero by adjusting the needle (in mechanical scales) or by taring (in case of electronic scales). Record the weight to the nearest accuracy possible on that scale. If only standing type of scale is available and the child is unable to stand (as in case of young, sick or uncooperative child), the mother and child can be weighed simultaneously. However, the sensitivity of the scale should be 0.1 kg for this purpose (as in UNICEF electronic scale). The bathroom scales with sensitivity of 0.5 kg are not suitable for this purpose. Ask the mother to stand on the scale. Record the weight and include the reading with one decimal point (e.g. 57.4 kgs). Pass the child to a person nearby. Record the second reading with just the mother (e.g. 50.8 kgs). The difference (e.g. 6.6 kgs) is the weight of the child.

5.2.3

Measuring mid-arm/mid-upper arm (MUAC) circumference (Figure 5.4)

Very young children can be held by their mother during this procedure. Ask the mother to remove clothing that may cover the child’s left arm. Calculate the midpoint of the child’s left upper arm by first locating the tip of the child’s shoulder with your finger tips. Bend the

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5.3 Measuring weight of a child using hanging scale

Measuring undernutrition and overnutrition in children

5.4 Measuring mid-upper arm circumference

115

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Public health nutrition in developing countries

child’s elbow to make a right angle. Place the tape at zero on the tip of the shoulder and pull the tape straight down past the tip of the elbow. Read the number at the tip of the elbow to the nearest centimeter and mark the midpoint with a pen on the arm. Straighten the child’s arm and wrap the tape around the arm at midpoint making sure the tape is flat around the skin. Make sure the tape has the proper tension and is not too tight or too loose. When the tape is in the correct position on the arm with the correct tension, record the measurement to the nearest 0.1 cm. Anthropometric indices The four building blocks or measures used to undertake anthropometric assessment are (i) age, (ii) sex, (iii) weight, and (iv) length (or height). Each of these variables provides one piece of information about a person. When they are used together they can provide important information about a person’s nutritional status. When two of these variables are used together they are called an index. The indices commonly used in assessing the nutritional status of children are “Weight-for-age”, “Length-for-age or Height-forage”, “Weight-for-length or Weight-for-height” and body mass index. There are many other anthropometric measures including mid-upper arm circumference (MUAC), waist-hip ratio and skin-fold thicknesses. Weight-for-age Low weight-for-age index identifies the condition of being underweight for a specific age. The advantage of this index is that it reflects both past (chronic) and/or present (acute), although it is unable to distinguish between the two and is recommended as the indicator to assess changes in the magnitude of malnutrition over time [4]. However, the disadvantage of this index is that it fails to distinguish between the low weight because of less height (stunting) or because of low muscle and fat mass (wasting). Another disadvantage is that this parameter may not detect or classify malnutrition accurately when there is a presence of increased extravascular fluid (as in edema or serous effusions) or tumor load as in cancer patients. In these conditions, any weight-based index is likely to underdiagnose malnutrition. Table 5.1 presents the weight for age index for boys and girls [5].

2.1 2.9 3.8 4.4 4.9 5.3 5.7 5.9 6.2 6.4 6.6 6.8 6.9 7.1 7.2 7.4 7.5 7.7 7.8 8.0 8.1 8.2 8.4 8.5 8.6 8.8 8.9 9.0 9.1 9.2 9.4

0:0 0:1 0:2 0:3 0:4 0:5 0:6 0:7 0:8 0:9 0:10 0:11 1:0 1:1 1:2 1:3 1:4 1:5 1:6 1:7 1:8 1:9 1:10 1:11 2:0 2:1 2:2 2:3 2:4 2:5 2:6

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30

–3SD

Month

Months

Year :

2.5 3.4 4.3 5.0 5.6 6.0 6.4 6.7 6.9 7.1 7.4 7.6 7.7 7.9 8.1 8.3 8.4 8.6 8.8 8.9 9.1 9.2 9.4 9.5 9.7 9.8 10.0 10.1 10.2 10.4 10.5

–2SD 2.9 3.9 4.9 5.7 6.2 6.7 7.1 7.4 7.7 8.0 8.2 8.4 8.6 8.8 9.0 9.2 9.4 9.6 9.8 10.0 10.1 10.3 10.5 10.7 10.8 11.0 11.2 11.3 11.5 11.7 11.8

–1SD 3.3 4.5 5.6 6.4 7.0 7.5 7.9 8.3 8.6 8.9 9.2 9.4 9.6 9.9 10.1 10.3 10.5 10.7 10.9 11.1 11.3 11.5 11.8 12.0 12.2 12.4 12.5 12.7 12.9 13.1 13.3

3.9 5.1 6.3 7.2 7.8 8.4 8.8 9.2 9.6 9.9 10.2 10.5 10.8 11.0 11.3 11.5 11.7 12.0 12.2 12.5 12.7 12.9 13.2 13.4 13.6 13.9 14.1 14.3 14.5 14.8 15.0

Median 1 SD

Boys

4.4 5.8 7.1 8.0 8.7 9.3 9.8 10.3 10.7 11.0 11.4 11.7 12.0 12.3 12.6 12.8 13.1 13.4 13.7 13.9 14.2 14.5 14.7 15.0 15.3 15.5 15.8 16.1 16.3 16.6 16.9

2SD 5.0 6.6 8.0 9.0 9.7 10.4 10.9 11.4 11.9 12.3 12.7 13.0 13.3 13.7 14.0 14.3 14.6 14.9 15.3 15.6 15.9 16.2 16.5 16.8 17.1 17.5 17.8 18.1 18.4 18.7 19.0

3SD 2.0 2.7 3.4 4.0 4.4 4.8 5.1 5.3 5.6 5.8 5.9 6.1 6.3 6.4 6.6 6.7 6.9 7.0 7.2 7.3 7.5 7.6 7.8 7.9 8.1 8.2 8.4 8.5 8.6 8.8 8.9

–3SD 2.4 3.2 3.9 4.5 5.0 5.4 5.7 6.0 6.3 6.5 6.7 6.9 7.0 7.2 7.4 7.6 7.7 7.9 8.1 8.2 8.4 8.6 8.7 8.9 9.0 9.2 9.4 9.5 9.7 9.8 10.0

–2SD

Table 5.1 WHO Growth Standards Weight-for-Age – boys and girls birth to 5 years (Z scores) [5]

2.8 3.6 4.5 5.2 5.7 6.1 6.5 6.8 7.0 7.3 7.5 7.7 7.9 8.1 8.3 8.5 8.7 8.9 9.1 9.2 9.4 9.6 9.8 10.0 10.2 10.3 10.5 10.7 10.9 11.1 11.2

–1SD 3.2 4.2 5.1 5.8 6.4 6.9 7.3 7.6 7.9 8.2 8.5 8.7 8.9 9.2 9.4 9.6 9.8 10.0 10.2 10.4 10.6 10.9 11.1 11.3 11.5 11.7 11.9 12.1 12.3 12.5 12.7

3.7 4.8 5.8 6.6 7.3 7.8 8.2 8.6 9.0 9.3 9.6 9.9 10.1 10.4 10.6 10.9 11.1 11.4 11.6 11.8 12.1 12.3 12.5 12.8 13.0 13.3 13.5 13.7 14.0 14.2 14.4

Median 1 SD

Girls

4.2 5.5 6.6 7.5 8.2 8.8 9.3 9.8 10.2 10.5 10.9 11.2 11.5 11.8 12.1 12.4 12.6 12.9 13.2 13.5 13.7 14.0 14.3 14.6 14.8 15.1 15.4 15.7 16.0 16.2 16.5

2SD 4.8 6.2 7.5 8.5 9.3 10.0 10.6 11.1 11.6 12.0 12.4 12.8 13.1 13.5 13.8 14.1 14.5 14.8 15.1 15.4 15.7 16.0 16.4 16.7 17.0 17.3 17.7 18.0 18.3 18.7 19.0

3SD

Measuring undernutrition and overnutrition in children 117

10.7 10.8 10.9 11.0 11.2 11.3 11.4 11.5 11.6 11.8 11.9 12.0 12.1 12.2 12.4 12.5 12.6 12.7 12.8 12.9 13.1 13.2 13.3 13.4 13.5 13.6 13.7 13.8 14.0 14.1

–2SD 12.0 12.1 12.3 12.4 12.6 12.7 12.9 13.0 13.1 13.3 13.4 13.6 13.7 13.8 14.0 14.1 14.3 14.4 14.5 14.7 14.8 15.0 15.1 15.2 15.4 15.5 15.6 15.8 15.9 16.0

–1SD 13.5 13.7 13.8 14.0 14.2 14.3 14.5 14.7 14.8 15.0 15.2 15.3 15.5 15.7 15.8 16.0 16.2 16.3 16.5 16.7 16.8 17.0 17.2 17.3 17.5 17.7 17.8 18.0 18.2 18.3

15.2 15.4 15.6 15.8 16.0 16.2 16.4 16.6 16.8 17.0 17.2 17.4 17.6 17.8 18.0 18.2 18.4 18.6 18.8 19.0 19.2 19.4 19.6 19.8 20.0 20.2 20.4 20.6 20.8 21.0

Median 1 SD

Boys

Source: http://www.who.int/childgrowth/standards/en/

9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.2 12.3 12.4

2:7 2:8 2:9 2:10 2:11 3:0 3:1 3:2 3:3 3:4 3:5 3;6 3:7 3:8 3:9 3:10 3:11 4:0 4:1 4:2 4:3 4:4 4:5 4:6 4:7 4:8 4:9 4:10 4:11 5:0

31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60

–3SD

Month

Months

Year :

17.1 17.4 17.6 17.8 18.1 18.3 18.6 18.8 19.0 19.3 19.5 19.7 20.0 20.2 20.5 20.7 20.9 21.2 21.4 21.7 21.9 22.2 22.4 22.7 22.9 23.2 23.4 23.7 23.9 24.2

2SD 19.3 19.6 19.9 20.2 20.4 20.7 21.0 21.3 21.6 21.9 22.1 22.4 22.7 23.0 23.3 23.6 23.9 24.2 24.5 24.8 25.1 25.4 25.7 26.0 26.3 26.6 26.9 27.2 27.6 27.9

3SD 9.0 9.1 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1

–3SD 10.1 10.3 10.4 10.5 10.7 10.8 10.9 11.1 11.2 11.3 11.5 11.6 11.7 11.8 12.0 12.1 12.2 12.3 12.4 12.6 12.7 12.8 12.9 13.0 13.2 13.3 13.4 13.5 13.6 13.7

–2SD 11.4 11.6 11.7 11.9 12.0 12.2 12.4 12.5 12.7 12.8 13.0 13.1 13.3 13.4 13.6 13.7 13.9 14.0 14.2 14.3 14.5 14.6 14.8 14.9 15.1 15.2 15.3 15.5 15.6 15.8

–1SD 12.9 13.1 13.3 13.5 13.7 13.9 14.0 14.2 14.4 14.6 14.8 15.0 15.2 15.3 15.5 15.7 15.9 16.1 16.3 16.4 16.6 16.8 17.0 17.2 17.3 17.5 17.7 17.9 18.0 18.2

14.7 14.9 15.1 15.4 15.6 15.8 16.0 16.3 16.5 16.7 16.9 17.2 17.4 17.6 17.8 18.1 18.3 18.5 18.8 19.0 19.2 19.4 19.7 19.9 20.1 20.3 20.6 20.8 21.0 21.2

Median 1 SD

Girls

16.8 17.1 17.3 17.6 17.9 18.1 18.4 18.7 19.0 19.2 19.5 19.8 20.1 20.4 20.7 20.9 21.2 21.5 21.8 22.1 22.4 22.6 22.9 23.2 23.5 23.8 24.1 24.4 24.6 24.9

2SD 19.3 19.6 20.0 20.3 20.6 20.9 21.3 21.6 22.0 22.3 22.7 23.0 23.4 23.7 24.1 24.5 24.8 25.2 25.5 25.9 26.3 26.6 27.0 27.4 27.7 28.1 28.5 28.8 29.2 29.5

3SD

118 Public health nutrition in developing countries

Measuring undernutrition and overnutrition in children

119

Height-for-age For children below 2 years of age, the term is length-for-age and for above 2 years of age, the index is referred to as height-for-age. Low length or heightfor-age index (stunting) identifies past undernutrition or chronic malnutrition. It is associated with a number of long-term factors including chronic insufficient protein and energy intake, frequent infection, sustained inappropriate feeding practices and poverty. This index cannot measure short term changes in malnutrition. Data on prevalence of stunting in a community may be used in problem analysis in designing interventions. Information on stunting for individual children is useful clinically as an aid to diagnosis. Stunting, based on height for-age, can be used for evaluation purposes but is not recommended for monitoring as it does not change in the short term such as 6–12 months [2, 4]. Another disadvantage of this index is that it fails to distinguish between short stature due to true nutritional cause or because of other problems such as genetic or hormonal. Tables 5.2 and 5.3 present the length-for-age and height-for-age index for age group birth to 2 years and 2 to 5 years. Weight-for-height It is calculated as the weight of each child in relation to the weight of a well-nourished reference child of the same sex and stature using the appropriate reference charts. Weight-for-height is expressed either using Z-scores (standard deviations from the reference median) or percentage of the reference median. Reporting using Z-score is preferred for assessments and surveys and weight-for-height percent of the median is preferred for admission into treatment [4, 5]. Tables 5.4 and 5.5 present weight-for-length and weight-for-length index for boys and girls birth to 2 years and 2 to 5 years respectively [5]. Low weight-for-height (weight-for-length in children under 2 years of age) is a measure of wasting. Wasting is the result of a weight falling significantly below the weight expected of a child of the same length or height. Wasting indicates current or acute malnutrition resulting from failure to gain weight or actual weight loss. Causes include inadequate food intake, incorrect feeding practices, disease, and infection or, more frequently, a combination of these factors. It is a very useful index when exact ages are difficult to determine. It is appropriate for examining shortterm effects such as seasonal changes in food supply or short-term nutritional stress brought about by illness. Wasting in individual children and population groups can change rapidly and thus used for screening or targeting purposes in emergency settings and is sometimes used for annual reporting. As with weight-for-age, this index also carries the limitation of

46.1 50.8 54.4 57.3 59.7 61.7 63.3 64.8 66.2 67.5 68.7 69.9 71.0 72.1 73.1 74.1 75.0 76.0 76.9 77.7 78.6 79.4 80.2 81.0 81.7

–2SD 48.0 52.8 56.4 59.4 61.8 63.8 65.5 67.0 68.4 69.7 71.0 72.2 73.4 74.5 75.6 76.6 77.6 78.6 79.6 80.5 81.4 82.3 83.1 83.9 84.8

–1SD 49.9 54.7 58.4 61.4 63.9 65.9 67.6 69.2 70.6 72.0 73.3 74.5 75.7 76.9 78.0 79.1 80.2 81.2 82.3 83.2 84.2 85.1 86.0 86.9 87.8

51.8 56.7 60.4 63.5 66.0 68.0 69.8 71.3 72.8 74.2 75.6 76.9 78.1 79.3 80.5 81.7 82.8 83.9 85.0 86.0 87.0 88.0 89.0 89.9 90.9

Median 1 SD

Boys

53.7 58.6 62.4 65.5 68.0 70.1 71.9 73.5 75.0 76.5 77.9 79.2 80.5 81.8 83.0 84.2 85.4 86.5 87.7 88.8 89.8 90.9 91.9 92.9 93.9

2SD 55.6 60.6 64.4 67.6 70.1 72.2 74.0 75.7 77.2 78.7 80.1 81.5 82.9 84.2 85.5 86.7 88.0 89.2 90.4 91.5 92.6 93.8 94.9 95.9 97.0

3SD 43.6 47.8 51.0 53.5 55.6 57.4 58.9 60.3 61.7 62.9 64.1 65.2 66.3 67.3 68.3 69.3 70.2 71.1 72.0 72.8 73.7 74.5 75.2 76.0 76.7

–3SD 45.4 49.8 53.0 55.6 57.8 59.6 61.2 62.7 64.0 65.3 66.5 67.7 68.9 70.0 71.0 72.0 73.0 74.0 74.9 75.8 76.7 77.5 78.4 79.2 80.0

–2SD 47.3 51.7 55.0 57.7 59.9 61.8 63.5 65.0 66.4 67.7 69.0 70.3 71.4 72.6 73.7 74.8 75.8 76.8 77.8 78.8 79.7 80.6 81.5 82.3 83.2

–1SD 49.1 53.7 57.1 59.8 62.1 64.0 65.7 67.3 68.7 70.1 71.5 72.8 74.0 75.2 76.4 77.5 78.6 79.7 80.7 81.7 82.7 83.7 84.6 85.5 86.4

51.0 55.6 59.1 61.9 64.3 66.2 68.0 69.6 71.1 72.6 73.9 75.3 76.6 77.8 79.1 80.2 81.4 82.5 83.6 84.7 85.7 86.7 87.7 88.7 89.6

Median 1 SD

Girls

52.9 57.6 61.1 64.0 66.4 68.5 70.3 71.9 73.5 75.0 76.4 77.8 79.2 80.5 81.7 83.0 84.2 85.4 86.5 87.6 88.7 89.8 90.8 91.9 92.9

2SD

54.7 59.5 63.2 66.1 68.6 70.7 72.5 74.2 75.8 77.4 78.9 80.3 81.7 83.1 84.4 85.7 87.0 88.2 89.4 90.6 91.7 92.9 94.0 95.0 96.1

3SD

*The standard for linear growth has a part based on length (length-for-age, 0 to 24 months) and another on height (height-for-age, 2 to 5 years). The two parts were constructed using the same model but the final curves reflect the average difference between recumbent length and standing height. By design, children between 18 and 30 months in the cross-sectional component of the MGRS had both length and height measurements taken. The resulting disjunction between the two standards thus in essence reflects the 0.7 cm difference between length and height.

44.2 48.9 52.4 55.3 57.6 59.6 61.2 62.7 64.0 65.2 66.4 67.6 68.6 69.6 70.6 71.6 72.5 73.3 74.2 75.0 75.8 76.5 77.2 78.0 78.7

0:0 0:1 0:2 0:3 0:4 0:5 0:6 0:7 0:8 0:9 0:10 0:11 1:0 1.1 1:2 1:3 1:4 1:5 1:6 1:7 1:8 1:9 1:10 1:11 2:0

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24

–3SD

Month

Months

Year :

Table 5.2 WHO Growth Standards Length-for-Age – boys and girls birth to 2 years (Z scores)* [5]

120 Public health nutrition in developing countries

78.0 78.6 79.3 79.9 80.5 81.1 81.7 82.3 82.8 83.4 83.9 84.4 85.0 85.5 86.0 86.5 87.0 87.5 88.0 88.4 88.9 89.4 89.8 90.3 90.7 91.2 91.6 92.1

2.0 2:1 2:2 2:3 2:4 2:5 2:6 2:7 2:8 2:9 2:10 2:11 3:0 3:1 3:2 3:3 3:4 3:5 3;6 3:7 3:8 3:9 3:10 3:11 4:0 4:1 4:2 4:3

24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51

–3SD

Month

Months

Year :

81.0 81.7 82.5 83.1 83.8 84.5 85.1 85.7 86.4 86.9 87.5 88.1 88.7 89.2 89.8 90.3 90.9 91.4 91.9 92.4 93.0 93.5 94.0 94.4 94.9 95.4 95.9 96.4

–2SD 84.1 84.9 85.6 86.4 87.1 87.8 88.5 89.2 89.9 90.5 91.1 91.8 92.4 93.0 93.6 94.2 94.7 95.3 95.9 96.4 97.0 97.5 98.1 98.6 99.1 99.7 100.2 100.7

–1SD 87.1 88.0 88.8 89.6 90.4 91.2 91.9 92.7 93.4 94.1 94.8 95.4 96.1 96.7 97.4 98.0 98.6 99.2 99.9 100.4 101.0 101.6 102.2 102.8 103.3 103.9 104.4 105.0

90.2 91.1 92.0 92.9 93.7 94.5 95.3 96.1 96.9 97.6 98.4 99.1 99.8 100.5 101.2 101.8 102.5 103.2 103.8 104.5 105.1 105.7 106.3 106.9 107.5 108.1 108.7 109.3

Median 1 SD

Boys

93.2 94.2 95.2 96.1 97.0 97.9 98.7 99.6 100.4 101.2 102.0 102.7 103.5 104.2 105.0 105.7 106.4 107.1 107.8 108.5 109.1 109.8 110.4 111.1 111.7 112.4 113.0 113.6

2SD 96.3 97.3 98.3 99.3 100.3 101.2 102.1 103.0 103.9 104.8 105.6 106.4 107.2 108.0 108.8 109.5 110.3 111.0 111.7 112.5 113.2 113.9 114.6 115.2 115.9 116.6 117.3 117.9

3SD 76.0 76.8 77.5 78.1 78.8 79.5 80.1 80.7 81.3 81.9 82.5 83.1 83.6 84.2 84.7 85.3 85.8 86.3 86.8 87.4 87.9 88.4 88.9 89.3 89.8 90.3 90.7 91.2

–3SD 79.3 80.0 80.8 81.5 82.2 82.9 83.6 84.3 84.9 85.6 86.2 86.8 87.4 88.0 88.6 89.2 89.8 90.4 90.9 91.5 92.0 92.5 93.1 93.6 94.1 94.6 95.1 95.6

–2SD

Table 5.3: WHO Growth Standards Height-for-Age – boys and girls 2 and 5 years (Z scores)* [5]

82.5 83.3 84.1 84.9 85.7 86.4 87.1 87.9 88.6 89.3 89.9 90.6 91.2 91.9 92.5 93.1 93.8 94.4 95.0 95.6 96.2 96.7 97.3 97.9 98.4 99.0 99.5 100.1

–1SD 85.7 86.6 87.4 88.3 89.1 89.9 90.7 91.4 92.2 92.9 93.6 94.4 95.1 95.7 96.4 97.1 97.7 98.4 99.0 99.7 100.3 100.9 101.5 102.1 102.7 103.3 103.9 104.5

88.9 89.9 90.8 91.7 92.5 93.4 94.2 95.0 95.8 96.6 97.4 98.1 98.9 99.6 100.3 101.0 101.7 102.4 103.1 103.8 104.5 105.1 105.8 106.4 107.0 107.7 108.3 108.9

Median 1 SD

Girls

92.2 93.1 94.1 95.0 96.0 96.9 97.7 98.6 99.4 100.3 101.1 101.9 102.7 103.4 104.2 105.0 105.7 106.4 107.2 107.9 108.6 109.3 110.0 110.7 111.3 112.0 112.7 113.3

2SD

95.4 96.4 97.4 98.4 99.4 100.3 101.3 102.2 103.1 103.9 104.8 105.6 106.5 107.3 108.1 108.9 109.7 110.5 111.2 112.0 112.7 113.5 114.2 114.9 115.7 116.4 117.1 117.7

3SD

Measuring undernutrition and overnutrition in children 121

96.9 97.4 97.8 98.3 98.8 99.3 99.7 100.2 100.7

–2SD 101.2 101.7 102.3 102.8 103.3 103.8 104.3 104.8 105.3

–1SD 105.6 106.1 106.7 107.2 107.8 108.3 108.9 109.4 110.0

109.9 110.5 111.1 111.7 112.3 112.8 113.4 114.0 114.6

Median 1 SD

Boys

Source: http://www.who.int/childgrowth/standards/en/ [5].

92.5 93.0 93.4 93.9 94.3 94.7 95.2 95.6 96.1

4:4 4:5 4:6 4:7 4:8 4:9 4:10 4:11 5:0

52 53 54 55 56 57 58 59 60

–3SD

Month

Months

Year :

114.2 114.9 115.5 116.1 116.7 117.4 118.0 118.6 119.2

2SD 118.6 119.2 119.9 120.6 121.2 121.9 122.6 123.2 123.9

3SD 91.7 92.1 92.6 93.0 93.4 93.9 94.3 94.7 95.2

–3SD 96.1 96.6 97.1 97.6 98.1 98.5 99.0 99.5 99.9

–2SD 100.6 101.1 101.6 102.2 102.7 103.2 103.7 104.2 104.7

–1SD 105.0 105.6 106.2 106.7 107.3 107.8 108.4 108.9 109.4

109.5 110.1 110.7 111.3 111.9 112.5 113.0 113.6 114.2

Median 1 SD

Girls

114.0 114.6 115.2 115.9 116.5 117.1 117.7 118.3 118.9

2SD 118.4 119.1 119.8 120.4 121.1 121.8 122.4 123.1 123.7

3SD

122 Public health nutrition in developing countries

2.4 2.5 2.6 2.7 2.8 2.9 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.8 3.9 4.0 4.1 4.3 4.4 4.5 4.7 4.8 5.0 5.1 5.3 5.4 5.6 5.7 5.9 6.0

2.7 2.8 2.9 3.0 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.8 3.9 4.0 4.1 4.2 4.4 4.5 4.7 4.8 5.0 5.1 5.3 5.4 5.6 5.7 5.9 6.1 6.2 6.4 6.5

1.9 1.9 2.0 2.1 2.1 2.2 2.3 2.3 2.4 2.5 2.6 2.7 2.7 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.6 3.7 3.8 3.9 4.0 4.1 4.3 4.4 4.5 4.6 4.7

45.0 45.5 46.0 46.5 47.0 47.5 48.0 48.5 49.0 49.5 50.0 50.5 51.0 51.5 52.0 52.5 53.0 53.5 54.0 54.5 55.0 55.5 56.0 56.5 57.0 57.5 58.0 58.5 59.0 59.5 60.0

2.2 2.3 2.4 2.5 2.5 2.6 2.7 2.8 2.9 3.0 3.0 3.1 3.2 3.3 3.5 3.6 3.7 3.8 3.9 4.0 4.2 4.3 4.4 4.6 4.7 4.9 5.0 5.1 5.3 5.4 5.5

Median 1 SD

2.0 2.1 2.2 2.3 2.3 2.4 2.5 2.6 2.6 2.7 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 4.0 4.1 4.2 4.3 4.5 4.6 4.7 4.8 5.0 5.1

Boys –1SD

(cm)

–2SD

–3SD

Length

3.0 3.1 3.1 3.2 3.3 3.4 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.1 5.3 5.4 5.6 5.8 5.9 6.1 6.3 6.4 6.6 6.8 7.0 7.1

2SD 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.2 4.3 4.4 4.5 4.7 4.8 5.0 5.1 5.3 5.4 5.6 5.8 6.0 6.1 6.3 6.5 6.7 6.9 7.1 7.2 7.4 7.6 7.8

3SD 45.0 45.5 46.0 46.5 47.0 47.5 48.0 48.5 49.0 49.5 50.0 50.5 51.0 51.5 52.0 52.5 53.0 53.5 54.0 54.5 55.0 55.5 56.0 56.5 57.0 57.5 58.0 58.5 59.0 59.5 60.0

(cm)

Length

1.9 2.0 2.0 2.1 2.2 2.2 2.3 2.4 2.4 2.5 2.6 2.7 2.8 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3 4.4 4.5

–3SD 2.1 2.1 2.2 2.3 2.4 2.4 2.5 2.6 2.6 2.7 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.1 4.3 4.4 4.5 4.6 4.7 4.8 4.9

–2SD

Table 5.4 WHO Growth Standards Weight-for-Length – boys and girls birth to 2 years (Z scores) [5]

2.3 2.3 2.4 2.5 2.6 2.6 2.7 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.2 4.3 4.4 4.5 4.6 4.8 4.9 5.0 5.1 5.3 5.4

–1SD 2.5 2.5 2.6 2.7 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.2 4.3 4.4 4.5 4.7 4.8 5.0 5.1 5.2 5.4 5.5 5.6 5.7 5.9

2.7 2.8 2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.2 4.3 4.4 4.6 4.7 4.8 5.0 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.2 6.3 6.4

Median 1 SD

Girls

3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.2 4.3 4.4 4.6 4.7 4.9 5.0 5.2 5.3 5.5 5.7 5.8 6.0 6.1 6.3 6.5 6.6 6.8 6.9 7.1

2SD 3.3 3.4 3.5 3.6 3.7 3.8 4.0 4.1 4.2 4.3 4.5 4.6 4.8 4.9 5.1 5.2 5.4 5.5 5.7 5.9 6.1 6.3 6.4 6.6 6.8 7.0 7.1 7.3 7.5 7.7 7.8

3SD

Measuring undernutrition and overnutrition in children 123

5.6 5.8 5.9 6.0 6.1 6.2 6.4 6.5 6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.3 7.5 7.6 7.7 7.8 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.8 8.9 9.0

6.1 6.3 6.4 6.5 6.7 6.8 6.9 7.0 7.1 7.3 7.4 7.5 7.6 7.8 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8

6.7 6.8 7.0 7.1 7.2 7.4 7.5 7.6 7.8 7.9 8.0 8.2 8.3 8.4 8.5 8.7 8.8 8.9 9.0 9.2 9.3 9.4 9.5 9.6 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.6 10.7

4.8 4.9 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 5.9 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.2 7.3 7.4 7.5 7.6 7.6 7.7

60.5 61.0 61.5 62.0 62.5 63.0 63.5 64.0 64.5 65.0 65.5 66.0 66.5 67.0 67.5 68.0 68.5 69.0 69.5 70.0 70.5 71.0 71.5 72.0 72.5 73.0 73.5 74.0 74.5 75.0 75.5 76.0 76.5

5.2 5.3 5.4 5.6 5.7 5.8 5.9 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.6 7.7 7.8 7.9 8.0 8.1 8.2 8.3 8.3

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

7.3 7.4 7.6 7.7 7.9 8.0 8.2 8.3 8.5 8.6 8.7 8.9 9.0 9.2 9.3 9.4 9.6 9.7 9.8 10.0 10.1 10.2 10.4 10.5 10.6 10.8 10.9 11.0 11.2 11.3 11.4 11.5 11.6

2SD 8.0 8.1 8.3 8.5 8.6 8.8 8.9 9.1 9.3 9.4 9.6 9.7 9.9 10.0 10.2 10.3 10.5 10.6 10.8 10.9 11.1 11.2 11.3 11.5 11.6 11.8 11.9 12.1 12.2 12.3 12.5 12.6 12.7

3SD 60.5 61.0 61.5 62.0 62.5 63.0 63.5 64.0 64.5 65.0 65.5 66.0 66.5 67.0 67.5 68.0 68.5 69.0 69.5 70.0 70.5 71.0 71.5 72.0 72.5 73.0 73.5 74.0 74.5 75.0 75.5 76.0 76.5

(cm)

Length

4.6 4.7 4.8 4.9 5.0 5.1 5.2 5.3 5.4 5.5 5.5 5.6 5.7 5.8 5.9 6.0 6.1 6.1 6.2 6.3 6.4 6.5 6.5 6.6 6.7 6.8 6.9 6.9 7.0 7.1 7.1 7.2 7.3

–3SD 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 5.9 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 6.9 6.9 7.0 7.1 7.2 7.3 7.4 7.4 7.5 7.6 7.7 7.8 7.8 7.9

–2SD 5.5 5.6 5.7 5.8 5.9 6.0 6.2 6.3 6.4 6.5 6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.7 7.8 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.5 8.6

–1SD 6.0 6.1 6.3 6.4 6.5 6.6 6.7 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.1 9.2 9.3 9.4

6.6 6.7 6.9 7.0 7.1 7.3 7.4 7.5 7.6 7.8 7.9 8.0 8.1 8.3 8.4 8.5 8.6 8.7 8.8 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3

Median 1 SD

Girls

7.3 7.4 7.6 7.7 7.8 8.0 8.1 8.3 8.4 8.6 8.7 8.8 9.0 9.1 9.2 9.4 9.5 9.6 9.7 9.9 10.0 10.1 10.2 10.3 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.4

2SD 8.0 8.2 8.4 8.5 8.7 8.8 9.0 9.1 9.3 9.5 9.6 9.8 9.9 10.0 10.2 10.3 10.5 10.6 10.7 10.9 11.0 11.1 11.3 11.4 11.5 11.7 11.8 11.9 12.0 12.2 12.3 12.4 12.5

3SD

124 Public health nutrition in developing countries

9.1 9.2 9.3 9.4 9.5 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.5

9.9 10.0 10.1 10.2 10.3 10.4 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.2 11.3 11.4 11.5 11.6 11.7 11.9 12.0 12.1 12.2 12.4 12.5 12.6 12.7 12.8 13.0 13.1 13.2 13.3 13.4 13.5

10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.2 12.4 12.5 12.6 12.8 12.9 13.0 13.2 13.3 13.4 13.5 13.7 13.8 13.9 14.1 14.2 14.3 14.4 14.6 14.7

7.8 7.9 7.9 8.0 8.1 8.2 8.2 8.3 8.4 8.5 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.7

77.0 77.5 78.0 78.5 79.0 79.5 80.0 80.5 81.0 81.5 82.0 82.5 83.0 83.5 84.0 84.5 85.0 85.5 86.0 86.5 87.0 87.5 88.0 88.5 89.0 89.5 90.0 90.5 91.0 91.5 92.0 92.5 93.0 93.5

8.4 8.5 8.6 8.7 8.7 8.8 8.9 9.0 9.1 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

11.7 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 13.0 13.1 13.2 13.3 13.5 13.6 13.7 13.9 14.0 14.2 14.3 14.5 14.6 14.7 14.9 15.0 15.1 15.3 15.4 15.6 15.7 15.8 16.0

2SD 12.8 13.0 13.1 13.2 13.3 13.4 13.6 13.7 13.8 13.9 14.0 14.2 14.3 14.4 14.6 14.7 14.9 15.0 15.2 15.3 15.5 15.6 15.8 15.9 16.1 16.2 16.4 16.5 16.7 16.8 17.0 17.1 17.3 17.4

3SD 77.0 77.5 78.0 78.5 79.0 79.5 80.0 80.5 81.0 81.5 82.0 82.5 83.0 83.5 84.0 84.5 85.0 85.5 86.0 86.5 87.0 87.5 88.0 88.5 89.0 89.5 90.0 90.5 91.0 91.5 92.0 92.5 93.0 93.5

(cm)

Length

7.4 7.4 7.5 7.6 7.7 7.7 7.8 7.9 8.0 8.1 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.1 10.2 10.3

–3SD 8.0 8.1 8.2 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2

–2SD 8.7 8.8 8.9 9.0 9.1 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.7 11.8 11.9 12.0 12.1 12.2

–1SD 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.9 11.0 11.1 11.2 11.3 11.5 11.6 11.7 11.8 12.0 12.1 12.2 12.3 12.5 12.6 12.7 12.8 13.0 13.1 13.2 13.3

10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.2 11.3 11.4 11.5 11.6 11.8 11.9 12.0 12.1 12.3 12.4 12.6 12.7 12.8 13.0 13.1 13.2 13.4 13.5 13.7 13.8 13.9 14.1 14.2 14.3 14.5 14.6

Median 1 SD

Girls

11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.3 12.4 12.5 12.6 12.8 12.9 13.1 13.2 13.3 13.5 13.6 13.8 13.9 14.1 14.2 14.4 14.5 14.7 14.8 15.0 15.1 15.3 15.5 15.6 15.8 15.9 16.1

2SD 12.6 12.8 12.9 13.0 13.1 13.3 13.4 13.5 13.7 13.8 13.9 14.1 14.2 14.4 14.5 14.7 14.9 15.0 15.2 15.4 15.5 15.7 15.9 16.0 16.2 16.4 16.5 16.7 16.9 17.0 17.2 17.4 17.5 17.7

3SD

Measuring undernutrition and overnutrition in children 125

12.6 12.7 12.8 12.9 13.1 13.2 13.3 13.4 13.5 13.6 13.7 13.9 14.0 14.1 14.2 14.4 14.5 14.6 14.8 14.9 15.0 15.2 15.3 15.4 15.6 15.7 15.9 16.0 16.2 16.3 16.5 16.6 16.8

13.7 13.8 13.9 14.0 14.1 14.3 14.4 14.5 14.6 14.8 14.9 15.0 15.2 15.3 15.4 15.6 15.7 15.9 16.0 16.2 16.3 16.5 16.6 16.8 16.9 17.1 17.3 17.4 17.6 17.8 17.9 18.1 18.3

14.8 14.9 15.1 15.2 15.3 15.5 15.6 15.7 15.9 16.0 16.2 16.3 16.5 16.6 16.8 16.9 17.1 17.3 17.4 17.6 17.8 17.9 18.1 18.3 18.5 18.6 18.8 19.0 19.2 19.4 19.6 19.8 20.0

10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 12.9 13.0 13.2 13.3 13.4 13.5 13.6 13.7 13.8 14.0 14.1 14.2

94.0 94.5 95.0 95.5 96.0 96.5 97.0 97.5 98.0 98.5 99.0 99.5 100.0 100.5 101.0 101.5 102.0 102.5 103.0 103.5 104.0 104.5 105.0 105.5 106.0 106.5 107.0 107.5 108.0 108.5 109.0 109.5 110.0

11.7 11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 12.9 13.0 13.2 13.3 13.4 13.5 13.6 13.7 13.9 14.0 14.1 14.2 14.4 14.5 14.6 14.7 14.9 15.0 15.1 15.3 15.4

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

16.1 16.3 16.4 16.5 16.7 16.8 17.0 17.1 17.3 17.5 17.6 17.8 18.0 18.1 18.3 18.5 18.7 18.8 19.0 19.2 19.4 19.6 19.8 20.0 20.2 20.4 20.6 20.8 21.0 21.2 21.4 21.7 21.9

2SD 17.6 17.7 17.9 18.0 18.2 18.4 18.5 18.7 18.9 19.1 19.2 19.4 19.6 19.8 20.0 20.2 20.4 20.6 20.8 21.0 21.2 21.5 21.7 21.9 22.1 22.4 22.6 22.8 23.1 23.3 23.6 23.8 24.1

3SD 94.0 94.5 95.0 95.5 96.0 96.5 97.0 97.5 98.0 98.5 99.0 99.5 100.0 100.5 101.0 101.5 102.0 102.5 103.0 103.5 104.0 104.5 105.0 105.5 106.0 106.5 107.0 107.5 108.0 108.5 109.0 109.5 110.0

(cm)

Length

10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.3 12.4 12.5 12.6 12.7 12.8 13.0 13.1 13.2 13.3 13.5 13.6 13.7 13.9 14.0

–3SD 11.3 11.4 11.5 11.6 11.7 11.8 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 13.0 13.1 13.2 13.3 13.5 13.6 13.7 13.8 14.0 14.1 14.3 14.4 14.5 14.7 14.8 15.0 15.1 15.3

–2SD 12.3 12.4 12.6 12.7 12.8 12.9 13.0 13.1 13.3 13.4 13.5 13.6 13.7 13.9 14.0 14.1 14.3 14.4 14.5 14.7 14.8 15.0 15.1 15.3 15.4 15.6 15.7 15.9 16.0 16.2 16.4 16.5 16.7

–1SD 13.5 13.6 13.7 13.8 14.0 14.1 14.2 14.4 14.5 14.6 14.8 14.9 15.0 15.2 15.3 15.5 15.6 15.8 15.9 16.1 16.2 16.4 16.5 16.7 16.9 17.1 17.2 17.4 17.6 17.8 18.0 18.1 18.3

14.7 14.9 15.0 15.2 15.3 15.4 15.6 15.7 15.9 16.0 16.2 16.3 16.5 16.6 16.8 17.0 17.1 17.3 17.5 17.6 17.8 18.0 18.2 18.4 18.5 18.7 18.9 19.1 19.3 19.5 19.7 20.0 20.2

Median 1 SD

Girls

16.2 16.4 16.5 16.7 16.8 17.0 17.1 17.3 17.5 17.6 17.8 18.0 18.1 18.3 18.5 18.7 18.9 19.0 19.2 19.4 19.6 19.8 20.0 20.2 20.5 20.7 20.9 21.1 21.3 21.6 21.8 22.0 22.3

2SD 17.9 18.0 18.2 18.4 18.6 18.7 18.9 19.1 19.3 19.5 19.6 19.8 20.0 20.2 20.4 20.6 20.8 21.0 21.3 21.5 21.7 21.9 22.2 22.4 22.6 22.9 23.1 23.4 23.6 23.9 24.2 24.4 24.7

3SD

126 Public health nutrition in developing countries

6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.2 9.3 9.4 9.5

7.4 7.6 7.7 7.8 7.9 8.0 8.1 8.2 8.4 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3

8.1 8.2 8.3 8.5 8.6 8.7 8.8 9.0 9.1 9.2 9.3 9.5 9.6 9.7 9.8 9.9 10.0 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2

5.9 6.0 6.1 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 6.9 6.9 7.0 7.1 7.2 7.3 7.4 7.4 7.5 7.6 7.7 7.7 7.8 7.9 8.0 8.0 8.1

65.0 65.5 66.0 66.5 67.0 67.5 68.0 68.5 69.0 69.5 70.0 70.5 71.0 71.5 72.0 72.5 73.0 73.5 74.0 74.5 75.0 75.5 76.0 76.5 77.0 77.5 78.0 78.5

6.3 6.4 6.5 6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.5 8.6 8.7 8.8

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

8.8 8.9 9.1 9.2 9.4 9.5 9.6 9.8 9.9 10.0 10.2 10.3 10.4 10.6 10.7 10.8 11.0 11.1 11.2 11.3 11.4 11.6 11.7 11.8 11.9 12.0 12.1 12.2

2SD 9.6 9.8 9.9 10.1 10.2 10.4 10.5 10.7 10.8 11.0 11.1 11.3 11.4 11.6 11.7 11.8 12.0 12.1 12.2 12.4 12.5 12.6 12.8 12.9 13.0 13.1 13.3 13.4

3SD 65.0 65.5 66.0 66.5 67.0 67.5 68.0 68.5 69.0 69.5 70.0 70.5 71.0 71.5 72.0 72.5 73.0 73.5 74.0 74.5 75.0 75.5 76.0 76.5 77.0 77.5 78.0 78.5

(cm)

Length

5.6 5.7 5.8 5.8 5.9 6.0 6.1 6.2 6.3 6.3 6.4 6.5 6.6 6.7 6.7 6.8 6.9 7.0 7.0 7.1 7.2 7.2 7.3 7.4 7.5 7.5 7.6 7.7

–3SD 6.1 6.2 6.3 6.4 6.4 6.5 6.6 6.7 6.8 6.9 7.0 7.1 7.1 7.2 7.3 7.4 7.5 7.6 7.6 7.7 7.8 7.9 8.0 8.0 8.1 8.2 8.3 8.4

–2SD 6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 8.0 8.1 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.7 8.8 8.9 9.0 9.1

–1SD

Table 5.5 WHO Growth Standards Weight-for-Height – boys and girls over 2 to 5 years (Z scores) [5]

7.2 7.4 7.5 7.6 7.7 7.8 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.6 9.7 9.8 9.9

7.9 8.1 8.2 8.3 8.4 8.5 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9

Median 1 SD

Girls

8.7 8.9 9.0 9.1 9.3 9.4 9.5 9.7 9.8 9.9 10.0 10.1 10.3 10.4 10.5 10.6 10.7 10.8 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 12.0

2SD

9.7 9.8 10.0 10.1 10.2 10.4 10.5 10.7 10.8 10.9 11.1 11.2 11.3 11.5 11.6 11.7 11.8 12.0 12.1 12.2 12.3 12.5 12.6 12.7 12.8 12.9 13.1 13.2

3SD

Measuring undernutrition and overnutrition in children 127

9.6 9.7 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.6 12.7

10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.7 11.8 11.9 12.0 12.2 12.3 12.4 12.5 12.6 12.8 12.9 13.0 13.1 13.2 13.4 13.5 13.6 13.7

11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.1 12.2 12.3 12.4 12.5 12.7 12.8 12.9 13.1 13.2 13.3 13.5 13.6 13.7 13.9 14.0 14.1 14.2 14.4 14.5 14.6 14.7 14.9

8.2 8.3 8.3 8.4 8.5 8.6 8.7 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9

79.0 79.5 80.0 80.5 81.0 81.5 82.0 82.5 83.0 83.5 84.0 84.5 85.0 85.5 86.0 86.5 87.0 87.5 88.0 88.5 89.0 89.5 90.0 90.5 91.0 91.5 92.0 92.5 93.0 93.5

8.8 8.9 9.0 9.1 9.2 9.3 9.3 9.4 9.5 9.6 9.7 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

12.3 12.4 12.6 12.7 12.8 12.9 13.0 13.1 13.3 13.4 13.5 13.7 13.8 13.9 14.1 14.2 14.4 14.5 14.7 14.8 14.9 15.1 15.2 15.3 15.5 15.6 15.8 15.9 16.0 16.2

2SD 13.5 13.6 13.7 13.8 14.0 14.1 14.2 14.4 14.5 14.6 14.8 14.9 15.1 15.2 15.4 15.5 15.7 15.8 16.0 16.1 16.3 16.4 16.6 16.7 16.9 17.0 17.2 17.3 17.5 17.6

3SD 79.0 79.5 80.0 80.5 81.0 81.5 82.0 82.5 83.0 83.5 84.0 84.5 85.0 85.5 86.0 86.5 87.0 87.5 88.0 88.5 89.0 89.5 90.0 90.5 91.0 91.5 92.0 92.5 93.0 93.5

(cm)

Length

7.8 7.8 7.9 8.0 8.1 8.2 8.3 8.4 8.5 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5

–3SD 8.4 8.5 8.6 8.7 8.8 8.9 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 10.9 11.0 11.1 11.2 11.3 11.4

–2SD 9.2 9.3 9.4 9.5 9.6 9.7 9.8 9.9 10.0 10.1 10.2 10.3 10.4 10.6 10.7 10.8 10.9 11.0 11.1 11.2 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.3 12.4

–1SD 10.0 10.1 10.2 10.3 10.4 10.6 10.7 10.8 10.9 11.0 11.1 11.3 11.4 11.5 11.6 11.8 11.9 12.0 12.1 12.3 12.4 12.5 12.6 12.8 12.9 13.0 13.1 13.3 13.4 13.5

11.0 11.1 11.2 11.3 11.4 11.6 11.7 11.8 11.9 12.1 12.2 12.3 12.5 12.6 12.7 12.9 13.0 13.2 13.3 13.4 13.6 13.7 13.8 14.0 14.1 14.3 14.4 14.5 14.7 14.8

Median 1 SD

Girls

12.1 12.2 12.3 12.4 12.6 12.7 12.8 13.0 13.1 13.3 13.4 13.5 13.7 13.8 14.0 14.2 14.3 14.5 14.6 14.8 14.9 15.1 15.2 15.4 15.5 15.7 15.8 16.0 16.1 16.3

2SD 13.3 13.4 13.6 13.7 13.9 14.0 14.1 14.3 14.5 14.6 14.8 14.9 15.1 15.3 15.4 15.6 15.8 15.9 16.1 16.3 16.4 16.6 16.8 16.9 17.1 17.3 17.4 17.6 17.8 17.9

3SD

128 Public health nutrition in developing countries

12.8 12.9 13.0 13.1 13.2 13.3 13.4 13.6 13.7 13.8 13.9 14.0 14.2 14.3 14.4 14.5 14.7 14.8 14.9 15.1 15.2 15.4 15.5 15.6 15.8 15.9 16.1 16.2 16.4 16.5

13.8 13.9 14.1 14.2 14.3 14.4 14.6 14.7 14.8 14.9 15.1 15.2 15.4 15.5 15.6 15.8 15.9 16.1 16.2 16.4 16.5 16.7 16.8 17.0 17.2 17.3 17.5 17.7 17.8 18.0

15.0 15.1 15.3 15.4 15.5 15.7 15.8 15.9 16.1 16.2 16.4 16.5 16.7 16.9 17.0 17.2 17.3 17.5 17.7 17.8 18.0 18.2 18.4 18.5 18.7 18.9 19.1 19.3 19.5 19.7

11.0 11.1 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.8 12.9 13.0 13.1 13.2 13.3 13.4 13.5 13.7 13.8 13.9 14.0

94.0 94.5 95.0 95.5 96.0 96.5 97.0 97.5 98.0 98.5 99.0 99.5 100.0 100.5 101.0 101.5 102.0 102.5 103.0 103.5 104.0 104.5 105.0 105.5 106.0 106.5 107.0 107.5 108.0 108.5

11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.8 12.9 13.0 13.1 13.2 13.3 13.4 13.6 13.7 13.8 13.9 14.0 14.2 14.3 14.4 14.5 14.7 14.8 14.9 15.1 15.2

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

16.3 16.5 16.6 16.7 16.9 17.0 17.2 17.4 17.5 17.7 17.9 18.0 18.2 18.4 18.5 18.7 18.9 19.1 19.3 19.5 19.7 19.9 20.1 20.3 20.5 20.7 20.9 21.1 21.3 21.5

2SD 17.8 17.9 18.1 18.3 18.4 18.6 18.8 18.9 19.1 19.3 19.5 19.7 19.9 20.1 20.3 20.5 20.7 20.9 21.1 21.3 21.6 21.8 22.0 22.2 22.5 22.7 22.9 23.2 23.4 23.7

3SD 94.0 94.5 95.0 95.5 96.0 96.5 97.0 97.5 98.0 98.5 99.0 99.5 100.0 100.5 101.0 101.5 102.0 102.5 103.0 103.5 104.0 104.5 105.0 105.5 106.0 106.5 107.0 107.5 108.0 108.5

(cm)

Length

10.6 10.7 10.8 10.8 10.9 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.8 12.9 13.0 13.1 13.3 13.4 13.5 13.7 13.8

–3SD 11.5 11.6 11.7 11.8 11.9 12.0 12.1 12.2 12.3 12.4 12.5 12.7 12.8 12.9 13.0 13.1 13.3 13.4 13.5 13.6 13.8 13.9 14.0 14.2 14.3 14.5 14.6 14.7 14.9 15.0

–2SD 12.5 12.6 12.7 12.8 12.9 13.1 13.2 13.3 13.4 13.5 13.7 13.8 13.9 14.1 14.2 14.3 14.5 14.6 14.7 14.9 15.0 15.2 15.3 15.5 15.6 15.8 15.9 16.1 16.3 16.4

–1SD 13.6 13.8 13.9 14.0 14.1 14.3 14.4 14.5 14.7 14.8 14.9 15.1 15.2 15.4 15.5 15.7 15.8 16.0 16.1 16.3 16.4 16.6 16.8 16.9 17.1 17.3 17.5 17.7 17.8 18.0

14.9 15.1 15.2 15.4 15.5 15.6 15.8 15.9 16.1 16.2 16.4 16.5 16.7 16.9 17.0 17.2 17.4 17.5 17.7 17.9 18.1 18.2 18.4 18.6 18.8 19.0 19.2 19.4 19.6 19.8

Median 1 SD

Girls

16.4 16.6 16.7 16.9 17.0 17.2 17.4 17.5 17.7 17.9 18.0 18.2 18.4 18.6 18.7 18.9 19.1 19.3 19.5 19.7 19.9 20.1 20.3 20.5 20.8 21.0 21.2 21.4 21.7 21.9

2SD 18.1 18.3 18.5 18.6 18.8 19.0 19.2 19.3 19.5 19.7 19.9 20.1 20.3 20.5 20.7 20.9 21.1 21.4 21.6 21.8 22.0 22.3 22.5 22.7 23.0 23.2 23.5 23.7 24.0 24.3

3SD

Measuring undernutrition and overnutrition in children 129

16.7 16.8 17.0 17.1 17.3 17.5 17.6 17.8 18.0 18.1 18.3 18.5 18.6 18.8 19.0 19.2 19.3 19.5 19.7 19.9 20.0 20.2 20.4

18.2 18.3 18.5 18.7 18.9 19.1 19.2 19.4 19.6 19.8 20.0 20.2 20.4 20.6 20.8 21.0 21.2 21.4 21.6 21.8 22.0 22.2 22.4

19.8 20.0 20.2 20.4 20.7 20.9 21.1 21.3 21.5 21.7 21.9 22.1 22.4 22.6 22.8 23.0 23.3 23.5 23.7 23.9 24.1 24.4 24.6

14.1 14.3 14.4 14.5 14.6 14.8 14.9 15.0 15.2 15.3 15.4 15.6 15.7 15.8 16.0 16.1 16.2 16.4 16.5 16.7 16.8 16.9 17.1

109.0 109.5 110.0 110.5 111.0 111.5 112.0 112.5 113.0 113.5 114.0 114.5 115.0 115.5 116.0 116.5 117.0 117.5 118.0 118.5 119.0 119.5 120.0

15.3 15.5 15.6 15.8 15.9 16.0 16.2 16.3 16.5 16.6 16.8 16.9 17.1 17.2 17.4 17.5 17.7 17.9 18.0 18.2 18.3 18.5 18.6

Median 1 SD

–1SD

–3SD

(cm)

–2SD

Boys

Length

21.8 22.0 22.2 22.4 22.7 22.9 23.1 23.4 23.6 23.9 24.1 24.4 24.6 24.9 25.1 25.4 25.6 25.9 26.1 26.4 26.6 26.9 27.2

2SD 23.9 24.2 24.4 24.7 25.0 25.2 25.5 25.8 26.0 26.3 26.6 26.9 27.2 27.5 27.8 28.0 28.3 28.6 28.9 29.2 29.5 29.8 30.1

3SD 109.0 109.5 110.0 110.5 111.0 111.5 112.0 112.5 113.0 113.5 114.0 114.5 115.0 115.5 116.0 116.5 117.0 117.5 118.0 118.5 119.0 119.5 120.0

(cm)

Length

13.9 14.1 14.2 14.4 14.5 14.7 14.8 15.0 15.1 15.3 15.4 15.6 15.7 15.9 16.0 16.2 16.3 16.5 16.6 16.8 16.9 17.1 17.3

–3SD 15.2 15.4 15.5 15.7 15.8 16.0 16.2 16.3 16.5 16.7 16.8 17.0 17.2 17.3 17.5 17.7 17.8 18.0 18.2 18.4 18.5 18.7 18.9

–2SD 16.6 16.8 17.0 17.1 17.3 17.5 17.7 17.9 18.0 18.2 18.4 18.6 18.8 19.0 19.2 19.4 19.6 19.8 19.9 20.1 20.3 20.5 20.7

–1SD 18.2 18.4 18.6 18.8 19.0 19.2 19.4 19.6 19.8 20.0 20.2 20.5 20.7 20.9 21.1 21.3 21.5 21.7 22.0 22.2 22.4 22.6 22.8

20.0 20.3 20.5 20.7 20.9 21.2 21.4 21.6 21.8 22.1 22.3 22.6 22.8 23.0 23.3 23.5 23.8 24.0 24.2 24.5 24.7 25.0 25.2

Median 1 SD

Girls

22.1 22.4 22.6 22.9 23.1 23.4 23.6 23.9 24.2 24.4 24.7 25.0 25.2 25.5 25.8 26.1 26.3 26.6 26.9 27.2 27.4 27.7 28.0

2SD 24.5 24.8 25.1 25.4 25.7 26.0 26.2 26.5 26.8 27.1 27.4 27.8 28.1 28.4 28.7 29.0 29.3 29.6 29.9 30.3 30.6 30.9 31.2

3SD

130 Public health nutrition in developing countries

Measuring undernutrition and overnutrition in children

131

being insensitive in the presence of edema or in cancer patients with large tumor load. Edema can be diagnosed by applying moderate thumb pressure to the back of the foot or ankle. The impression of the thumb will remain for some time when edema is present. The presence of edema in individuals should be recorded when using any weight-based index. When a child has edema, it is automatically included with children counted as severely malnourished, independently of its wasting, stunting, or underweight status. This is due to the strong association between edema and mortality. Body mass index (BMI) BMI is measured as weight (in kg) divided by height2 (in meters2). Body mass index is known to track significantly from childhood to adolescence and then to adulthood. However, both sex and pubertal development are associated with dramatic changes in body composition and the values may require adjustment as per the sexual maturity. BMI has been used since the 1960s to assess obesity in adults and more recently in children. With the availability of BMI cut-offs for children and WHO BMI reference charts from 0–19 years, the use of BMI can be extended for assessing thinness in children and adolescence [7]. Table 5.6 presents BMI for age index for both boys and girls from birth to 5 years. Mid-upper arm circumference (MUAC) It is relatively easy to measure and a good predictor of immediate risk of death. It is used for rapid screening of acute malnutrition in the age group of 1–5 years. MUAC can be used for screening in emergency situations and for estimating the prevalence of malnutrition in the populations but is not typically used for evaluation purposes. Though grossly mid-arm circumference may be considered an age independent index in children between 1 and 5 years of age, recently age specific cut-offs for mid-arm circumference have been released by WHO [5]. MUAC is also recommended for rapid identification of severe acute malnutrition (SAM) in a community – MUAC of less than 115 mm being indicative of SAM.

5.3

Comparison of indices with references

Once value of any index is obtained or calculated, it has to be compared with the expected value and interpretation is to be made. References are used to standardize a child’s measurement by comparing the child’s measurement with the average measure for healthy children of the same

10.2 11.3 12.5 13.1 13.4 13.5 13.6 13.7 13.6 13.6 13.5 13.4 13.4 13.3 13.2 13.1 13.1 13.0 12.9 12.9 12.8 12.8 12.7 12.7 12.7 12.9 12.8 12.8 12.7 12.7 12.7

0:0 0:1 0:2 0:3 0:4 0:5 0:6 0:7 0:8 0:9 0:10 0:11 1:0 1.1 1:2 1:3 1:4 1:5 1:6 1:7 1:8 1:9 1:10 1:11 2:0 2.0 2:1 2:2 2:3 2:4 2:5

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 24 25 26 27 28 29

–3SD

Months

Month

Year:

11.1 12.4 13.7 14.3 14.5 14.7 14.7 14.8 14.7 14.7 14.6 14.5 14.4 14.3 14.2 14.1 14.0 13.9 13.9 13.8 13.7 13.7 13.6 13.6 13.6 13.8 13.8 13.7 13.7 13.6 13.6

–2SD 12.2 13.6 15.0 15.5 15.8 15.9 16.0 16.0 15.9 15.8 15.7 15.6 15.5 15.4 15.3 15.2 15.1 15.0 14.9 14.9 14.8 14.7 14.7 14.6 14.6 14.8 14.8 14.8 14.7 14.7 14.7

–1SD 13.4 14.9 16.3 16.9 17.2 17.3 17.3 17.3 17.3 17.2 17.0 16.9 16.8 16.7 16.6 16.4 16.3 16.2 16.1 16.1 16.0 15.9 15.8 15.8 15.7 16.0 16.0 15.9 15.9 15.9 15.8

14.8 16.3 17.8 18.4 18.7 18.8 18.8 18.8 18.7 18.6 18.5 18.4 18.2 18.1 18.0 17.8 17.7 17.6 17.5 17.4 17.3 17.2 17.2 17.1 17.0 17.3 17.3 17.3 17.2 17.2 17.1

Median 1 SD

Boys

16.3 17.8 19.4 20.0 20.3 20.5 20.5 20.5 20.4 20.3 20.1 20.0 19.8 19.7 19.5 19.4 19.3 19.1 19.0 18.9 18.8 18.7 18.7 18.6 18.5 18.9 18.8 18.8 18.7 18.7 18.6

2SD 18.1 19.4 21.1 21.8 22.1 22.3 22.3 22.3 22.2 22.1 22.0 21.8 21.6 21.5 21.3 21.2 21.0 20.9 20.8 20.7 20.6 20.5 20.4 20.3 20.3 20.6 20.5 20.5 20.4 20.4 20.3

3SD 10.1 10.8 11.8 12.4 12.7 12.9 13.0 13.0 13.0 12.9 12.9 12.8 12.7 12.6 12.6 12.5 12.4 12.4 12.3 12.3 12.2 12.2 12.2 12.2 12.1 12.4 12.4 12.3 12.3 12.3 12.3

–3SD 11.1 12.0 13.0 13.6 13.9 14.1 14.1 14.2 14.1 14.1 14.0 13.9 13.8 13.7 13.6 13.5 13.5 13.4 13.3 13.3 13.2 13.2 13.1 13.1 13.1 13.3 13.3 13.3 13.3 13.3 13.2

–2SD

Table 5.6 WHO Growth Standards BMI-for-Age – boys and girls birth to 5 years (Z scores) [5]*

12.2 13.2 14.3 14.9 15.2 15.4 15.5 15.5 15.4 15.3 15.2 15.1 15.0 14.9 14.8 14.7 14.6 14.5 14.4 14.4 14.3 14.3 14.2 14.2 14.2 14.4 14.4 14.4 14.4 14.3 14.3

–1SD 13.3 14.6 15.8 16.4 16.7 16.8 16.9 16.9 16.8 16.7 16.6 16.5 16.4 16.2 16.1 16.0 15.9 15.8 15.7 15.7 15.6 15.5 15.5 15.4 15.4 15.7 15.7 15.6 15.6 15.6 15.6

14.6 16.0 17.3 17.9 18.3 18.4 18.5 18.5 18.4 18.3 18.2 18.0 17.9 17.7 17.6 17.5 17.4 17.3 17.2 17.1 17.0 17.0 16.9 16.9 16.8 17.1 17.1 17.0 17.0 17.0 17.0

Median 1 SD

Girls

16.1 17.5 19.0 19.7 20.0 20.2 20.3 20.3 20.2 20.1 19.9 19.8 19.6 19.5 19.3 19.2 19.1 18.9 18.8 18.8 18.7 18.6 18.5 18.5 18.4 18.7 18.7 18.7 18.6 18.6 18.6

2SD

17.7 19.1 20.7 21.5 22.0 22.2 22.3 22.3 22.2 22.1 21.9 21.8 21.6 21.4 21.3 21.1 21.0 20.9 20.8 20.7 20.6 20.6 20.4 20.4 20.3 20.6 20.5 20.6 20.5 20.5 20.4

3SD

132 Public health nutrition in developing countries

13.6 13.5 13.5 13.5 13.4 13.4 13.4 13.3 13.3 13.3 13.2 13.2 13.2 13.2 13.1 13.1 13.1 13.1 13.1 13.0 13.0 13.0 13.0 13.0 13.0 13.0 12.9 12.9 12.9 12.9 12.9

–2SD 14.6 14.6 14.6 14.5 14.5 14.5 14.4 14.4 14.4 14.3 14.3 14.3 14.3 14.2 14.2 14.2 14.2 14.2 14.1 14.1 14.1 14.1 14.1 14.1 14.0 14.0 14.0 14.0 14.0 14.0 14.0

–1SD 15.8 15.8 15.7 15.7 15.7 15.6 15.6 15.6 15.5 15.5 15.5 15.5 15.4 15.4 15.4 15.4 15.4 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.2 15.2 15.2 15.2 15.2 15.2

17.1 17.1 17.0 17.0 17.0 16.9 16.9 16.9 16.8 16.8 16.8 16.8 16.8 16.7 16.7 16.7 16.7 16.7 16.7 16.7 16.7 16.6 16.6 16.6 16.6 16.6 16.6 16.6 16.6 16.6 16.6

Median 1 SD

Boys

18.6 18.5 18.5 18.5 18.4 18.4 18.4 18.3 18.3 18.3 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.2 18.3 18.3 18.3

2SD 20.2 20.2 20.1 20.1 20.0 20.0 20.0 19.9 19.9 19.9 19.9 19.9 19.8 19.8 19.8 19.8 19.8 19.9 19.9 19.9 19.9 19.9 19.9 20.0 20.0 20.0 20.1 20.1 20.2 20.2 20.3

3SD 12.3 12.2 12.2 12.2 12.2 12.1 12.1 12.1 12.1 12.0 12.0 12.0 12.0 11.9 11.9 11.9 11.9 11.8 11.8 11.8 11.8 11.8 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.6 11.6

–3SD 13.2 13.2 13.2 13.1 13.1 13.1 13.1 13.1 13.0 13.0 13.0 13.0 12.9 12.9 12.9 12.9 12.9 12.8 12.8 12.8 12.8 12.8 12.8 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7

–2SD 14.3 14.3 14.3 14.2 14.2 14.2 14.2 14.1 14.1 14.1 14.1 14.1 14.0 14.0 14.0 14.0 14.0 14.0 14.0 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9

–1SD 15.5 15.5 15.5 15.5 15.4 15.4 15.4 15.4 15.4 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.2 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3

16.9 16.9 16.9 16.9 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.8 16.9 16.9 16.9 16.9

Median 1 SD

Girls

18.5 18.5 18.5 18.5 18.5 18.4 18.4 18.4 18.4 18.4 18.4 18.4 18.4 18.4 18.5 18.5 18.5 18.5 18.5 18.5 18.6 18.6 18.6 18.6 18.7 18.7 18.7 18.7 18.8 18.8 18.8

2SD 20.4 20.4 20.4 20.3 20.3 20.3 20.3 20.3 20.3 20.3 20.3 20.4 20.4 20.4 20.4 20.5 20.5 20.5 20.6 20.6 20.7 20.7 20.7 20.8 20.8 20.9 20.9 21.0 21.0 21.0 21.1

3SD

*The WHO length- and height-based BMI-for-age standards do not overlap, i.e. the length-based interval ends at 730 days and the height-based interval starts at 731 days.

12.6 12.6 12.5 12.5 12.5 12.4 12.4 12.4 12.3 12.3 12.3 12.2 12.2 12.2 12.2 12.2 12.1 12.1 12.1 12.1 12.1 12.1 12.0 12.0 12.0 12.0 12.0 12.0 12.0 12.0 12.0

2:6 2:7 2:8 2:9 2:10 2:11 3:0 3:1 3:2 3:3 3:4 3:5 3:6 3:7 3:8 3:9 3:10 3:11 4:0 4:1 4:2 4:3 4:4 4:5 4:6 4:7 4:8 4:9 4:10 4:11 5:0

30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60

–3SD

Months

Month

Year:

Measuring undernutrition and overnutrition in children 133

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Public health nutrition in developing countries

age and sex [8]. Taking age and sex into consideration, differences in measurements can be expressed in a number of ways: ● ● ●

Percentage of the median Standard deviation units, or Z-scores Percentiles

Percentage of the median The percentage of the median is defined as the ratio of a measured or observed value of the individual to the median value of the reference data for the same age or height for the specific sex, expressed as a percentage. The median is the average or 50th percentile value. If a child’s measurement is exactly the same as the median of the reference population we say that it is 100% of the median. This can be calculated as:

Observed value × 100

Percent of median = Median value of reference population Z-Scores The Z-score or standard deviation unit (SD) is defined as the difference between the value for an individual and the median value of the reference population for the same age or height, divided by the standard deviation of the reference population [9]. This can be written in equation form as:

(Observed value) – (Median reference value)

Z-score (or SD Score) = Standard deviation of reference population

Z-scores are more commonly used by the international nutrition community because they offer two major advantages. First, using Z-scores allows us to identify a fixed point in the distributions of different indices and across different ages. For all indices for all ages, 2.28% of the reference population lies below a cut-off of –2 Z-scores. The percent of the median does not have this characteristic. For example, because weight and height have different distributions (variances), –2 Z-scores on the weight-for-age distribution is about 80% of the median, and –2 Z-scores on the height-forage distribution is about 90% of the median. Further, the proportion of the population identified by a particular percentage of the median varies at different ages on the same index. The second major advantage of using Z-scores is that useful summary statistics can be calculated from them. The approach allows the mean and standard deviation to be calculated for the Z-scores for a group of children. The Z-score application is considered the

Measuring undernutrition and overnutrition in children

135

simplest way of describing the reference population and making comparisons to it. It is the statistic recommended for use when reporting results of nutritional assessments. The distribution of Z-scores follows a normal (bellshaped or Gaussian) distribution.

Percentiles The percentile is the rank position of an individual on a given reference distribution, stated in terms of what percentage of the group the individual equals or exceeds. The percentiles can be thought of as the percentage of children in the reference population below the equivalent cut-off. For example, 10 percent of children would be expected to be below 10 th percentile in a normally distributed population. The commonly used cutoffs of –3, –2, and –1 Z-scores are respectively, the 0.13th, 2.28th , and 15.8th percentiles.

5.4

Cut-offs

Cut-offs are used for identifying children who are at higher risk of adverse outcomes either due to undernutrition or overnutrition. The most commonly used cut-off with Z-scores is “–2 standard deviations” irrespective of the indicator used. This means children with a Z-score below -2 SD for weight-for-age, height-for-age or weight-for-height are considered underweight, stunted and wasted, respectively. (Tables 5.1, 5.2, 5.3, 5.4 and 5.5). Children having Z-scores below –3 SD are considered to be having severe forms of these conditions. For example, a child with a Z-score for weight-for-height of –2.5 is classified as being wasted whereas a child with a Z-score of –1.9 is not considered wasted. In the reference population, by definition, 2.3% of the children would be below -2 SD and 0.13% would be below -3 SD. WHO Classification of Undernutrition is based on this currently accepted nomenclature. This classification is used for assessing the magnitude of malnutrition amongst under-five children in national health programs (Table 5.1). In some classifications, the cut-off for defining malnutrition used is –1 SD. The use of –1 SD as cut-off over-estimates malnutrition as a significant proportion (15.8%) of healthy children normally would fall below this cut-off. Using the percentile method, the cut-offs of –3, –2, and –1 Z-scores are, respectively the 0.13 th , 2.28 th , and 15.8 th percentiles [2]. For practical purpose, the cut-off for defining malnutrition (wasting or stunting) of –2 SD (Z-score) is taken as less than 3 rd percentile. The percentile method of classification also retains the advantage of Z-score in terms of uniformity in classifications for all indicators (underweight,

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Public health nutrition in developing countries

wasting or stunting). However, this method is less useful for classifying the extreme forms (e.g. < 3 SD or >3 SD) of malnutrition as the equivalent percentile values become extremely small and difficult to calculate or represent. The cut-offs can also decided by percentage of reference median. This carries the advantage of ease of calculation as the only parameter required for this is observed value and the expected (median reference) value. However, the disadvantage is that the cut-off would be different for different parameters depending on the variability of the parameter in the population. Also, these derivations are approximate and there might be few subjects who are wrongly classified as being or not being malnourished by percentage method in comparison to Z-score technique. A comparison of cut-offs for percent of median and Z-scores illustrates the following: 80% 90% 85% 80% 70%

for for for for for

weight-for-age = –2 Z-score (Underweight) height-for-age = –2 Z-score (Stunting) height-for-age = –3 Z-score (Severe stunting) weight-for-height = –2 Z-score (Wasting) weight-for-height = –3 Z-score (Severe wasting)

For BMI cut-offs, adult values of overweight and obesity in childhood have been used to construct statistical models for children [10]. The choice of cut-off is fundamentally important to identify correctly those children at risk and ideally should be related to known outcomes for morbidity and mortality. Yet while adult body mass index values of 25 (overweight) and 30 (obesity) are related to morbidity, evidence on morbidity related to cut-offs for thinness, particularly in children, is less clear. Recently, this work has been extended to provide cut-offs for body mass index to define “thinness” in children and adolescents [11, 12].

5.5

Growth references

When the comparisons of the anthropometric indices are to be made using percentile, percentage or Z-score method, reference tables/charts/curves are required. It is important that the reference chosen is reflective of a good nutritional status and thus should be based on the growth of children who had optimum nutrition and not having any adverse health constraints. The growth charts obtained from such reference population are called growth references.

Local (country-specific) references Growth charts are widely used throughout the world for assessing the

Measuring undernutrition and overnutrition in children

137

nutritional status of young children. When these began to be widely disseminated in the 1970s, there was considerable debate as to whether separate growth references should be developed for each country or whether a single international reference would suffice. Some argued that the growth of children of high socio-economic status was very similar throughout the world, irrespective of ethnic background. Others believed that although international references were useful for comparing across populations, country-specific references were essential for assessing the growth of individual children. Country-specific and sometimes even geographicspecific references are available for many settings. For India, locally derived references are available but require frequent updating as India is still experiencing secular trends of increasing weight and height because of continuous improvement in nutritional and socio-economic structure of the country.

NCHS growth references for children The NCHS reference was developed in the United States in 1975 by pooling four different sources of data [13]. The reference for 2–18 year olds was based on three representative surveys conducted in the US between 1960 and 1975. For children less than 2 years of age the data came from the Fels Longitudinal Study carried out in Yellow Springs, Ohio, from 1929 to 1975. The group was of homogeneous genetic, geographic, and socio-economic backgrounds. For older children, the data came from nationally representative cross-sectional surveys of children in the United States and include all ethnic groups and social classes. These growth references have been used for decades all over the world to assess the growth of individual children and for comparisons across populations. However, recently concerns have been raised about validity of these references for healthy breastfed children as these reflect the growth of children who were fed primarily infant formula and in whom complementary feeding often was initiated before 4 months [14, 15].

WHO child growth references A comprehensive review of the uses and interpretation of anthropometric undertaken by WHO in the 1990s concluded that new growth curves were needed to replace the existing international reference [16]. To develop new references, a multi-country study was carried out to collect primary growth data and related information from 8440 healthy breastfed infants and young children from diverse ethnic backgrounds and cultural settings (Brazil, Ghana, India, Norway, Oman

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Public health nutrition in developing countries

and the USA). The growth references represent the description of physiological growth for children under-5 years of age, under optimal environmental conditions [17]. The children included in the study were raised in environments that minimized constraints to growth such as poor diets and infection. In addition, their mothers followed health practices such as breastfeeding their children and not smoking during and after pregnancy. These growth charts were released in 2006 [5]. Based on these simplified field tables were developed. These are presented in Tables 5.1, 5.2, 5.3, 5.4, 5.5, 5.6 and 5.7, (length/height-for-age, weight-for-age, weight-for-length, weight-for-height, body mass index-for-age, Recently, WHO proceeded to reconstruct the 1977 NCHS/WHO growth reference from 5 to 19 years, using the original sample (a non-obese sample with expected heights) supplemented with data from the WHO Child Growth References (to facilitate a smooth transition at 5 years) and applying complex statistical methods [6]. The 2007 height-for-age and BMI-forage charts extend to 19 years, which is the upper age limit of adolescence as defined by WHO. The weight-for-age charts extend to 10 years for the benefit of countries that routinely measure only weight and would like to monitor growth throughout childhood. Weight-for-age is inadequate for monitoring growth beyond childhood due to its inability to distinguish between relative height and body mass, hence, the provision here of BMI-for-age to complement height-for-age in the assessment of thinness (low BMI-for-age), overweight and obesity (high BMI-for-age) and stunting (low height-for-age) in school-aged children and adolescents. The new WHO growth charts are likely to change the current estimates of undernutrition and overnutrition in children [18]. A notable effect is that stunting (low height-for-age) will be greater throughout childhood when assessed using the new WHO references compared to the previous international reference. There will be a substantial increase in underweight rates during the first half of infancy (i.e., 0–6 months) and a decrease thereafter. For wasting (low weight-for-length/height), the main difference between the new references and the old reference is during infancy (i.e., up to about 70 cm length) when wasting rates will be substantially higher using the new WHO references. With respect to overweight, use of the new WHO references will result in a greater prevalence that will vary by age, sex and nutritional status of the index population.

12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.1 12.2 12.2 12.2 12.2 12.2 12.2 12.2 12.2 12.2 12.2 12.3 12.3 12.3 12.3 12.3

5:1 5:2 5:3 5:4 5:5 5:6 5:7 5:8 5:9 5:10 5:11 6:0 6:1 6:2 6:3 6:4 6:5 6:6 6:7 6:8 6:9 6:10 6:11 7:0 7:1 7:2 7:3 7:4

61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88

–3SD

Months

Month

Year:

13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.0 13.1 13.1 13.1 13.1 13.1 13.1 13.1 13.1 13.1 13.1 13.1 13.2 13.2 13.2 13.2

–2SD 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.1 14.2 14.2 14.2 14.2 14.2 14.2 14.2 14.3 14.3

–1SD 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.4 15.4 15.4 15.4 15.4 15.4 15.4 15.5 15.5 15.5 15.5 15.5 15.6

16.6 16.6 16.7 16.7 16.7 16.7 16.7 16.7 16.7 16.7 16.7 16.8 16.8 16.8 16.8 16.8 16.9 16.9 16.9 16.9 17.0 17.0 17.0 17.0 17.1 17.1 17.1 17.2

Median 1 SD

Boys

18.3 18.3 18.3 18.3 18.3 18.4 18.4 18.4 18.4 18.5 18.5 18.5 18.6 18.6 18.6 18.7 18.7 18.7 18.8 18.8 18.9 18.9 19.0 19.0 19.1 19.1 19.2 19.2

2SD 20.2 20.2 20.2 20.3 20.3 20.4 20.4 20.5 20.5 20.6 20.6 20.7 20.8 20.8 20.9 21.0 21.0 21.1 21.2 21.3 21.3 21.4 21.5 21.6 21.7 21.8 21.9 22.0

3SD 11.8 11.8 11.8 11.8 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.7 11.8 11.8 11.8 11.8 11.8

–3SD 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.7 12.8 12.8 12.8

–2SD

Table 5.7 WHO Growth Standards BMI for Age boys and girls over 5 to 19 years (Z scores) [5]

13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 13.9 14.0 14.0 14.0

–1SD 15.2 15.2 15.2 15.2 15.2 15.2 15.2 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.3 15.4 15.4 15.4 15.4 15.4 15.4 15.5 15.5

16.9 16.9 16.9 16.9 16.9 16.9 16.9 17.0 17.0 17.0 17.0 17.0 17.0 17.0 17.1 17.1 17.1 17.1 17.2 17.2 17.2 17.2 17.3 17.3 17.3 17.4 17.4 17.4

Median 1 SD

Girls

18.9 18.9 18.9 18.9 19.0 19.0 19.0 19.1 19.1 19.1 19.2 19.2 19.3 19.3 19.3 19.4 19.4 19.5 19.5 19.6 19.6 19.7 19.7 19.8 19.8 19.9 20.0 20.0

2SD

21.3 21.4 21.5 21.5 21.6 21.7 21.7 21.8 21.9 22.0 22.1 22.1 22.2 22.3 22.4 22.5 22.6 22.7 22.8 22.9 23.0 23.1 23.2 23.3 23.4 23.5 23.6 23.7

3SD

Measuring undernutrition and overnutrition in children 139

12.3 12.3 12.3 12.3 12.4 12.4 12.4 12.4 12.4 12.4 12.4 12.4 12.5 12.5 12.5 12.5 12.5 12.5 12.5 12.6 12.6 12.6 12.6 12.6 12.6 12.7 12.7 12.7 12.7 12.7

7:5 7:6 7:7 7:8 7:9 7:10 7:11 8:0 8:1 8:2 8:3 8:4 8:5 8:6 8:7 8:8 8:9 8:10 8:11 9:0 9:1 9:2 9:3 9:4 9:5 9:6 9:7 9:8 9:9 9:10

89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118

–3SD

Months

Month

Year:

13.2 13.2 13.2 13.2 13.3 13.3 13.3 13.3 13.3 13.3 13.3 13.4 13.4 13.4 13.4 13.4 13.4 13.5 13.5 13.5 13.5 13.5 13.5 13.6 13.6 13.6 13.6 13.6 13.7 13.7

–2SD 14.3 14.3 14.3 14.3 14.3 14.4 14.4 14.4 14.4 14.4 14.4 14.5 14.5 14.5 14.5 14.5 14.6 14.6 14.6 14.6 14.6 14.7 14.7 14.7 14.7 14.8 14.8 14.8 14.8 14.9

–1SD 15.6 15.6 15.6 15.6 15.7 15.7 15.7 15.7 15.8 15.8 15.8 15.8 15.9 15.9 15.9 15.9 16.0 16.0 16.0 16.0 16.1 16.1 16.1 16.2 16.2 16.2 16.3 16.3 16.3 16.4

17.2 17.2 17.3 17.3 17.3 17.4 17.4 17.4 17.5 17.5 17.5 17.6 17.6 17.7 17.7 17.7 17.8 17.8 17.9 17.9 18.0 18.0 18.0 18.1 18.1 18.2 18.2 18.3 18.3 18.4

Median 1 SD

Boys

19.3 19.3 19.4 19.4 19.5 19.6 19.6 19.7 19.7 19.8 19.9 19.9 20.0 20.1 20.1 20.2 20.3 20.3 20.4 20.5 20.5 20.6 20.7 20.8 20.8 20.9 21.0 21.1 21.2 21.2

2SD 22.0 22.1 22.2 22.4 22.5 22.6 22.7 22.8 22.9 23.0 23.1 23.3 23.4 23.5 23.6 23.8 23.9 24.0 24.2 24.3 24.4 24.6 24.7 24.9 25.0 25.1 25.3 25.5 25.6 25.8

3SD 11.8 11.8 11.8 11.8 11.8 11.9 11.9 11.9 11.9 11.9 11.9 11.9 12.0 12.0 12.0 12.0 12.0 12.1 12.1 12.1 12.1 12.1 12.2 12.2 12.2 12.2 12.3 12.3 12.3 12.3

–3SD 12.8 12.8 12.8 12.8 12.8 12.9 12.9 12.9 12.9 12.9 12.9 13.0 13.0 13.0 13.0 13.0 13.1 13.1 13.1 13.1 13.2 13.2 13.2 13.2 13.3 13.3 13.3 13.4 13.4 13.4

–2SD 14.0 14.0 14.0 14.0 14.1 14.1 14.1 14.1 14.1 14.2 14.2 14.2 14.2 14.3 14.3 14.3 14.3 14.4 14.4 14.4 14.5 14.5 14.5 14.6 14.6 14.6 14.7 14.7 14.7 14.8

–1SD 15.5 15.5 15.5 15.6 15.6 15.6 15.7 15.7 15.7 15.7 15.8 15.8 15.8 15.9 15.9 15.9 16.0 16.0 16.1 16.1 16.1 16.2 16.2 16.3 16.3 16.3 16.4 16.4 16.5 16.5

17.5 17.5 17.5 17.6 17.6 17.6 17.7 17.7 17.8 17.8 17.9 17.9 18.0 18.0 18.1 18.1 18.2 18.2 18.3 18.3 18.4 18.4 18.5 18.6 18.6 18.7 18.7 18.8 18.8 18.9

Median 1 SD

Girls

20.1 20.1 20.2 20.3 20.3 20.4 20.5 20.6 20.6 20.7 20.8 20.9 20.9 21.0 21.1 21.2 21.3 21.3 21.4 21.5 21.6 21.7 21.8 21.9 21.9 22.0 22.1 22.2 22.3 22.4

2SD 23.9 24.0 24.1 24.2 24.4 24.5 24.6 24.8 24.9 25.1 25.2 25.3 25.5 25.6 25.8 25.9 26.1 26.2 26.4 26.5 26.7 26.8 27.0 27.2 27.3 27.5 27.6 27.8 27.9 28.1

3SD

140 Public health nutrition in developing countries

12.8 12.8 12.8 12.8 12.8 12.9 12.9 12.9 12.9 13.0 13.0 13.0 13.0 13.1 13.1 13.1 13.1 13.2 13.2 13.2 13.2 13.3 13.3 13.3 13.4 13.4 13.4 13.5 13.5 13.5

9:11 10:0 10:1 10:2 10:3 10:4 10:5 10:6 10:7 10:8 10:9 10:10 10:11 11:0 11:1 11:2 11:3 11:4 11:5 11:6 11:7 11:8 11:9 11:10 11:11 12:0 12:1 12:2 12:3 12:4

119 120 121 122 123 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148

–3SD

Months

Month

Year:

13.7 13.7 13.8 13.8 13.8 13.8 13.9 13.9 13.9 13.9 14.0 14.0 14.0 14.1 14.1 14.1 14.1 14.2 14.2 14.2 14.3 14.3 14.3 14.4 14.4 14.5 14.5 14.5 14.6 14.6

–2SD 14.9 14.9 15.0 15.0 15.0 15.0 15.1 15.1 15.1 15.2 15.2 15.2 15.3 15.3 15.3 15.4 15.4 15.5 15.5 15.5 15.6 15.6 15.7 15.7 15.7 15.8 15.8 15.9 15.9 16.0

–1SD 16.4 16.4 16.5 16.5 16.6 16.6 16.6 16.7 16.7 16.8 16.8 16.9 16.9 16.9 17.0 17.0 17.1 17.1 17.2 17.2 17.3 17.3 17.4 17.4 17.5 17.5 17.6 17.6 17.7 17.8

18.4 18.5 18.5 18.6 18.6 18.7 18.8 18.8 18.9 18.9 19.0 19.0 19.1 19.2 19.2 19.3 19.3 19.4 19.5 19.5 19.6 19.7 19.7 19.8 19.9 19.9 20.0 20.1 20.2 20.2

Median 1 SD

Boys

21.3 21.4 21.5 21.6 21.7 21.7 21.8 21.9 22.0 22.1 22.2 22.3 22.4 22.5 22.5 22.6 22.7 22.8 22.9 23.0 23.1 23.2 23.3 23.4 23.5 23.6 23.7 23.8 23.9 24.0

2SD 25.9 26.1 26.2 26.4 26.6 26.7 26.9 27.0 27.2 27.4 27.5 25.7 25.9 28.0 28.2 28.4 28.5 28.7 28.8 29.0 29.2 29.3 29.5 29.6 29.8 30.0 30.1 30.3 30.4 30.6

3SD 12.4 12.4 12.4 12.4 12.5 12.5 12.5 12.5 12.6 12.6 12.6 12.7 12.7 12.7 12.8 12.8 12.8 12.9 12.9 12.9 13.0 13.0 13.0 13.1 13.1 13.2 13.2 13.2 13.3 13.3

–3SD 13.4 13.5 13.5 13.5 13.6 13.6 13.6 13.7 13.7 13.7 13.8 13.8 13.8 13.9 13.9 14.0 14.0 14.0 14.1 14.1 14.2 14.2 14.3 14.3 14.3 14.4 14.4 14.5 14.5 14.6

–2SD 14.8 14.8 14.9 14.9 15.0 15.0 15.0 15.1 15.1 15.2 15.2 15.3 15.3 15.3 15.4 15.4 15.5 15.5 15.6 15.6 15.7 15.7 15.8 15.8 15.9 16.0 16.0 16.1 16.1 16.2

–1SD 16.6 16.6 16.7 16.7 16.8 16.8 16.9 16.9 17.0 17.0 17.1 17.1 17.2 17.2 17.3 17.4 17.4 17.5 17.5 17.6 17.7 17.7 17.8 17.9 17.9 18.0 18.1 18.1 18.2 18.3

19.0 19.0 19.1 19.2 19.2 19.3 19.4 19.4 19.5 19.6 19.6 19.7 19.8 19.9 19.9 20.0 20.1 20.2 20.2 20.3 20.4 20.5 20.6 20.6 20.7 20.8 20.9 21.0 21.1 21.1

Median 1 SD

Girls

22.5 22.6 22.7 22.8 22.8 22.9 23.0 23.1 23.2 23.3 23.4 23.5 23.6 23.7 23.8 23.9 24.0 24.1 24.2 24.3 24.4 24.5 25.7 24.8 24.9 25.0 25.1 25.2 25.3 25.4

2SD 28.2 28.4 28.5 28.7 28.8 29.0 29.1 29.3 29.4 29.6 29.7 29.9 30.0 30.2 30.3 30.5 30.6 30.8 30.9 31.1 31.2 31.4 31.5 31.6 31.8 31.9 32.0 32.2 32.3 32.4

3SD

Measuring undernutrition and overnutrition in children 141

13.6 13.6 13.6 13.7 13.7 13.7 13.8 13.8 13.8 13.9 13.9 14.0 14.0 14.0 14.1 14.1 14.1 14.2 14.2 14.3 14.3 14.3 14.4 14.4 14.5 14.5 14.5 14.6 14.6 14.6

12:5 12:6 12:7 12:8 12:9 12:10 12:11 13:0 13:1 13:2 13:3 13:4 13:5 13:6 13:7 13:8 13:9 13:10 13:11 14:0 14:1 14:2 14:3 14:4 14:5 14:6 14:7 14:8 14:9 14:10

149 150 151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175 176 177 178

–3SD

Months

Month

Year:

14.6 14.7 14.7 14.8 14.8 14.8 14.9 14.9 15.0 15.0 15.1 15.1 15.2 15.2 15.2 15.3 15.3 15.4 15.4 15.5 15.5 15.6 15.6 15.7 15.7 15.7 15.8 15.8 15.9 15.9

–2SD 16.0 16.1 16.1 16.2 16.2 16.3 16.3 16.4 16.4 16.5 16.5 16.6 16.6 16.7 16.7 16.8 16.8 16.9 17.0 17.0 17.1 17.1 17.2 17.2 17.3 17.3 17.4 17.4 17.5 17.5

–1SD 17.8 17.9 17.9 18.0 18.0 18.1 18.2 18.2 18.3 18.4 18.4 18.5 18.6 18.6 18.7 18.7 18.8 18.9 18.9 19.0 19.1 19.1 19.2 19.3 19.3 19.4 19.5 19.5 19.6 19.6

20.3 20.4 20.4 20.5 20.6 20.7 20.8 20.8 20.9 21.0 21.1 21.1 21.2 21.3 21.4 21.5 21.5 21.6 21.7 21.8 21.8 21.9 22.0 22.1 22.2 22.2 22.3 22.4 22.5 22.5

Median 1 SD

Boys

24.1 24.2 24.3 24.4 24.5 24.6 24.7 24.8 24.9 25.0 25.1 25.2 25.2 25.3 25.4 25.5 25.6 25.7 25.8 25.9 26.0 26.1 26.2 26.3 26.4 26.5 26.5 26.6 26.7 26.8

2SD 30.7 30.9 31.0 31.1 31.3 31.4 31.6 31.7 31.8 31.9 32.1 32.2 32.3 32.4 32.6 32.7 32.8 32.9 33.0 33.1 33.2 33.3 33.4 33.5 33.5 33.6 33.7 33.8 33.9 33.9

3SD 13.3 13.4 13.4 13.5 13.5 13.5 13.6 13.6 13.6 13.7 13.7 13.8 13.8 13.8 13.9 13.9 13.9 14.0 14.0 14.0 14.1 14.1 14.1 14.1 14.2 14.2 14.2 14.3 14.3 14.3

–3SD 14.6 14.7 14.7 14.8 14.8 14.8 14.9 14.9 15.0 15.0 15.1 15.1 15.2 15.2 15.2 15.3 15.3 15.4 15.4 15.4 15.5 15.5 15.6 15.6 15.6 15.7 15.7 15.7 15.8 15.8

–2SD 16.2 16.3 16.3 16.4 16.4 16.5 16.6 16.6 16.7 16.7 16.8 16.8 16.9 16.9 17.0 17.0 17.1 17.1 17.2 17.2 17.3 17.3 17.4 17.4 17.5 17.5 17.6 17.6 17.6 17.7

–1SD 18.3 18.4 18.5 18.5 18.6 18.7 18.7 18.8 18.9 18.9 19.0 19.1 19.1 19.2 19.3 19.3 19.4 19.4 19.5 19.6 19.6 19.7 19.7 19.8 19.9 19.9 20.0 20.0 20.1 20.1

21.2 21.3 21.4 21.5 21.6 21.6 21.7 21.8 21.9 22.0 22.0 22.1 22.2 22.3 22.4 22.4 22.5 22.6 22.7 22.7 22.8 22.9 22.9 23.0 23.1 23.1 23.2 23.3 23.3 23.4

Median 1 SD

Girls

25.5 25.6 25.7 25.8 25.9 26.0 26.1 26.2 26.3 26.4 26.5 26.6 26.7 26.8 26.9 27.0 27.1 27.1 27.2 27.3 27.4 27.5 27.6 27.7 27.7 27.8 27.9 28.0 28.0 28.1

2SD 32.6 32.7 32.8 33.0 33.1 33.2 33.3 33.4 33.6 33.7 33.8 33.9 34.0 34.1 34.2 34.3 34.4 34.5 34.6 34.7 34.7 34.8 34.9 35.0 35.1 35.1 35.2 35.3 35.4 35.4

3SD

142 Public health nutrition in developing countries

14.7 14.7 14.7 14.8 14.8 14.8 14.9 14.9 15.0 15.0 15.0 15.0 15.1 15.1 15.1 15.2 15.2 15.2 15.3 15.3 15.3 15.3 15.4 15.4 15.4 15.4 15.5 15.5 15.5 15.5

14:11 15:0 15:1 15:2 15:3 15:4 15:5 15:6 15:7 15:8 15:9 15:10 15:11 16:0 16:1 16:2 16:3 16:4 16:5 16:6 16:7 16:8 16:9 16:10 16:11 17:0 17:1 17:2 17:3 17:4

179 180 181 182 183 184 185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208

–3SD

Months

Month

Year:

16.0 16.0 16.1 16.1 16.1 16.2 16.2 16.3 16.3 16.3 16.4 16.4 16.5 16.5 16.5 16.6 16.6 16.7 16.7 16.7 16.8 16.8 16.8 16.9 16.9 16.9 17.0 17.0 17.0 17.1

–2SD 17.6 17.6 17.7 17.8 17.8 17.9 17.9 18.0 18.0 18.1 18.1 18.2 18.2 18.2 18.3 18.3 18.4 18.4 18.5 18.5 18.6 18.6 18.7 18.7 18.7 18.8 18.8 18.9 18.9 18.9

–1SD 19.7 19.8 19.8 19.9 20.0 20.0 20.1 20.1 20.2 20.3 20.3 20.4 20.4 20.5 20.6 20.6 20.7 20.7 20.8 20.8 20.9 20.9 21.0 21.0 21.1 21.1 21.2 21.2 21.3 21.3

22.6 22.7 22.8 22.8 22.9 23.0 23.0 23.1 23.2 23.3 23.3 23.4 23.5 23.5 23.6 23.7 23.7 23.8 23.8 23.9 24.0 24.0 24.1 24.2 24.2 24.3 24.3 24.4 24.4 24.5

Median 1 SD

Boys

26.9 27.0 27.1 27.1 27.2 27.3 27.4 27.4 27.5 27.6 27.7 27.7 27.8 27.9 27.9 28.0 28.1 28.1 28.2 28.3 28.3 28.4 28.5 28.5 28.6 28.6 28.7 28.7 28.8 28.9

2SD 34.0 34.1 34.1 34.2 34.3 34.3 34.4 34.5 34.5 34.6 34.6 34.7 34.7 34.8 34.8 34.8 34.9 34.9 35.0 35.0 35.0 35.1 35.1 35.1 35.2 35.2 35.2 35.2 35.3 35.3

3SD 14.3 14.4 14.4 14.4 14.4 14.5 14.5 14.5 14.5 14.5 14.5 14.6 14.6 14.6 14.6 14.6 14.6 14.6 14.6 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7

–3SD 15.8 15.9 15.9 15.9 16.0 16.0 16.0 16.0 16.1 16.1 16.1 16.1 16.2 16.2 16.2 16.2 16.2 16.2 16.3 16.3 16.3 16.3 16.3 16.3 16.3 16.4 16.4 16.4 16.4 16.4

–2SD 17.7 17.8 17.8 17.8 17.9 17.9 17.9 18.0 18.0 18.0 18.1 18.1 18.1 18.2 18.2 18.2 18.2 18.3 18.3 18.3 18.3 18.3 18.4 18.4 18.4 18.4 18.4 18.4 18.5 18.5

–1SD 20.2 20.2 20.3 20.3 20.4 20.4 20.4 20.5 20.5 20.6 20.6 20.6 20.7 20.7 20.7 20.8 20.8 20.8 20.9 20.9 20.9 20.9 21.0 21.0 21.0 21.0 21.1 21.1 21.1 21.1

23.5 23.5 23.6 23.6 23.7 23.7 23.8 23.8 23.9 23.9 24.0 24.0 24.1 24.1 24.1 24.2 24.2 24.3 24.3 24.3 24.4 24.4 24.4 24.4 24.5 24.5 24.5 24.6 24.6 24.6

Median 1 SD

Girls

28.2 28.2 28.3 28.4 28.4 28.5 28.5 28.6 28.6 28.7 28.7 28.8 28.8 28.9 28.9 29.0 29.0 29.0 29.1 29.1 29.1 29.2 29.2 29.2 29.3 29.3 29.3 29.3 29.4 29.4

2SD 35.5 35.5 35.6 35.7 35.7 35.8 35.8 35.8 35.9 35.9 36.0 36.0 36.0 36.1 36.1 36.1 36.1 36.2 36.2 36.2 36.2 36.2 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.3

3SD

Measuring undernutrition and overnutrition in children 143

15.6 15.6 15.6 15.6 15.6 15.7 15.7 15.7 15.7 15.7 15.7 15.8 15.8 15.8 15.8 15.8 15.8 15.8 15.8 15.9

17:5 17:6 17:7 17:8 17:9 17:10 17:11 18:0 18:1 18:2 18:3 18:4 18:5 18:6 18:7 18:8 18:9 18:10 18:11 19:0

209 210 211 212 213 214 215 216 217 218 219 220 221 222 223 224 225 226 227 228

–3SD

Months

Month

Year:

17.1 17.1 17.1 17.2 17.2 17.2 17.3 17.3 17.3 17.3 17.4 17.4 17.4 17.4 17.5 17.5 17.5 17.5 17.5 17.6

–2SD 19.0 19.0 19.1 19.1 19.1 19.2 19.2 19.2 19.3 19.3 19.3 19.4 19.4 19.4 19.5 19.5 19.5 19.6 19.6 19.6

–1SD 21.4 21.4 21.5 21.5 21.6 21.6 21.7 21.7 21.8 21.8 21.8 21.9 21.9 22.0 22.0 22.0 22.1 22.1 22.2 22.2

24.5 24.6 24.7 24.7 24.8 24.8 24.9 24.9 25.0 25.0 25.1 25.1 25.1 25.2 25.2 25.3 25.3 25.4 25.4 25.4

Median 1 SD

Boys

28.9 29.0 29.0 29.1 29.1 29.2 29.2 29.2 29.3 29.3 29.4 29.4 29.5 29.5 29.5 29.6 29.6 29.6 29.7 29.7

2SD 35.3 35.3 35.4 35.4 35.4 35.4 35.4 35.4 35.4 35.5 35.5 35.5 35.5 35.5 35.5 35.5 35.5 35.5 35.5 35.5

3SD 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7 14.7

–3SD 16.4 16.4 16.4 16.4 16.4 16.4 16.4 16.4 16.5 16.5 16.5 16.5 16.5 16.5 16.5 16.5 16.5 16.5 16.5 16.5

–2SD 18.5 18.5 18.5 18.5 18.5 18.5 18.6 18.6 18.6 18.6 18.6 18.6 18.6 18.6 18.6 18.6 18.7 18.7 18.7 18.7

–1SD 21.1 21.2 21.2 21.2 21.2 21.2 21.2 21.3 21.3 21.3 21.3 21.3 21.3 21.3 21.4 21.4 21.4 21.4 21.4 21.4

24.6 24.6 24.7 24.7 24.7 24.7 24.8 24.8 24.8 24.8 24.8 24.8 24.9 24.9 24.9 24.9 24.9 24.9 25.0 25.0

Median 1 SD

Girls

29.4 29.4 29.4 29.5 29.5 29.5 29.5 29.5 29.5 29.6 29.6 29.6 29.6 29.6 29.6 29.6 29.6 29.6 29.7 29.7

2SD 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.3 36.2 36.2 36.2 36.2 36.2 36.2 36.2 36.2

3SD

144 Public health nutrition in developing countries

Measuring undernutrition and overnutrition in children

5.6

145

Undernutrition

Undernutrition is the most widely prevalent form of malnutrition among children. Nutritional status of children is an indicator of nutritional profile of the entire community. Protein energy malnutrition (PEM) affects every fourth child world-wide. About 129 million are underweight while 195 million are stunted [19]. Despite an overall decrease of stunting in developing countries, child malnutrition still remains a major public health problem in developing countries. In India, there has been a significant decline in extreme forms of protein energy malnutrition (classical kwashiorkor and extreme forms of marasmus) over the past few decades but the decline has been only modest for anthropometrically measured undernutrition. The proportion of children under-5 years of age who were underweight decreased from 53 percent in National Family Health Survey-1 (NFHS-1) conducted in 1992–93 to 47 percent in NFHS-2 (1998–99) and 46 percent in NFHS-3 (2005– 2006). Similarly, prevalence of stunting decreased from 52% in NFHS-1 to 45% in NFHS-2 and 38% in NFHS-3 [20].

Classification Undernutrition is the result of food intake that is continuously insufficient to meet dietary energy requirements, poor absorption and/or poor biological use of nutrients consumed. This usually results in loss of body weight. Contrary to common usage, the term “malnutrition” correctly includes both undernutrition and overnutrition. Several systems are used for classifying undernutrition. Mild, moderate and severe are different in each of the classification systems. Thus, it is important to use the same system to analyze and present data while making the comparisons or describing trends. PEM may be classified according to the severity, course and the relative contributions of energy or protein deficit. Some classifications based on anthropometric measurements, mainly weight and height are described below: (i) Indian Academy of Pediatrics (IAP) classification based on weightfor-age. IAP takes a weight of more than 80% of the expected weightfor-age as normal. Grades of malnutrition are Grade I (71–80%), II (61–70%), III (51–60%) and IV (<50%) of the expected weight for that age. Alphabet K is post-fixed in presence of edema. For example, a male child weighing 8 kg at 2 years of age with pedal edema (50th percentile for 2 years is 12.3 kg) is classified as PEM Grade II (k) as per IAP classification. IAP classification is simple and the cut-offs are suitable for Indian

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population. However, the disadvantage is that it does not take in account the child’s height. The weight is also dependent on height besides the built; thus children who are short statured (not necessarily because of nutritional deprivation) are also misclassified as PEM by this classification. (ii) Welcome Trust Classification is also based on deficit in body weight for age and presence or absence of edema. Children weighing between 60% and 80% of their expected weight-for-age with edema are classified as kwashiorkor. Those weighing between 60% and 80% of the expected weight without edema are known as having undernutrition. Those without edema and weighing less than 60 per cent of their expected weight-for-age are considered to be having marasmus. Marasmic kwashiorkor is applied to children with edema and body weight less than 60% of the expected. (iii) WHO classification. The above referred classifications measure undernutrition and are based on weight-for-age alone. However, it is important to distinguish undernutrition from wasting (deficits in weight-for-height) and stunting (deficits in height-for-age). WHO Classification of malnutrition is based on the statistical cut-offs for defining wasting and stunting as those below –2 SD (Table 5.2, 5.3, 5.4, 5.5). Severe wasting and stunting are defined when the weightfor-height and height-for-age, respectively are less than 3 SD scores. Severe wasting (weight-for-height <3 SD or < 70% of median) is used as an admission criteria to identify individual children for inpatient management of severe malnutrition (Table 5.8). (iv) Age-independent anthropometric indices. Some anthropometric indices which are ratios of weight or height and are based on circumference such as Dugale’s, Rao’s and Kanawati do not require consideration of age. These serve as useful one time indicators to assess nutritional status in clinical practice, where exact age of the child is not known (e.g., orphanages, street children, etc.). However, most of these indices are no longer used now as these are difficult to calculate and interpret. Also, these are not truly age independent but the effect of age on these indices is less pronounced especially in under-5 children.

Overnutrition (overweight and obesity) Overnutrition refers to a chronic condition where intake of food is in excess of dietary energy requirements, resulting in overweight and/or obesity. Obesity may be defined as an excessive storage of energy as fat relative to the lean body mass. Body fat expressed as a percentage of body weight

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Table 5.8 WHO Classification for Undernutrition

Symmetrical edema Weight for height (measure of wasting) Height for age (measure of stunting)

Moderate undernutrition

Severe undernutrition

No

Yes (a) Edematous malnutrition

SD score -2 to –3 (70–79% of expected (b)) Wasting

SD score < -3 (<70% of expected) Severe wasting

SD score -2 to –3 (85–89% of expected (b))

SD score < -3 (<85% of expected)

Stunting

Severe stunting

This includes kwashiorkar and marasmic kwashiorkar Median (50th percentile of NCHS references)

(a)

(b)

(% body fat) is the most relevant measure against which all anthropometric measures is correlated. Estimates of body composition can be made by dual energy X-ray absorbiometry (DEXA). The complex nature, high cost and difficult methodology of direct estimation of body fat content has ensured that this is limited to research purpose only. This led to the search for other measurements which can be easily performed and correlate satisfactorily with the percentage of body fat. Skin-fold thickness provides a reliable estimate of body fat and its distribution. It can be measured at several sites including triceps, biceps, axilla, mid-abdominal, subscapular and suprailiac. The biceps and the triceps skin-fold thickness estimate the peripheral body fat, whereas subscapular and suprailiac skin-folds reflect the central adiposity. Skin-fold thicknesses above the 85th percentile for age and sex suggest obesity and above the 95th percentile suggest superobesity. Triceps skin-fold thickness is the most common site of measurement. Although accurate under research settings, the use of this method for epidemiologic assessment of obesity is hindered by methodological problems. In contrast, the high reliability of measurement of weight and height suggests that an anthropometric parameter based on these indices would provide a more useful measure of adiposity for comparison within and between populations. Traditionally, obesity in children has been defined as a weight-for-height above the 90th percentile on the growth charts from the National Centre of Heath Statistics or weight in excess of 120% of the median weight for a given height. Super-obesity is defined as a weight for height above the 95th percentile and weight in excess of 140% of the median weight for a given height. Body mass index [weight (kg)/height2 (meter2)] is widely accepted as a convenient measure of a person’s fatness. It is a rather robust index which is extremely useful for large-scale epidemiological work. For adults the BMI categories are underweight <18.5, ideal 18.5–24.9, preobese 25.0–

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29.9, obese class I 30.0–34.9, obese class II 35.0–39.9 and obese class III >40 kg/m 2 (Table 5.9). The risk for medical complications in adults has a direct correlation with the BMI. In recent years, there was a growing debate on whether there are possible needs for developing lower BMI cut-off points for Asian populations due to their different body composition. The proportion of Asian people with a high risk of type 2 diabetes and cardiovascular disease is substantial at BMI’s lower than the existing WHO cut-off point for overweight i.e. 25 kg/m2. However, the cut-off point for observed risk varies from 22 to 25 kg/m 2 in different Asian populations, and for high risk it varies from 26 to 31 kg/m2. The current WHO BMI cut-off points (Table 5.9) is the international classification. However, the cut-off points of 23, 27.5, 32.5 and 37.5 kg/m2 are important and need to be considered as points for public health action. It means that the public health action for prevention of overweight and obesity in Indian populations should start at BMI >23 kg/m 2 despite the person being defined as normal as per the International classification. BMI in children changes substantially with age. It is obvious that a single cut-off point for defining obesity cannot be used. The 85th and the 95th percentiles of BMI for age and sex have been recommended to identify overweight and obesity. Given the relative ease of measurement and its accuracy vis-à-vis other parameters, BMI is the most acceptable indicator of body fatness. International BMI cut-offs for child overweight and obesity, based on data from six countries, have been developed. The international BMI cut-offs for child overweight and obesity cover the age Table 5.9 The International classification of nutritional status in adults according to BMI [21] Classification

BMI (kg/m 2) Principal cut-off points

Additional cut-off points (a)

Underweight Severe thinness Moderate thinness Mild thinness

<18.50 <16.00 16.00–16.99 17.00–18.49

<18.50 <16.00 16.00–16.99 17.00–18.49

Normal range

18.50–24.99

Overweight Pre-obese

> 25.00 25.00–29.99

Obese Obese class I

> 30.00 30.00–34.99

Obese class II

35.00–39.99

Obese class III

> 40.00

18.50–22.99 23.00–24.99 > 25.00 25.00–27.49 27.50–29.99 > 30.00 30.00–32.49 32.50–34.99 35.00–37.49 37.50–39.99 > 40.00

The additional cut-off points in these categories are important for public health action in Asian populations. (a)

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range 2–18 years and are based on the adult cut-offs of 25 and 30 at 18 years. BMI charts developed by WHO for children and adolescents up to the ages of 19 years are presented in the chapter.

Types of obesity: android and gynecoid Obesity should also be evaluated in terms of distribution of body fat. Adipose tissue accumulates in two main sites – intra-abdominal and subcutaneous. Intra-abdominal fat comprises fat surrounding the omentum and mesentery with the retroperitoneal fat whereas subcutaneous fat is distributed all over the body. In males both kinds of fat accumulation is more prominent in the upper segment of the body, visible as an apple shaped distribution. In females the tissue is more subcutaneous and over the thighs in a pear shaped distribution. This is important because it has been demonstrated that in comparison to obese individuals with pelvic or “gynecoid” fat distribution, equally obese individuals with central or ‘android obesity’ are more likely to develop obesity related disorders including insulin resistance, Non Insulin Dependent Diabetes Mellitus (NIDDM), hypertension and hyperlipidemias. The distribution of body fat can be estimated using the waist–hip ratio (WHR). WHR>0.8 is the cut-off point associated with above listed clinical problems. However in children no correlation has been shown between WHR and visceral fat. The visceral subcutaneous fat ratio (VSR) measured with the help of the CT scan has been shown to be a better index of fat distribution. There is no controversy with respect to the importance of visceral fat as a determinant of adult health. Unfortunately, there is a paucity of similar data for pediatric population largely because of absence of a method other than radiological for its measurement.

References 1. WHO Working Group (1986). Use and interpretation of anthropometric indicators of nutritional status. Bull WHO vol. 64, pp. 929–941. 2. COGILL B (2003). Anthropometric Indicators Measurement Guide. Food and Nutrition Technical Assistance Project, Academy for Educational Development, Washington, D.C. 3. How to Weigh and Measure Children: Assessing the Nutritional Status of Young Children in Household Surveys, United Nations Department of Technical Cooperation for Development and Statistical Office, 1986. 4. GORSTEIN J, SULLIVAN K, YIP R , DE ONIS M , TROWBRIDGE F , FAJANS P , CLUGSTON G (1994). Issues in the assessment of nutritional status using anthropometry. Bull WHO vol. 72, pp. 273–283. 5. World Health Organization. Growth standards (2006). Available at http:// www.who.int/childgrowth/standards.

150 6.

7.

8.

9. 10.

11.

12. 13.

14. 15. 16.

17.

18.

19. 20. 21.

Public health nutrition in developing countries Physical Status: the Use and Interpretation of Anthropometry. Report of a WHO Expert Committee. Geneva, World Health Organization, 1995 (WHO Technical Report Series, No. 854). DE ONIS M, ONYANGO AW , BORGHI E , SIYAM A , NISHIDAA C, SIEKMANNA J (2007). Development of a WHO growth reference for school-aged children and adolescents. Bull WHO vol. 85, pp. 660–667. DIBLEY MJ et al (1987). Development of normalized curves for the international growth reference: historical and technical considerations. Am J Clin Nutr vol. 46, pp. 736–748. DIBLEY MJ et al (1987). Interpretation of z-score anthropometric indicators derived from the international growth reference. Am J Clin Nutr vol. 46, pp. 749–762. COLE TJ , BELLIZZI MC , FLEGAL KM , DIETZ WH (2000). Establishing a standard definition for child overweight and obesity: international survey. BMJ vol. 320, pp. 1240–1243. COLE TJ , FLEGAL KM , NICHOLLS D , JACKSON AA (2007). Body mass index cutoffs to define thinness in children and adolescents: international survey. BMJ vol. 335, p. 194. CAMERON N (2007). Body mass index cut offs to define thinness in children and adolescents. BMJ vol. 335, pp. 166–167. National Center for Health Statistics (1977). In: Hamill, PVV et al., (eds) Growth curves for children birth-18 years United States. Washington, DC, National Center for Health Statistics (Vital and health statistics. Series 11: No. 165 (DHEW publication (PHS) #78-1650)), 1977. DE ONIS M (1997). Time for a new growth reference. Pediatrics vol. 100, p. e8. VICTORA CG , MORRIS SS , BARROS FC , DE ONIS M, YIP R (1998). The NCHS reference and the growth of breast- and bottle-fed infants. J Nutr vol. 128, pp. 1134–1138. DE ONIS M, GARZA C, VICTORA CG , BHAN MK , NORUM KR (2004). The WHO Multicentre Growth Reference Study (MGRS): rationale, planning and implementation. Food Nutr Bull vol. 25 (Suppl. 1). WHO Multicentre Growth Reference Study Group (2006). Enrolment and baseline characteristics in the WHO Multicentre Growth Reference Study. Acta Paediatrica Suppl 450, pp. 7–15. DE ONIS M, ONYANGO AW, BORGHI E , GARZA C , YANG H , for the WHO Multicentre Growth Reference Study Group. Comparison of the WHO Child Growth Standards and the NCHS growth reference: implications for child health programs. (In press) UNICEF (2009). Tracking progress on child and maternal nutrition. www.unicef.org National Family Health Survey (NFHS-3), India, 2005–2006. Mumbai, International Institute for Population Sciences and ORC Macro, 2007. WHO. Global database on Body Mass Index: http://apps.who.int/bmi/index.jsp? introPage=intro_3html

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Essential new-born care and child survival Richa Singh Pandey and Sheila C. Vir

Richa Singh Pandey, MD, has several years of experience in the field of public health and nutrition. Dr. Singh is currently a nutrition specialist with UNICEF (India). Prior to joining UNICEF, Dr. Pandey worked on an important newborn care project with Saksham Study Group of Johns Hopkins–King George Medical College Collaborative Centre and as a consultant with UNICEF on maternal & child health and nutrition issues. Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

6.1

Neonatal period – a risky start to childhood

The greatest risk to life is in its beginning. A good start in life begins well before birth, however it is just before, during and in the very first hours and days that life is most at risk [1]. A newborn is known a “neonate” during the first 28 days of life and this period is referred to as the neonatal period. On the basis of survival, the neonatal period is further classified into early neonatal period 0–7 days and late neonatal period 8–28 days (Figure 6.1). The probability of dying in first month of life is known as neonatal mortality [2] and when expressed as “deaths within the first twenty eight days per 1000 live births” the term is known as neonatal mortality rate. The neonatal period is only 28 days and yet accounts for 38% of all deaths in children younger than age 5 years in age. The remaining 62% of deaths in under five arise over a period of 1800 days, i.e. 59 months [3].

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152

Thus, the average daily mortality rate during the neonatal period nearly 30-fold higher than during the post-neonatal period. Within the neonatal period, early neonatal period is more risky with 50–70% of fatal and life threatening illnesses occur during the first 7 days [1, 4].

6.1.1

Neonatal mortality – global magnitude

Globally, more than 4 million newborns die within the first 28 days of coming into this world. Amongst the developing nations, countries of Africa

6.1 Neonatal period [5].

(28%) and South East Asia (36%) account for two-thirds of total neonatal deaths, with rates being highest in Africa (Figure 6.2) and numbers in Asia [3, 6]. Ten countries account for two-thirds of neonatal deaths [3].

6.2 Variations between countries in NMR [3].

Owing to its large population size, India’s contribution to neonatal mortality is highest in terms of numbers (Table 6.1).

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Table 6.1 Countries with largest number of neonatal deaths worldwide (2000) [3] Countries

Number of neonatal deaths (1000s)

India China Pakistan Nigeria Bangladesh Ethiopia Democratic Republic of Congo Indonesia Afghanistan United Republic of Tanzania Total

6.2

1098 416 298 247 153 147 116 82 63 62 2682

Percentage of global neonatal deaths 27% 10% 7% 6% 4% 4% 3% 2% 2% 2% 67%

NMR (per 1000 live births) 43 21 57 53 36 51 47 18 60 43

Millennium development goal 4 (MDG-4) and neonatal mortality

The fourth goal (MDG-4) commits the international community to reducing child mortality (under five mortality rate) by two-thirds between 1990 and 2015. Inherent in this goal is reduction in neonatal mortality rates. Available data shows that decline in neonatal mortality rates is not commensurate with decline in IMR or child mortality rates Between 1980 and 2000, child mortality after the first month of life – i.e. from month 2 to age 5 years – fell by a third, whereas the neonatal mortality rate (NMR) was reduced by only about a quarter [3] (Figure 6.3). Even in neonatal mortality, the visible reduction was primarily due to reduction in late neonatal mortality with almost no change in the early neonatal mortality (Figure 6.3).

6.3 Trends in child and neonatal mortality [3].

Public health experts predict that MDG-4 cannot be met unless neonatal mortality is at least halved [7]. Concerted efforts, with focus on reducing

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NMR in high mortality countries of South East Asia which constitute 25% of global population but have more than 36% share in global neonatal burden [8], are critical to success; Indian subcontinent has a key role achieving the success.

6.3

Neonatal mortality – an Indian perspective

The Indian subcontinent accounts for nearly 27–30% of global burden of neonatal deaths [9]. The Government of India has set a target of reducing the infant mortality rate from 64 to 30 per 1000 live births by the year 2010, which can only be possible if neonatal mortality is reduced by 54%, i.e. from 44/1000 live births to 20/1000 live births in this period. However, there has been only a 15% decline in neonatal mortality during the 1990s which has plateaued in recent years [10]. A Lancet study of 2005 puts this reduction further lower at just 11% [3]. The modest drop in neonatal mortality rate (NMR) is largely the result of late neonatal mortality reductions (deaths after the first week of life), in part due to a fall in deaths from tetanus [3]. The country has not been able to reduce early neonatal deaths. Moreover, the burden of neonatal deaths continues to be primarily from with five northern states (Bihar, Madhya Pradesh, Uttar Pradesh, Rajasthan) of the country contributing to more than half of all neonatal deaths [9]. The recent National Family Health Survey(NFHS) data confirms that India is also following global trend of rapid fall in U5MR (from 109 to 74) and Infant mortality (from 79 to 57) rate but has stagnant NMR which has reduced marginally from 49 to only 39 [11] ( from 49 to 39) (Figure 6.4).

6.4 Trend in child mortality rates in India [12].

Essential new-born care and child survival

6.4

155

Neonatal mortality – direct and underlying determinants

The distribution of causes of neonatal death varies between countries and correlates closely with the degree of neonatal mortality [3]. Based on the data of 193 countries, the major causes of neonatal death globally are estimated to be infections (35%) – this includes (sepsis/pneumonia, tetanus, and diarrhea), preterm birth (28%), and asphyxia (23%) [13]. In India, a study conducted in Gadhchiroli, a small district in Maharashtra ascribed sepsis/pneumonia (52.5%), asphyxia (20%), prematurity <32 weeks (15%), hypothermia (2.5%), and other/not known (10%) as the primary cause of neonatal deaths in India.

6.4.1

Low birth weight – an important contributor to neonatal mortality

On the basis of birth weight, newborn is categorized into normal (>2500 g), low birth weight (<2500 g), very low birth weight (<1500 g), and extremely low birth weight (<1000 g) groups [14]. Low birth weight can be an outcome of pre-term delivery (gestational age <37 completed weeks) or prematurity (intrauterine growth retardation or IUGR), or both. Prematurity or IUGR is a greater risk with fifty percent of the 4 million neonatal deaths per year occurring in babies who are small for their age [15]. The lower the birth weight, higher the chances of mortality. The Lancet malnutrition series 2008 observes that infants born at term weighing 1500– 1999 g are 8.1 times more likely to die and those weighing 2000–2499 g are 2.8 times more likely to die from all causes during the neonatal period than those weighing more than 2499 g at birth. Birth weight is also an important predictor of clinical complications. It has been shown that LBW plays an important role in almost 60% of neonatal deaths occurring due to birth asphyxia and infections [16]. The national neonatal perinatal database reports that nearly about onethird of all neonates born in major hospitals of India every year are LBW. In India, nearly 82% neonatal deaths occur among LBW (NNF, 1995), which is the highest in the world [17]. Newborn care entails efforts directed at reducing not only neonatal mortality but also ensuring that each newborn is given an environment and a healthy beginning which allows them to survive and develop to their full potential. Most of the causes leading to neonatal death have their origin in the antenatal period. Reducing neonatal mortality requires efforts directed throughout pregnancy, through delivery and after birth, that is, care along the continuum.

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6.5

Continuum of care – a comprehensive approach to saving newborn lives

Neonatal health is intrinsically linked to the health and nutrition of the mother and the care she receives before, during and immediately after giving birth [1]. Cost-effective prenatal and delivery interventions that improve maternal health and nutrition and save mothers’ lives can save most newborns too [18]. This principle of care which extends and links two or more phases (maternal health and child health) is often termed as continuum of care. The continuum of care has recently been highlighted as a core principle of programmes for maternal, newborn, and child health, and as a means to reduce the burden of half a million maternal deaths, 4 million neonatal deaths, and 6 million children [19]. According to World Health Report 2005, the term “continuum of care” encompasses both person and place, i.e. care provided as a continuum throughout the lifecycle, including adolescence, pregnancy, childbirth and childhood and secondly care provided in a continuum that spans the home, the community, the health center and the hospital – Figs. 6.5a and 6.5b. The interventions for saving newborn lives “Essential newborn care” is based on the principles of continuum of care. A d olescen t a nd

P re gn a ncy

B irth

P o st pa rtu m

M atern al h ea lth

L in king a cro ss the tim es o f care g ivin g N e on ata l

In fa ncy

C h ild h oo d

6.5a Connecting care giving across the continuum for maternal, newborn and child health.

Ho usehold

Co mm unity

Linking the places of care givin g He alth Fa cility

6.5b Connecting care giving across the continuum between households and health facilities to reduce maternal, newborn and child deaths.

Essential new-born care and child survival

6.6

157

Essential newborn care interventions

Essential newborn care is a comprehensive strategy designed to improve the health of newborns through interventions before conception, during pregnancy, at and soon after birth, and in the postnatal period [20]. On the basis of birth weight and gestational age, WHO proposes two types of essential newborn care: basic care and special care. Basic care means interventions for all infants to meet their physiological needs. Basic newborn care assures survival of those that are born wellequipped to survive (term, well-grown newborns without malformations) and give good start for preterm and small newborns. Simple, effective, low cost interventions notably, tetanus toxoid vaccination, exclusive breastfeeding, kangaroo mother care come under basic interventions. Special care is required for a small group of newborns because of diseases acquired before, during or after birth and/or because they were born too soon and/or too small. Figure 6.6 given below shows the package of interventions (both basic and special) which have a proven role in promoting health and preventing deaths in newborns, the linkages between the physiological stage and subsequent outcome and the type of care provider needed for providing the care. Labour and delivery care

Postnatal c are

Skilled Atte ndance

Provid er contacts/visits

Antenatal ca re

Ba s ic ca re

Provid er conta ct/visits Tetanus toxoid im m unization A dequate diet Iron Folic Acid(+ iodine) Syphilis detection & treatm ent M alaria prophylaxis Breastfeeding couns elin g Birth preparednes s

C lean d eliv ery Prevention of hypotherm ia Im m ediate breastfeeding Prophylactic eye care

Exclusive breastfeedin g W arm th H ygiene, C ord C are Im m uniza tion M aternal nutrition Birth spacing counseling

S pe cia l ca re

D AN G E R SIG N S M aternal and fetal com plic ations Prevention of m other to child trans m iss ion if m other HIV pos itiv e M an agement or referral of obstetric or neonatal com plic ations

Birth asphyx ia R esuscitation

Low birth weight Special w arm th

Post resuscitation care

Kangaroo m other care

R eferral, if necessary

H ygiene, cord care Assisted feeding --R eferral, if necessary

Infections , m alformations and other Antibiotics for infection Supportive care Antiretrov iral therap y, if m other H IV positive R eferral if necessary

6.6 Essential newborn care interventions across the continuum of care [18].

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Following sections give a brief insight into selected basic essential newborn care interventions as recommended by WHO.

Basic care (a) Protecting newborn against infections Almost 75% deliveries in India occur at home in presence of unskilled birth attendants/family members thereby exposing the mother and the newborn to the risk of infection, inappropriate management of pregnancy complications and poor hygiene during the delivery. Tetanus and sepsis are the commonest infection during the early neonatal period and are a manifestation of unhygienic delivery practices. Ensuring clean delivery and clean cord is essential for minimizing the risk of neonatal tetanus and sepsis. Clean delivery – The hands of the birth attendant should be clean (washed with water and soap) and the delivery surface should be sterile. Clean cord – The cord should be cut with a new blade, stump should be short (length approximately 1.5–2.0 cm) to prevent soiling from urine (Figure 6.7) and nothing should be applied on the cut surface of umbilical cord. The cut surface should be inspected for bleeding within 2–4 hours after birth. The shriveled dry cord normally falls within 5–10 days.

C la m ps

P o in t o f incisio n

6.7 Clamping and cutting umbilical cord [21].

(b) Thermal protection Newborn’s vulnerability to hypothermia – The normal body temperature of the newborn infant is 36.5–37.5°C. Hypothermia occurs when the body temperature drops below 36.5°C. Relatively large surface area, poor thermal insulation, small body mass to produce and conserve heat, little ability to conserve heat by changing posture and no ability to adjust its own clothing in response to thermal stress put a newborn at risk to hypothermia. Hypothermia can easily occur in a cold environment, if newborn is left wet, naked and unprotected from cold while waiting for the placenta to be

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delivered or cord to be cut. Hypothermia can also occur if the newborn is bathed soon after birth. Preventing hypothermia – Ensuring delivery of the baby in a warm room, drying the head, body and face (preferably in that order) thoroughly after birth, wrapping it in layers of clean, dry warm cloth taking care to cover the head and the feet and giving it to the mother as soon as possible are the simplest measures for preventing hypothermia. Early skin-to-skin contact (kangaroo mother care – Box 6.1) for the first few hours after birth is the simplest and most effective way for providing warmth. The newborn should be kept away from draft and should be bathed only after temperature stabilizes, preferably after 24 hours. Box 6.1 Kangaroo mother care [22, 23] Kangaroo care is a method of holding a baby that involves skin-to-skin contact. The baby, who is naked except for a diaper and a piece of cloth covering his or her back (either a receiving blanket or the parent’s clothing), is placed in an upright position against a parent’s bare chest. This snuggling of the infant inside the pouch of their parent’s shirt, much like a kangaroo’s pouch, led to the creation of the term “kangaroo care.

Kangaroo Mother Care was designed to reduce hypothermia by keeping mother and newborn together but it has other benefits too. Kangaroo Care also encourages mother and child to bond emotionally and enables the baby to breastfeed at will, giving the baby the energy to produce its own body heat. The action reduces the need for incubators, which are prohibitively expensive in developing countries. Kangaroo mother Care is a universally available and biologically sound method of care for all newborns, but in particular for premature babies

(c) Early, exclusive breastfeeding and newborn nutrition Intrauterine growth and gestational age are important determinants of nutritional status of a newborn. The transition from fetal to extra fetal life

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poses a serious challenge for a term normal newborn. The goal of neonatal nutrition is to meet the metabolic requirements of developing organ systems, satisfy normal growth requirements and avoid deficiency or excess states without imposing detrimental stress on developing metabolic or excretory systems [24]. Just as the nutritional requirements of an infant are different from those of an adult, the nutritional requirements of the term neonate differ from those of the preterm neonate. Babies born after less than 37 weeks in the womb (preterm) have different nutritional needs than babies born at term (38–42 weeks). Preterm babies because of their short gestational age do not have enough stored up nutrients and they usually need supplements. Most neonates need 100–120 calories per kilogram of weight per day (cal/ kg/d) in order to grow properly. Infants who have health problems may need extra nutrition – up to 160–180 cal/kg/d. Table 6.2 compares daily requirement of selected nutrients in healthy versus preterm neonate. Table 6.2 Daily requirements of selected nutrients in healthy term and preterm infants [25] Normal requirement Nutrient Energy Total (kcal/kg) Carbohydrate (g/kg) Fat (g/kg) Protein (g/kg) Mineral and Trace elements Sodium (mEq/kg) Potassium (mEq/kg) Calcium (mg/kg) Orthophosphate (mg/kg) Magnesium (mg/kg) Iron (mg/kg) Vitamins A (IU/kg) E (IU) (a) (b)

Term(a)

Preterm

100 10 3.3–6.0 1.5–2.2

120 12.0–14.0 4.0–7.0 3.0–4.0

1 to 3 1 to 2 45 to 60 25 to 40 6 to 8 1(b)

2 to 4 2 to 4 120 to 230 60 to 140 7.9 to 15 2 to 4(b)

333 3 to 25

700 to 1500 5 to 25

Based on infants fed human milk. Iron supplementation starts at 2 weeks postnatal age.

(1) Principles of feeding a newborn The neonate’s gastric capacity ranges from 40 to 60 ml during the first 24 hours after delivery. Nutrient needs must be met through frequent, smallvolume feedings. Gastric emptying time – typically 2 to 4 hours – varies with feeding volume and the neonate’s age. As the newborn gains weight, the stomach capacity also increases and so does the daily intake of feeds. The given feed must meet the special nutrient requirements of the neonate with organ systems that are still developing and must not exceed the limited

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concentrations that these same premature organ systems can tolerate [14]. In institutional settings, preterm newborns are kept in the neonatal intensive care unit (NICU), where they are carefully monitored to make sure they are getting the right balance of fluids, minerals such as sodium and potassium (electrolytes), and nutrition until their bodies mature and they are able to suckle breast milk. The NICU is equipped with careful temperature control, often with an incubator or special warmer which helps to reduce excess calorie needs. Humidified (moistened) air helps maintain body temperature and avoid fluid loss. Table 6.3 summarizes the usual principles adopted while feeding newborns with different gestational ages Early exclusive breastfeeding is dealt in another chapter in this book. (2) Benefits of breastfeeding in context of neonatal health ●

●

In the first week of life, breastfeeding can help prevent hypothermia and hypoglycemia in newborns, which are contributory causes of death. Suckling increases body temperature, and the nearness to the mother that breastfeeding provides is beneficial in reducing hypothermia. Delaying first feed leads to starvation which increases the risk of hypoglycemia. Recent research evidence from Ghana (Box 6.2) highlights that neonatal deaths will be reduced by 22%, if all newborns are exclusively breastfed within an hour of their birth. WHO recommends that infants should be put to breast within one hour after birth and should not go without breastfeeding for more than 3 hours between feeds. Studies in Brazil and Philippines have shown that breastfeeding has a greater role in preventing late neonatal deaths (from 8 to 28 days) – deaths that are primarily due to infections such as sepsis, pneumonia, meningitis, umbilical infection, and diarrhea. A study in Brazil has shown that there are substantial benefits of exclusive breastfeeding over partial breastfeeding. The relative risk of death found to be 24.7 for infants not breastfed, and 3.1 for infants partially breastfed, compared to 1 for those exclusively breastfed [27].

(d) Initiation of breathing, resuscitation During the intrauterine life, the fetal lungs are filled with fluid and they do not serve ventilatory purpose since placenta supplies oxygen to the fetus. Most babies have a smooth transition from fetal to neonatal life and establish spontaneous breathing without any active assistance. About 3.5–7.5% of babies are likely to experience difficulty in breathing termed as “birth asphyxia” and need active resuscitation. The operational definition of birth asphyxia is a delay in initiating breathing at birth. If a newborn infant does not cry after initial stimulation by drying, it must be assessed for breathing. If the infant is not breathing or the breathing is poor, it needs active resuscitation.

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Table 6.3 Feeding guidelines for neonates with different gestational ages [26]

Pre-term/Premature <34 weeks Problem

Process and type of nutrition

Can’t feed from a bottle or breast because of immature reflexes and trouble coordinating sucking, breathing, and swallowing. Also they may have accompanying medical problems like breathing problems, very low oxygen levels, gagging, circulatory problems, blood infection, or other illnesses might not be able to feed through a nipple (orally). Very premature babies get nutrition and fluids through a vein (intravenously)—parenteral nutrition. As they get bigger and their systems mature, they can be given breast milk or formula through a small tube inserted through the nose or mouth into the stomach (gavage feeding). Premature babies are fed very slowly to reduce the risk of getting an intestinal infection

Term 34–37 weeks

38–42 weeks

Often can be fed from Exclusive a bottle or the mother's breastfeeding breast. Sometimes it’s easier for a premature baby to drink expressed breast milk from a bottle with a large hole in the nipple than from the breast. Babies who are breastfed may need a supplement called human milk fortifier added to the breast milk. This supplement contains the extra protein, calories, iron, calcium, and vitamins that premature babies need. If it is not possible for the baby to take breast milk, special preterm formulas can be used. Those fed formula may need to take added supplements of certain nutrients, including vitamins A, C, and D and folic acid. These formulas have a higher amount of fat and protein to meet the special growth needs of premature babies. Once babies reach 34–36 weeks gestation, they can be switched to regular formula.

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Box 6.2 The Ghana study [28] Objective – The primary objective was to evaluate the association between the timing of initiation of breastfeeding and neonatal mortality. The secondary objective was to assess whether the different types of breastfeeding (exclusive, predominant, and partial breastfeeding) were associated with substantially different risks of neonatal death. Methodology – The study took advantage of the 4-weekly surveillance system from a large ongoing maternal vitamin A supplementation trial in rural Ghana involving all women of childbearing age and their infants. The analysis was based on 10,947 breastfed singleton infants born between July 2003 and June 2004 who survived to day 2 and whose mothers were visited in the neonatal period. Women were visited once every 4 weeks by a network of trained village-based fieldworkers to distribute vitamin A capsules and collect data on morbidity and mortality. When a birth was reported, the fieldworker administered a “birth” questionnaire, which included details on delivery and newborn care practices including early breastfeeding practices. The mother was asked when she initiated breastfeeding and was prompted for the exact timing (within 1 hour, after 1 hour but first day, day 2, day 3, day 4– 7, or after day 7). She was then asked what she offered her child to eat or drink in the 24 hours before the interview. After noting the unprompted response, the mother was asked if she offered her own breast milk, breast milk from a wet nurse, animal milk, infant formula, milk-based fluids, water-based fluids, or solid foods. The mother was also asked about the infant’s health on the day of birth and in the previous 24 hours. At the next 4-week visit, an “infant” questionnaire was administered to obtain additional outcome data (infant morbidity and mortality) and information about infant feeding practices. Infants were followed up at subsequent visits every 4 weeks until they reached 12 months of age. Results – Breastfeeding was initiated within the first day of birth in 71% of the infants and by the end of day 3 in all but 1.3% of them; 70% of the infants were exclusively breastfed during the neonatal period. The risk of neonatal death was fourfold higher in children given milk-based fluids or solids in addition to breast milk. Late initiation (after day 1) was associated with a 2.4-fold increase in risk. The study concluded that 16 % of neonatal deaths could be saved if all infants were breastfed from day 1 and 22% if breastfeeding started within the first hour. The risk of neonatal death increased approximately fourfold if milk-based fluids or solids were provided.

Birth asphyxia should be recognized promptly and management should follow the basic principles of resuscitation: open airway (aspiration of mouth and nostrils), initiating breathing (by tactile stimulation and or end ventilation with positive pressure) and maintaining circulation through external cardiac massage. As asphyxia management entails involvement of a trained person, it should be preferably done in institutional setting. Asphyxia should ideally be managed in institutional settings. If done at home, presence of a trained attendant is important. (e) Immunization At birth BCG, OPV-0 and Hepatitis B vaccines are recommended by WHO as a part of overall immunization. BCG should be given as soon after birth as possible in all populations at high risk of tuberculosis infection. A single dose of OPV at birth or in the two weeks after birth is recommended to increase early protection.

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6.8 Resuscitating a newborn using bag and mask ventilation.

Where perinatal infections of Hepatitis B are common it is important to administer the first dose as soon as possible after birth. (f) Management of newborn illness Danger signs in the newborn period are non-specific and can be a manifestation of almost any newborn disease. The most common initial presentation of illness in an infant who has been doing well after birth is that it stops feeding well, is irritable and is cold to the touch. The initial signs may advance to fast and difficult breathing sometimes accompanied with grunting and intercostal retractions; the infant become lethargic, hypotonic and may or may not wake for feeds. Alternatively, the newborn may vomit; have diarrhoea and a distended abdomen. Pus draining from red swollen eyes or from the umbilicus is a sure indication of underlying infection. Jaundice on the first day and convulsions are always a sign of a serious illness. The danger signs of newborn illnesses need to be recognized early by family members and grass-root health functionaries for speedy referral. The underlying pathological condition needs management by a clinical specialist. (g) Care of the preterm and/or low birth weight newborn The World Health Organization (WHO), on the basis of world wide data, recommends that newborns with birth weight (b wt) less than 2500 g may be considered to fall in the low birth weight (LBW) category. Globally, more than 20 million infants are born with low birth weight (Table 6.4). The number of low birth weight babies is concentrated in two

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Table 6.4 Percentage of LBW by UN regions [30] World Africa Asia Europe Latin America and Caribbean North America Oceania

15.5 14.3 18.3 6.4 10 7.7 10.5

regions of the developing world: Asia and Africa. Seventy-two per cent of low birth weight infants in developing countries are born in Asia where most births also take place and 22 per cent are born in Africa. India with 30% LBW alone accounts for 40 per cent of low birth weight births in the developing world and more than half of those in Asia. It is estimated there are more than 8 million newborns born every year in India with LBW [29]. LBW is governed by two major processes: a short gestational period, i.e. the infant is born too soon and is qualified as premature (birth weight <2500 g and gestational age <37 weeks), or a retarded intrauterine growth rate (IUGR), i.e. the infant is small for gestational age (birth weight <2500 g and gestation age >37 weeks) [31]. In the developed countries, the overwhelming majority of LBW infants are pre-terms, whereas in the developing nations, including South Asia, majority of LBW are IUGR [32]. Two-third LBW neonates born in India fall in IUGR category [31]. IUGR is caused predominately by maternal malnutrition, either before conception or during pregnancy [33]. Three factors have maximum impact: poor maternal nutritional status before conception, short stature (due mostly to undernutrition and infections during childhood or onset of pregnancy during adolescence which interferes with the normal growth velocity), and poor nutrition during pregnancy. LBW especially IUGR babies, carry relatively greater risks of perinatal and neonatal morbidity and mortality, and substandard growth and development in later life [33, 34]. Additionally, there is now increasing evidence (Box 6.3 Barker’s hypothesis) that LBW is associated with an increased prevalence of diseases such as diabetes, hypertension, ischaemic heart disease and stroke in adult life. The latter is often known as fetal origin of adult disease. Reduced weight, poor immunity and a poor insulation because of lack of fat as the source of energy makes low birth weight babies susceptible to the risk of frequent infection, hypothermia and poor growth, impact of which is maximum during the neonatal period. Given below are few elements of care which should essentially be provided to all LBW newborns: Prevention of hypothermia – Skin-to-skin contact, adequately clothing the baby, provision of additional heat and regularly recording the temperature will help prevent hypothermia.

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Box 6.3 Barker’s hypothesis [35] Barker’s Hypothesis is named after David J. P. Barker a researcher at the University of Southampton who published the theory in 1997 (Ref). The theory states that reduced fetal growth is strongly associated with a number of chronic conditions later in life. This increased susceptibility results from adaptations made by the fetus in an environment limited in its supply of nutrients. These chronic conditions include coronary heart disease, stroke, diabetes, and hypertension. Barker hypothesis explains that malnutrition in utero has a far-reaching impact on the future health of the newborn. The undernourished fetus (mainly IUGR) adapts to its nutrition deficient environment by undergoing changes in the body’s structure, metabolism, hormonal sensitivity and physiology to ensure its continual survival and growth, but in the process compromising development of certain organs or processes. IUGR infants, having failed to attain full growth potential are at greater risks of suffering from the consequences of chronic diseases. Barker’s hypothesis asserts the need of a public health strategy which targets women in different point of their life cycle-starting before birth, infancy, adolescence, to adulthood, i.e. a preventive strategy having focus on continuum of care.

Traditional practice of giving both soon after birth needs to be avoided to prevent hypothermia. Provision of early and exclusive breastfeeding – In a low birth weight baby nutrient stores at birth are low, feeding, digestion and absorption systems are immature and there are high requirements for rapid growth. Concomitant illnesses may interfere with growth potential ,add to organ dysfunction and further increase the demand for energy and nutrients [24]. The window of tolerance of nutrient intake is extremely narrow for these infants. LBW babies must be frequently fed (preferably 2 hours or more frequently) because initially most of them suck briefly and consume small quantities of milk with each feed. Some LBW babies suck poorly during the first few days even though they are active. Expressed milk stored in a clean vessel and fed with a spoon could be practiced where acceptable. Early initiation of breastfeeding helps in averting hypoglycemia. It is important that bottle feeding is completely avoided as it increases the risk of infection. Prevention of infection – Because of low immunity, LBW are especially vulnerable to infection. Adoption of clean hygienic feeding practices, restriction of entry of family members suffering from infection like seasonal cold, avoiding pre lacteal feeds and water and wrapping the baby in a clean cloth are some of the precautions that need to be taken.

6.7

Delivering essential newborn care (ENBC) interventions through public health systems – opportunities and challenges

Despite the public health significance, few programs target neonatal health in developing countries. Interventions to reduce neonatal deaths have been traditionally covered by two health system programmes namely maternal health

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as well as child health. Maternal health programmes focus on pregnancy, childbirth and immediate care of the newborn while the child health programmes concentrates on late neonatal period, infancy and childhood. Much too often neonatal care “falls between the cracks” in maternal and child health programmes [7]. Though Essential Newborn Care (ENBC) has been acknowledged and incorporated in most of the maternal child health programmes across the countries but lack of integration and implementation bottlenecks have resulted in very little impact. Additionally, countries have continued to spend millions on provision of institution based care for maternal and newborn complications with little efforts and funds directed at providing services along the continuum, i.e. from household, community to health facility. This has created two parallel levels of care – a community governed family based care and an institution based clinical care. Both the levels work independently with little synergy between the two. The picture is especially true for low resource settings countries like India where almost 80% of deliveries are conducted at home with assistance from unskilled family members or community approved person. The services received by a newborn delivered at home are often those that are approved by community and practiced by majority. The “essentials” of newborn care like drying and wrapping the baby, immediate initiation of breastfeeding and resuscitation are severely compromised in home settings. An understanding of community practices throughout the continuum of care, i.e. from maternal through neonate and from home to outreach to facility (care seeking behaviour—recognition, labeling and seeking treatment for an illness) is critical for success of ENBC. Factors contributing to poor care seeking like poverty, illiteracy, poor maternal health, traditional barriers, harmful traditional practices and inadequate health care facilities and transport need to be studied and taken into consideration before introducing interventions which do not conform to their traditional beliefs and customs. In recent years, renewed global interest and generation of large body of evidence regarding neonatal health has seen a revival and the belief is taking ground that neonatal mortality is, in fact, amenable to simple effective public health initiatives including community-based interventions [8]. The importance of community involvement and participation in impacting neonatal health has also been demonstrated through successful community trials such as (Shivgarh study and Warmi project [35, 36]). These projects have provided the needed evidence that family/Community engagement can avoid many deaths by ensuring that families are equipped with appropriate healthcare messages on danger signs and care-seeking. Boxes 6.4 and 6.5 give a brief account of successful projects undertaken with support of people residing within the community.

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Box 6.4 The Warmi project [36] Background – The Warmi, conducted from July 1990 to June 1993, attempted to improve maternal and child health through involving communities in health care. An intervention to improve maternal and child health was conducted in a remote Bolivian province of Inquivisi with limited access to modern medical facilities. Methodology – Fifty communities in Inquivisi Province participated in the Warmi project. The total population in the demonstration area is 15 000. There were a variety of types of women’s groups in the Inquivisi area, including women’s organizations, cooperatives, mothers’ clubs, and agrarian unions. The groups’ functions varied together with their degrees of effectiveness. The project staff considered women’s organizations best able to organize women around health issues. Consequently, the staff focused on these groups, initiating or strengthening 50 women’s organizations. Study personnel included five to six teams, each consisting of two auxiliary nurses Monthly or more frequently, each team met individually with all women’s organizations, At these meetings, attended by approximately 10–30 group members, a technique called “autodiagnosis” was employed to address community problems. Autodiagnosis consists of the following four steps: (a) identification and prioritization of problems, (b) group development of a formal action plan, (c) implementation of the plan, and (d) evaluation. Each community identified a different set of problems and approaches, and accordingly, specific interventions varied by community. However, certain objectives were addressed by all the women’s groups: to (a) increase knowledge of reproduction, contraceptive use, danger signs of complications, and self-care, (b) improve immediate newborn care, and (c) increase the percentage of women who receive delivery care from trained birth attendants. Intervention – The intervention focused on initiating and strengthening women’s organizations, developing women’s skills in problem identification and prioritization, and training community members in safe birthing techniques. Results – The impact was evaluated by comparing perinatal mortality rates and obstetric behavior among 409 women before and after the intervention. Perinatal mortality decreased from 117 deaths per 1 000 births before the intervention to 43.8 deaths per 1 000 births after. There was a significant increase in the number of women participating in women’s organizations following the intervention, as well as in the number of organizations. The proportion of women receiving prenatal care and initiating breast-feeding on the first day after birth was also significantly larger. The number of infants attended to immediately after delivery likewise increased, but the change was not statistically significant. One of the greatest changes observed in this study was a doubling of participation in women’s organizations.

6.8

Addressing neonatal health in India – initiatives by Government of India

Over a period of three decades, a review of strategy and approach of maternal and child health programmes initiated by Government of India (GoI) shows that the maternal and child health programmes in India have retained their focus on provision of antenatal care and prevention of post neonatal deaths through diarrhea, pneumonia and immunization programmes (Box 6.6).

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Box 6.5 Shivgarh trial [37] Background – In rural India, most births take place in the home, where high-risk care practices are common. In Shivgarh trial the intervention developed was behavior change management, with a focus on prevention of hypothermia, aimed at modifying practices and reducing neonatal mortality. Methods – Cluster-randomised controlled efficacy trial in Shivgarh, a rural area in Uttar Pradesh. Thirty-nine village-administrative units (population 104, 123) were allocated to one of three groups: a control group, which received the usual services of governmental and non-governmental organizations in the area; an intervention group, which received a preventive package of interventions for essential newborn care (birth preparedness, clean delivery and cord care, thermal care (including skinto-skin care), breastfeeding promotion, and danger sign recognition) and another intervention group, which received the package of essential newborn care plus use of a liquid crystal hypothermia indicator (ThermoSpot). In the intervention clusters, community health workers delivered the packages via collective meetings and two antenatal and two postnatal household visitations. Outcome measures included changes in newborn-care practices and neonatal mortality rate compared with the control group. Results – Improvements in birth preparedness, hygienic delivery, thermal care (including skin-to-skin care), umbilical cord care, skin care, and breastfeeding were seen in intervention arms. There was little change in care-seeking. Compared with controls, neonatal mortality rate was reduced by 54% in the essential newborn-care intervention and by 52% in the essential newborn care plus Thermo Spot arm. Interpretation – A socio-culturally contextualized, community-based intervention, targeted at high-risk newborn-care practices, can lead to substantial behavioural modification and reduction in neonatal mortality. This approach can be applied to behaviour change along the continuum of care, harmonise vertical interventions and build community capacity for sustained development.

Box 6.6 – Child health programmes in India 1977 1978 1985 1990 1992 1997 2002 2005

– – – – – – – –

Family Planning changed to Family Welfare Programme Diarrhoeal Disease Control programme launched Universal Immunization programme (UIP) launched Acute Respiratory Infection Control Programme Child Survival and Safe Mother (CSSM) Programme launched Reproductive and Child Health (RCH) Programme – Phase I/RCH I Reproductive and Child Health Programme (Phase II) National Rural Health Mission (NRHM)

It is interesting to note that though reduction of neonatal mortality rate was one of the objectives of National health policy drafted in 1983, and essential newborn care was included as one of the components in Child Survival and Safe Motherhood Programmes (CSSM) launched in 1992, apart from neonatal tetanus immunization of pregnant mother, other activities failed to achieve any success in improving neonatal health due in part to lack of reliable information on the magnitude and causes of neonatal deaths. Being one of the signatory countries to United Nations Millennium Development Goals (MDGs), India has lately initiated several measures toward improving the neonatal health scenario in the country towards

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achieving MDG 4 and MDG 5. In addition to giving renewed thrust to ENBC through ongoing RCH II programme (being implemented under the umbrella of National Rural Health Mission) across the entire country, Government of India has also launched “Integrated Management of Childhood Illnesses (IMCI)” strategy in selected districts of the country, added “newborn” to it and renamed it as “Integrated Management of Neonatal and Childhood Illnesses” or IMNCI which is a key strategy within the RCH-II programme. Additionally, several governmental and non-governmental agencies, both national and international, have joined hands to support a nationwide Neonatal Health Research Initiative (NHRI) [8]. This has been under the auspices of the India Clinical Epidemiology Network (IndiaCLEN) with the active support of National Neonatology Forum, Ministry of HealthGovernment of India, Saving Newborn Lives, Johns Hopkins University and USAID. Under NHRI several multi-centric studies for identifying simple and better ways for promoting newborn health in community settings are being undertaken in various centers representing the entire country.

6.9

Integrated Management of Childhood Illnesses (IMCI) – the global strategy

IMCI is an integrated approach to child health that focuses on the wellbeing of the whole child. IMCI includes both preventive and curative elements that are implemented by families and communities as well as by health facilities. The success of IMCI in reducing childhood mortality depends on improvements of overall health systems as well as improvement of family and community health care practices [38]. Developed in mid-nineties by WHO and UNICEF, the global IMCI strategy focused primarily on the most common causes of child mortality like – diarrhea, pneumonia, measles, malaria and malnutrition, illnesses affecting children aged 1 week to 2 months and 2 months to 5 years, including both preventive and curative elements to be implemented by families and communities as well as by health facilities [39]. It promotes all the essential new born components except safe delivery. IMCI acknowledges contribution of malnutrition to child morbidity and mortality and includes nutrition assessment and counseling for all sick infants and children. The health workers are trained to follow an algorithmic systematic approach health to assess a sick child and address several medical conditions that often co-exist rather than only the main presenting symptom [39]. IMCI helps workers broaden their approach to consider and respond to the child and manage the different factors that could be

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contributing to child’s sickness [40]. For instance, all children, during an IMCI consultation are screened for malnutrition and assessed for immunization status, and given age appropriate feeding advice and immunization services.

6.10

Integrated Management of Neonatal Care and Childhood Illnesses (IMNCI)

The Indian adaptation gives thrust to neonatal component, the most critical period affecting infant and child mortality. A community-component for routine care of all newborn children has been added to the initiative. Box 6.6 gives information on such changes made in the IMNCI strategy in Indian adaptation. Box 6.7 Differences between generic IMCI and Indian IMNCI [41]

1 2 3 4 5

6 7 8 9

Features

Generic IMCI

India’s IMNCI

Scope Includes birth to 7 d of life (early newborn period) Target providers Facility-based providers such as physicians Community-based providers (auxiliary nurse midwives/ Anganwadi workers) Training program Training time – newborn and young infant Sequence of training

No

Yes

Yes

Yes

No

Yes

~20% (2 of 11 days)

50% (4 of 8 days)

First, the child (2 months to 5 years) module, followed by young infant (7 days to 2 months) No

First, the newborn and young infant (0–2 months) module; then the child (2 months to 5 years) Yes

yes

Yes

No

Yes

No

Yes

Training for home visits for postnatal care of newborn Implementation – facility-based application Community-based application (3 home contacts within first 10 days) Implement only young infant or older child package

The incorporation of home visits in India’s adaptation of IMNCI is an effort to ensure continuum of care from home to outreach to facility. Trained front-line workers extend quality inputs of the health system to household; helping to prevent illness and ensuring timely referral to a health facility

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for severe cases. During home visits, all newborns are assessed, any problems are identified and referred if necessary. In addition, and mother are taught ways to prevent illnesses and counseling to practice exclusive breastfeeding, keeping baby warm, and other essential newborn care. During these visits, mothers are also taught to keys signs of illnesses – when and where to seek timely care. Outreach health workers (the auxiliary nurse-midwives and ASHAs) and community nutrition and child development workers (grass-root workers or anganwadi workers of Integrated Child Development Services or ICDS) are mandated to visit all neonates at home three times (within 24 hours, 3–4 days and 7–10 days) within the first 10 days, starting soon after birth, to provide home-based preventive care/health promotion and to detect neonates with sickness requiring referral. For ensuring appropriate growth and feeding of low birth weight babies, nutritional counseling through extra contacts are also proposed in IMNCI on day 14, day 21 and day 28. These visits will also be used to provide post-partum care to the mother [42]. The specific newborn components that have been added to IMNCI include early and exclusive breastfeeding, warmth, care-seeking for severe illness, LBW care and treatment of umbilical sepsis.

6.11

Conclusion

Translating knowledge on effective interventions into a successful public health programme which integrates the continuum of care is a daunting task for countries struggling to achieve MDGs. The challenge becomes more in context of developing countries where incidence of low birth weight is high, service delivery structures are poor and utilization of health services is determined by care-seeking behavior of families and communities. In case of newborns, care seeking is more an outcome of prevalent and accepted cultural practices and traditions. Changing behaviours or developing a health care system responsive to newborns requires an understanding and appreciation of community practices, health education, dedicated health professionals, proper channeling of human and financial resources as well as political will, all of which continue to remain a challenge in developing countries. Identifying simple, acceptable and practiced by communities, require little modification should be introduced and promoted first These selected interventions should be such that these can be delivered by the primary care system and the community health care provider. The acceptability of other complex interventions will increase when communities start perceiving benefits of these simple interventions thereby contributing to reduced neonatal mortality rates in developing countries.

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23. Essential Newborn nursing for small hospitals. In resource restricted countries, Learner’s guide. Department of Paediatrics, WHO collaborating Centre for training and Research in Newborn Care. All India Institute of Medical Sciences, New Delhi. 24. WINN HN and HOBBINS JC (2000). Clinical Maternal-Fetal Medicine. Parthenon Publishing, p. 877. 25. PREMER DM and GEORGIEFF MK (1990). Nutrition for Ill Neonates. Pediatrics in Review vol. 20, pp. e56–e62. 26. GREENE A (2007). Neonatal weight gain and nutrition. Medline Plus: A service of U.S. National Library of Medicine and the National Institutes of Health: Adam. 27. Reducing perinatal and neonatal mortality. Child Health Research Project. Report of a Meeting Baltimore, Maryland May 10–12, 1999, vol. 3, no. 1. 28. EDMOND KM , et al. (2006). Delayed breastfeeding initiation increases risk of neonatal mortality. Pediatrics vol. 117, no. 3. 29. Saving newborn lives and national neonatology forum; State of India’s Newborn. 30. UNICEF and WHO, Low birth weight: Country Regional and Global Estimates. 2004. 31. NORTON R . Maternal nutrition during pregnancy as it affects infant growth, development and health. [Available from: http://www.unsystem.org/scn/archives/ scnnews11/ch06]. 32. SACHDEV HPS (2001). Low birth weight in South Asia. Int I of Diab Dev Countries vol. 21, pp. 13–31. 33. GALLOWAY R. Pre-pregnancy nutritional status and its impact on birth weight. [Available from: http://www.unsystem.org/scn/archives/scnnews11/ch06]. 34. TOMKINS A, MURRAY S ,RONDO P , FILTEAU S ; Impact of Maternal Infection on Foetal Growth and Nutrition. [cited; Available from: http://www.unsystem.org/scn/ archives/scnnews11/ch08 35. BARKER DJP (1997). Maternal nutrition, fetal nutrition, and disease in later life. Nutrition vol. 13, p. 807. 36. O’ROURKE K, HOWARD- GRABMAN L and SEOANE G (1998). Impact of community organization of women on perinatal outcomes in rural Bolivia. Pan Am J Public Health vol. 3, no. 1, pp. 9–14. 37. KUMAR V, MOHANTY S , KUMAR A et al (2008). Effect of community-based behaviour change management on neonatal mortality in Shivgarh, Uttar Pradesh, India: a cluster-randomised controlled trial. The Lancet vol. 372, pp. 1151–1162. 38. Funding Research Activities [Publications]. Available from: Funding Research, Child Health and Nutrition Research Initiatives. 39. THACKER N (2007). Integrated management of neonatal and childhood illnesses: a new hope for child survival. Indian Pediatrics vol. 44, pp. 169–171. 40. INGLE GK and MALHOTRA C (2007). Integrated management of neonatal and childhood illness: an overview. Indian J of Comm Medicine vol. 32, no. 2, pp. 108–110. 41. BHANDARI N, MAZUMDAR S and DUBE B . Evaluation of the Impact of Integrated Management of Neonatal and Childhood Illness (IMNCI) Strategy on Neonatal and Infant Mortality in Haryana, India, Society for Applied Studies, New Delhi. 42. MARTINES J, PAUL VK, BHUTTA ZA, KOBLINSKY M, SOUCAT A, WALKER N, BAHL R, FOGSTAD H , COSTELLO A , for the Lancet Neonatal Survival Steering Team (2005); Neonatal Survival 4 Neonatal survival: a call for action; Lancet vol. 365 pp. 43–51.

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Integrating breastfeeding in public health programming – scientific facts, current status and future directions Kajali Paintal

Kajali Paintal, MSc, PhD, is a Nutrition Specialist (Infant and Young Child Nutrition) at UNICEF, New Delhi. Formely, she was a nutritionist at PATH India working for the Ultra Rice and Sure Start programmes. She was rewarded Senior Research Fellowship by the Indian Council of Medical Research (ICMR) for research projects on pediatric health and nutrition. Dr. Paintal has research and field experience in the area of breastfeeding and reproductive child health issues and has worked on short-/long-term projects with CARE (Delhi), Indian Social Science Institute (Delhi) and Breast Feeding Promotion Network of India (BPNI).

7.1

Introduction

The future potential of human societies largely depends on children’s optimal physical growth and psycho-social development. For a decent start in life, meeting the nutritional needs of infants and providing adequate care in the early years is fundamental for physical, motor, cognitive, social and emotional development. At this critical stage of life, a neonate is extremely vulnerable and primarily dependant on the mother for nourishment that is provided through breastfeeding [1]. Optimal nourishment at this stage of life has not only short-term effect on growth, body composition/functions, but also long-term effect on morbidity and mortality risks in adulthood. If not managed in time, malnutrition disturbs the foundation of life, growth and development and its ill effects become virtually irreversible after 2 years of age. “Malnutrition has been responsible, directly or indirectly, for 35% of the 8.7 million deaths that occur annually among under-5 children; over two-thirds of these deaths are often associated with inappropriate feeding practices in first year of life” [2, 3].

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Box 7.1 WHO/UNICEF definitions of breastfeeding practices ● ●

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●

Early initiation of breastfeeding – Proportion of children born in the last 24 months who were put to the breast within one hour of birth. Exclusive breastfeeding under 6 months – Proportion of infants (0 to <6 months) fed with only breast milk (including milk expressed or from a wet nurse) including ORS, drops, syrup (vitamins, minerals, medicines) in the previous 24 hours. Predominant breastfeeding – Proportion of infants predominantly fed with breast milk (including milk expressed or from a wet nurse) as the main source of nourishment in the previous 24 hours. Breastfeeding – Proportion of infants being fed with breast milk (including milk expressed or from a wet nurse) in the previous 24 hours [4].

In developing countries, breastfeeding is a cultural norm and most children are breast-fed during the first year of life; yet the irony is that malnutrition owing to faulty feeding practices is associated with 35% of the young child deaths. The Lancet 2008 series indicate that sub-optimal breastfeeding increases the risk of poor nutrient intake, illness and malnutrition due to poor feeding practices. It is estimated that sub-optimum breastfeeding, especially non-exclusive breastfeeding in the first six months of life is responsible for 1.4 million child deaths and 44 million global childhood DALYs1 (10% of the disease burden in children younger than 5 years) [5]. In India, alone 2.4 million child deaths occur annually; two thirds of which are attributed to inappropriate infant feeding practices. The Lancet 2003 series on child survival identified breastfeeding interventions to have the potential to prevent 13% of all under-5 deaths in developing areas of the world, ranking it as the most important preventive approach for saving child lives, more than any other preventive intervention. Presently in Asia, only about one third of babies (<6 months) are exclusively breast fed; in order to achieve a reasonable reduction in the prevalence of child morbidity, malnutrition and mortality, ideally the exclusive breastfeeding rates should be 90–100% [6]. Lancet 2008 estimates that a universal coverage in breastfeeding promotion and support can reduce infant mortality by nearly 12% and that the benefits from exclusive breastfeeding would be much more [7]. Standing Committee on Nutrition of the United Nations Working Group on Breastfeeding and Complementary Feeding (2003), in its endeavour to reach the Millennium Development Goals (MDGs) has stated that governments should keep in mind that “Inappropriate feeding practices and their consequences are major obstacles to sustainable socio-economic development and poverty reduction. Governments will be unsuccessful in their efforts to accelerate significant long term economic development until optimal child growth and development, especially through appropriate feeding practices are ensured” [8, 9]. 1 DALYs i.e., Disability Adjusted Life Years is a measure of overall disease burden.

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Optimal infant and young child feeding practices rank among the most effective interventions to improve child health. It has been estimated that optimal breastfeeding of children under two years of age has the potential to prevent 1.4 million deaths in children under five in the developing world annually [5]. In developing countries, less than 40% of the 136 million babies born each year benefit from early initiation of breastfeeding and similarly, 37% are exclusively breastfed in the first six months of life. Early cessation of breastfeeding in favour of commercial breast milk substitutes, giving water and other liquids along with breast milk, needless supplementation and poorly timed introduction of solid, semi-solid and soft foods, often of poor quality, are far too common. Professional and commercial influences combine to discourage breastfeeding, as do continued gaps in maternity legislation. To improve this situation, mothers and families need support to initiate and sustain appropriate infant and young child feeding practices. Overall, increasing the rates of early initiation of breastfeeding and of exclusive breastfeeding is critical in improving young child survival and development [5, 6]. Child health in general, and infant and young child feeding more specifically is often not well addressed in the basic training of doctors, nurses and other allied health professionals. Because of lack of adequate knowledge and skills, health professionals are often barriers to improved feeding practices. For example, they may not know how to assist a mother to initiate and sustain exclusive breastfeeding; they may recommend tooearly introduction of supplements when there are feeding problems, and they may overtly or covertly promote breast-milk substitutes. Other sociocultural constraints to improving infant feeding practices include lack of counseling and support in the community; poor awareness of populations on benefits of breastfeeding, early initiation and exclusive breastfeeding; absence of effective and ongoing communication strategies; lack of workplace support; lack of effective legislation on marketing of breastmilk substitutes; poor empowerment of women; exposure to domestic violence, financial independence; autonomy in decision-making, etc. Health care professionals can play a critical role in providing that support, through influencing decisions about feeding practices among mothers and families. Therefore, it is critical for health professionals to have basic knowledge and skills to give appropriate advice. This scientific knowledge needs to be integrated into health and nutrition programmes to enable health professionals and service providers to counsel and help solve feeding difficulties, and know when and where to refer a mother who experiences more complex feeding problems [10].

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7.2

Breastfeeding – the science for integrating scientific facts into programming

The high mortality and disease burden resulting from nutrition related factors make a compelling case for the urgent implementation of proven interventions. Breastfeeding promotion has been identified to be one of the most effective interventions for reducing child deaths and future disease burden. Countries should focus resources on proven interventions and scale them up as quickly as possible [5, 11, 12].

7.2.1

Breastfeeding – foundation of infant care

Breastfeeding is much more than providing food to a baby; it is the foundation of infant care that goes a long way in protecting against the early onset of malnutrition. Caring for women and children for survival, growth and development has gained significant importance only in the last one to two decades. Breastfeeding is one of the most important caring activities that has a positive influence on the infant’s nutritional status and also increases chances of survival even under extreme conditions of poverty and food insecurity. Box 7.2 highlights how breastfeeding can support the baby in the transition from fetal life to the external environment. Inadequate care has been identified as one of the underlying causes of malnutrition amongst children. In addition, a mother’s health status, quality of care provided is closely interlinked to the baby’s health, growth and survival. A caregiver plays a critical role in providing the physical and emotional environment in which the infant can balance and regulate both internal and external stimuli as well as achieve their full growth potential [13]. Box 7.2 Breastfeeding supports the transition from fetal life to the external environment Before birth, the foetus in a sterile, protected, moist and warm environment of the womb and gets all necessary nutrients/ oxygen for its metabolic, digestive and sensory functions through the umbilical cord. After birth, the placental-uterine metabolic inter-relationship between the mother and her infant continues through breastfeeding. Mother’s milk is a part of the naturally ordained system uniquely adapted to meet the metabolic requirements of the new-born. It is intended to help the infant adapt to the sudden change(s) from fully dependant and secure intrauterine existence to an independent way of life in hostile extero-gestate environment. Breast milk provides the necessary nutrients and protective factors to the neonate to facilitate this transition [14, 15].

7.2.2

Benefits of breastfeeding

Breastfeeding protects the infant not only from disastrous consequences of malnutrition but also from degenerative diseases later in life. It has been

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well documented that breast milk is thus a natural resource of tremendous value, with medical and nutritional benefits. In addition to individual benefits, breastfeeding provides significant social and economic benefits to the family and nation. At the family level, breastfeeding results in reduced health care costs and abated absenteeism for care attributable to child’s illness. The significantly lower incidence of illness in the breast fed infants allows parents more time for attention to siblings and other family responsibilities. Thus, it provides direct economic benefits to the family by reducing work absenteeism and loss in earnings. The economic benefits of breastfeeding is evident from the fact that the estimated cost of purchasing breastmilk substitutes is double than the cost of increased maternal food intake [16]. Successful lactation is a complex interaction between the mother and her new born which is not entirely instinctive but is based on learned behaviour that helps to build a close psychological relationship between the mother-infant dyad during early months of life. Optimum quantity and quality of breast milk coupled with adequate care helps in the healthy growth and psycho-social development of a child.

7.2.3

Lactation process: anatomy and physiology

Estro us cyc le s

Pre gn anc y

Fe tal D e velopm e nt

P artuition

C o nce ption

Lactation cycle begins with growth of the breast (mammogenesis), initiation of milk synthesis and secretion (lactogenesis 1 and lactogenesis 2), established lactation (galactopoiesis), regression of the breast during and after weaning (involution) [17]. Figure 7.1 presents different stages in the lactation cycle starting from Mammogenesis (getting ready for lactation) to lactogenesis (initiation and establishment of lactation) to galactopoiesis (maintenance of lactation).

Lac tation

N e on ata l D ev elop m en t

M am m og ene sis

G alacto poie s is Lac toge ne sis

7.1 Lactational cycle.

(i) Mammogenesis is a stage when the mammary gland develops its histological and bio-chemical capacity to synthesize milk. This stage is characterized by increase in number and size of the alveoli, where milk is secreted and stored [18, 19].

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(ii) Lactogenesis is a stage where the body secretes and produces milk for the baby. In humans, lactogenesis (referred to as the time when milk ‘comes in’) starts about 40 hours before the infant’s birth and is largely complete within five days. During this stage, a profound and rapid series of changes in the activity of differentiated mamary epithelial cells from a quiescent state to a fully active secretory state occurs. Lactogenesis has 2 stages: the first stage, lactogenesis 1 occurs by mid pregnancy, when the mammary gland becomes competent to secrete milk. The secretion of milk, however, is held in check by high circulating levels of progesterone and estrogen [18]. The second stage, lactogenesis 2 occurs around the time of delivery and is defined as the onset of copious milk secretion. The hormonal changes during parturition and the subsequent removal of the placenta act as a lactogenic trigger which is necessary for initiation of milk secretion [20]. For the ongoing synthesis and secretion of human milk, continuous hormonal signals received by the mammary gland (due to stimulation of nipple and areola), relayed to the central nervous system are essential to induce milk secretion [21]. Milk is secreted more or less continuously into alveolar lumens and stored until the let-down reflex induces milk ejection where it exits through ducts into small sinuses near the areola and then opens directly on the nipple [22]. Hence, an infant’s mouth placement during breastfeeding is important so that these sinuses are not blocked and ensure free milk secretion. Breastfeeding initiation is a commonly used term which is used when a neonate is put to the breast. When the infant starts suckling at the breast, it causes the stimulation of touch receptors that are densely located around the nipple and areola (Box 7.3). Tactile sensations (created by infant’s suckling) create impulses that ascend the spinal cord, creating a neuronal pathway between the hypothalamus and pituitary gland which release oxytocin resulting in the expulsion of stored milk from alveoli into the sinuses through the nipple pore. Once milk secretion has started, suckling by the neonate influences subsequent functioning of the mammary that is jointly controlled by the nervous/endocrine systems through the release of appropriate hormones as well as transfer of nerve impulses [23]. Box 7.3 Suckling reflex Immediately after birth, the sucking reflex is strongest and babies are more active and alert during the first 30-60 minutes. If a baby is put to the mother’s breast within this period, exclusive breastfeeding and establishment of optimal breastfeeding is more likely. Early initiation of breastfeeding also ensures the intake of colostrum which is considered to be the first immunization for the baby. Findings from the Ghana study also demonstrated ensuring initiation of breastfeeding within 1 hour could reduce 22% of all neonatal mortality [24].

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Milk ‘coming in’, which is sensed by mothers as a sudden heaviness of their breasts with milk, is an event that occurs 2–3 days after delivery [25]. The physiological significance of this sensation of ‘milk coming in’ can perhaps be explained by the transition from an endocrine promoted lactogenesis to established lactation. Over the first few days post-partum, the maternal plasma levels of progesterone and estrogen fall by 3–5 times, while oxytocin and prolactin increase; these hormonal changes release the mammary cells from the inhibition. However, milk ejection reflex is also sensitive to minor emotional and psychological disturbances which may influence breast milk availability to the baby [26, 27]. Box 7.4 Prelacteal feeding and its harmful effects Honey is one of the most commonly used prelacteals in South Asia. Honey is primarily given because it is believed to be a laxative to help clean the meconium or as means to “bless and welcome the baby at birth”. However, modern science has found that honey is a known source of the heat resistant organism Clostridium botulinum, which can lead to infant botulism. With ingestion of honey, colonization may occur in the gut, especially in babies under six months as (i) they have immature immune systems, (ii) gut lacks the clostridium inhibiting bile acids and (iii) their gut flora has not been sufficiently well established to prevent colonization. Once colonized the bacterial spores release a fatal neurotoxin resulting in severe constipation (=3 days). Over the next few weeks, infants with botulism get lethargic, are afebrile, have a weak cry, droopy eyelids, listlessness, diminished appetite or activity, have either absent or diminished spontaneous movements, decreased suckling, floppy head and decreased motor response to stimuli. If untreated, these symptoms may progress to cause paralysis of the arms, legs, trunk and respiratory muscles. Botulism can even result in death due to respiratory failure. The symptoms of botulism appear around 8 to 36 hours after consuming the honey or other contaminated food. Further, antibiotic treatment is not recommended as killing the bacteria may increase the amount of toxin released into the body. Hence, the best recommendation is to avoid feeding honey to infants less than 1 year of age. Microbiologic surveys of honey products in USA have reported the presence of clostridial spores in up to 25% of honey products. However, no published information is available from India [28, 29].

Prelacteal feeding is a harmful practice that adversely effects on the establishment of breastfeeding, increases susceptibility to infections and increase the likelihood of early termination of exclusive breastfeeding (Box 7.4). (iii) Galactopoiesis is the maintenance of lactation. Once lactation has been established, prolactin is the primary hormone involved in maintenance of milk production. In the first few weeks post partum, maternal serum prolactin levels are continuously high and undergo further elevation (5- to 10-fold) with each nursing episode. Once breast enzyme systems are activated, lactation can continue with normal prolactin levels (essential to maintain lactation).

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However, suckling, i.e. actual removal of milk, is required to maintain lactation. Without frequent emptying of the mammary gland, milk synthesis will not continue in spite of adequate hormonal status. Hence, intense suckling by the infant, milk removal, autocrine control of lactation, milk secretion rate, milking interval, and milking frequency all contribute towards maintenance of lactation. Breastfeeding the baby in the first few days of life is important for establishment of lactation. Frequent feeding in the early days increases the number of prolactin receptor sites within the breast, indicating that these receptors could have a greater control in breast milk output rather than serum prolactin levels [17]. Successful establishment of lactation depends on the proper development of adequate prolactin receptors (laid down in the first 3 months post-partum) which in turn appears to be correlated with frequency of feedings – with more frequent breastfeeds, the stimulation for receptor development is greater [30, 31, 32]. Increase in milk volume is perceived by the parturient woman as ‘coming in’ of milk. This phenomenon is brought about by a substantial increase in the rates of synthesis and/or secretion of almost all the components of mature milk, which result in the increase in milk volume [33, 34]. Amongst the other nutrients, concentration of secretory immunoglobulin A and lactoferrin (protective proteins) increase dramatically and remain high for approximately 48 hours after birth; however, as the milk volume increases, their concentration falls rapidly, indicating that breastfeeding is an extension of maternal protection that helps the infant to transition [35]. (iv) Involution is a transitional phase of the mammary gland from lactating to non-lactating state. If milk is not removed from the breasts, the glands become distended. After termination of breastfeeding, milk continues to accumulate for 48 hours before the rate of milk synthesis and its secretion begin to decrease rapidly and dries out. One of the most serious problems leading to termination of breastfeeding is maternal perception of breast milk insufficiency. In addition, psychological factors like maternal self-confidence and her attitude are the strongest predictors perceived breast milk inadequacy. An anxious mother may suckle her infant less often, which may result in impaired milk volume [36]. Further, insecurity about the adequacy of her milk may cause the mother to wean her infant completely/introduce supplementary foods, which may reduce suckling frequency and impair milk synthesis leading to milk stasis. Regular removal of milk, adequate maternal diet, positive psychological attitude towards nursing and an intact hypothalamic

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pituitary axis are key factors to successful nursing. Failure to remove milk adequately results in the reduction of milk synthesis because the ‘milk dilated alveoli’ obstruct the mammary capillary blood flow. Initially, the intraductal pressure rises due to milk stasis (a plugged duct/breast engorgement – precursor of mastitis); with consequent flattening of alveolar cells and development of spaces between these cells some components (mainly immuno-proteins and sodium) cross from plasma into the milk and from milk into the interstitial tissue through this space, inducing an inflammatory response. The accumulated milk, the inflammatory response, and the resulting tissue damage facilitate the establishment of the infection, usually by Staphylococcus (aureus and albus), occasionally by Escherichia coli or Streptococcus [37]. Moreover, in the absence of suckling stimulus, secretion of prolactin or oxytocin is adversely affected, resulting in cessation of lactation [38, 39, 40, 41, 42]. Box 7.5 further elaborates upon the phenomenon during failed lactogenesis. Box 7.5 Failed lactogenesis After childbirth and expulsion of the placenta, the maternal serum levels of progesterone decrease drastically, the consequent prolactin secretion by the anterior pituitary gland stimulates lactogenesis phase II and the milk secretion begins. Oxytocin secreted from the posterior pituitary gland causes contraction of the myoepithelial cells allowing milk to be secreted. Breast milk synthesis in the initial phase is controlled by hormonal action and ‘ it comes in,’ by the third to fourth day after delivery even without the infant’s suckling). After that, lactogenesis phase III (galactopoiesis) begins lasting up to the end of lactation; it is controlled by autocrine mechanisms and basically depends on emptying of the breast. Therefore at this stage, the quality (vigorousness) and quantity (frequency and duration) of suckling by the infant regulate the synthesis of breast milk. With the degree of suckling and transfer of milk to the infant, the hypothalamus inhibits dopamine secretion (prolactin inhibitory factor); the decreased dopamine levels stimulate prolactin secretion, which in turn promotes milk secretion. The integrity of hypothalamic-pituitary axis (which regulates prolactin and oxytocin levels) is essential to trigger and maintain the synthesis of breast milk. An elevated breast milk sodium concentration is a reflection of failed lactogenesis, which may be a marker of poor interaction between the baby and breast resulting in low consumption of breast milk. Lowered breast milk consumption / high breast milk sodium concentrations on or before day 3 were observed in cases where the infant failed to latch on properly [44, 45]. High sodium concentration was found to be statistically related to impending lactation failure and could be reversed by effective milk removal, suggesting that milk removal and/or effective suckling are necessary to increase in milk volume secretion [46].

Studies have reported that on one hand oxytocin secretion can occur in response to conditioned stimuli such as thought, sight, vision, smell, infant’s cry as well as emotional factors such as motivation, self-confidence and tranquility; while on the other hand, pain, discomfort, stress, anxiety, fear and lack of self-confidence may inhibit the let-down reflex; thus

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hampering lactation. Acute maternal stress can also temporarily reduce the flow of breast milk, which the mother may perceive that the milk has ‘dried up’; however with adequate support the mother can resume breastfeeding [43]. A mother needs to be counseled and assured that her milk is sufficient for the baby. She also needs to be supported during the breastfeeding episodes so that lactation is re-established. WHO has guidelines for counseling and extending support to mothers with perceived breast milk insufficiency.

7.2.4

Composition of human milk – quality and quantity

Breast milk volume and composition is not uniform; concentration of many of its constituents varies not only inter and intra-individually as well as during the course of lactation. Further, there are variations during the course of the day as well as during the course of suckling (differences between fore and hind milk). These changes are the greatest and occur rapidly during the first week post partum after which the levels stabilize [47, 48, 38, 49]. Maternal age, parity, diet/nutritional status, regional differences and, in some situations season also influence breast milk composition. Human milk evolves to meet the changing needs of baby during growth and maturation; depending upon the stage of lactation, breast milk is designated as colostrum (3–5 days post partum), transitional milk (5–15 days) and mature milk (>15 days). (i) Colostrum – The volume of colostrum in the first 12 hours post partum is reported to be 44 ± 4.83 mL; while in the first 24 hours, the volume ranges from 7 mL to 123 mL [17, 50, 51]. With the infants’ suckling, the volume increases by nearly ten fold by 36 hours after birth and levels off to 500 mL by the 4th day; the dramatic changes in volume in the 0–72 hours period can be attributed to a fall in sodium and chloride concentration coupled with an increase in lactose [52]. This stage is known as the “coming in” of milk. In this stage, breast milk starts to be produced in larger amounts between the 2 and 4 days after delivery, making the breasts feel full; the milk is then said to have ‘come-in’. On the 3rd day, an infant is normally takes about 300–400 ml of milk in 24 hours and on the 5th day it is 500–800 ml. Human colostrum is rich in protein, fat-soluble vitamins and minerals essentially for meeting the need for rapid cellular growth as well as protecting the newborn against infections. It is thick and sticky due to high lactose content in the milk. ● The comparatively higher protein content of colostrum (than mature milk) aids in the development of certain digestive enzymes. Its

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high levels non-specific anti-microbial factors such as lactoferrin (inhibits proliferation of iron binding micro-organisms in the gut). Colostrum contains bifidus factor that promotes the removal of intestinal meconium and facilitates the establishment of bifidus flora in digestive tract of the new born. The bifidus factor provides resistance against pathogenic bacteria and also influenza virus activities [27, 42]. It has been observed that the epidermal growth factor and insulin are high in colostrum (as compared to mature milk) especially in the 1–3 days post partum indicating that their important role in the proliferation and differentiation of infant tissues [53]. Most immune bodies directed against various pathogens are provided transplacentally to the foetus; however, after birth, it is completed via a postnatal transfer of through the colostrum (passive immunization); this is critical for child survival in the first few months of life [46]. The yellowish colour of colostrum is due to the presence of âcarotene and therefore is the major source of vitamin A for the infants. Carotenoids have an important role to play in immunoenhancement and are found to be upto five times greater in colostrum (p<0.05) than the mature breast milk [54].

Hence, colostrum provides the important immune protection to a neonate who is newly been exposed to the micro-organisms in the environment and because of its immense beneficial properties it is called the first natural vaccination for the infant. Factors such as nutritional status of the mothers have an influence on the colostrum composition of breast milk. Garg et al (1988) found lower fat concentrations in the colostrum of undernourished as compared to the well-nourished Indian mothers [55]. Table 7.1 Nutrient composition of colostrum [60] Protein Triglycerides Cholesterol Phospholipid Vitamin A Vitamin E Calcium Zinc Iron

5.36 g/dL 5.4 g/dL 67.5 mg/dL 36.36 mg/dL 61.2 IU/dL 1180 ìg/dL 0.996 g/dL 3.9 mg/dL 0.42 ìg/dL

Studies indicate that although maternal nutritional status did not influence the serum immunoglobulin concentrations during pregnancy, but IgA, IgG and lysozyme concentrations in both colostrum and mature milk of

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malnourished mothers were only half as compared to the well-nourished ones [56–58]. No significant relationship has been demonstrated between maternal age, income, BMI, parity and the micronutrient contents of colostrum [59]. (ii) Transitional milk – Transitional milk can appear as early as twelve hours after delivery and may continue for 7–14 days. It retains some of the yellow color of colostrum. The concentration of immunoglobulins and total protein decreases, while lactose, fat as well as the total calorific value increases. There is also an increase in the water-soluble vitamins. By the 14th day, a white colour (due to emulsified lipids and presence of calcium caseinate) emerges. (iii) Mature milk – Breast milk secreted after approx 15 days post partum is the mature milk. At this stage, the composition of most milk constituents become stable and their levels remain more or less similar. Not only are there variations in the composition of colostrum, transitional and mature milk but there are following variations in the nutrient composition of mature milk itself. ● Variations in nutrient concentration during the course of lactation. During the first six months of lactation, a significant increase in lactose, glucose, pH and ionized calcium (for growing bones); while decrease in protein, sodium, potassium, chloride and calcium concentrations has been observed. ● Daily variations in nutrient composition in breast milk. There are day-to-day fluctuations observed in certain breast milk constituents like fat and water soluble vitamins. ● Within feed variations in breast milk. The fore milk has a lower fat content, appears thin and bluish in colour. Over the next several minutes of breastfeeding, fat content increases (hind milk) and the milk attains a light cream colour, appears comparatively thicker and helps in satiating the infant. Studies show that although total lipid content rises during individual feeds, diurnally and with the length of nursing; the fat composition of milk remains relatively constant [61, 62]. In a research study, it was observed that the fat content of milk increased from 3.0 g/100mL to 5.0 g/100mL in the course of feeds lasting 7 minutes; hind milk may contain almost twice as much fat as fore milk [63]. DaCunha et al (2005) reported that the fat content of milk varies with the duration and intensity of suckling; hind milk has three-fold fat content than foremilk. Diurnally, the fat rises from 2- to 5-folds early morning to a plateau at about mid-day [64].

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Quantity of breast milk

The vital stimulants to milk production are infants’ size, health status and activity which determine the frequency/length of feeding, strength of their suckling as well as appetite. Further, time of introduction, type and amount of complementary feeds are as important as mother’s emotional state and physical health can influence both the milk production and let-down reflex [65]. In order to stimulate the prolactin and oxytocin secretion, it is necessary to put the infant to mother’s breast within a few hours post partum, preferably within the first hour when the baby is alert and the suckling reflex is the strongest. In the first few days post partum, 3 minutes of suckling at each breast at 3–4 hourly intervals is sufficient for the milk flow; thereafter the suckling period can be increased by 1 minute every day [42]. Theoretically, WHO/FAO recommended that the breast milk requirement for a 50 th centile male child at 3 months is 900 mL/day and at 6 months 1,250 mL/day [66]. In Indian studies, average milk yield of mothers from the low socio-economic group was reported to be 450–600 g/day in the first 6 months of lactation; the average yield being lower than the reported values of 700–800 g for developed countries [67]. However, in a 2006 study, carried out in rural and urban India, the infants were reported to consume slightly higher amounts of breast milk in the first six months – 679.2±209.8 g/day [691.8±212.2 g (rural), 623.5±163.8 g (urban poor) and 709.8±241.6 g (urban elite)] [68]. Volume of breast milk secreted is according to the infant’s requirement and is related to the degree of emptiness or fullness of the breast. The emptier breast produces milk faster than the fuller one. It has been noted that there are individual differences in the breast milk intake of babies. Some babies drink large volumes of milk at a single feed and smaller number of feeds in a day, while others drink smaller volumes of milk but feed more frequently. Day-to-day differences have also been noted in the breast milk intakes of a baby [69]. The breast milk consumption of an exclusively breast fed infant was found to be positively correlated to the infant’s current weight and negatively with the amount of other liquids given in the early days post partum; it was also found to be related to the number of breast feeds given and child rearing practices [38, 70].

7.3

Trends in exclusive breastfeeding practices

Poor breastfeeding and complementary feeding practices are widespread. Worldwide, it is estimated that only 37% of infants are exclusively breastfed for the first 6 months of life, the majority receiving some other food or fluid in the early months [2].

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WHO/UNICEF (2008) defines exclusive breastfeeding means the infant receives only breast milk and no other liquids, not even water or complementary foods with the exception of undiluted vitamin/mineral drops or syrups, ORS and medicines for the first 6 months of life (see Box 7.1) [4]. There are limitations in the existing definition of the indicator has been described in Box 7.6. Box 7.6 Limitation of the exclusive breastfeeding indicator A limitation of the exclusive breastfeeding indicator is that it does not reflect the exclusive breastfeeding status of an infant for the entire six months period. At the time of survey, the data collected on exclusive breastfeeding denotes the status in the previous 24 hour period, whereas reality is that even if a woman has practiced exclusive breastfeeding for the last 24 hours it does not necessarily imply that she has exclusively breastfed her baby in the entire six month period. This issue still needs to be addressed in the new WHO publication which defines breastfeeding status of infants [4].

(a)

Exclusive breastfeeding for 6 months

The advantages of exclusive breastfeeding compared to partial breastfeeding were recognized in 1984, when a review of available studies found that the risk of death from diarrhoea of partially breastfed infants 0–6 months of age was 8.6 times the risk for exclusively breastfed children. For those who received no breast milk the risk was 25 times that of those who were exclusively breastfed. A study in Brazil in 1987 found that compared with exclusive breastfeeding, partial breastfeeding was associated with 4.2 times the risk of death, while no breastfeeding had 14.2 times the risk. More recently, a study in Dhaka, Bangladesh found that deaths from diarrhoea and pneumonia could be reduced by one third if infants were exclusively instead of partially breastfed for the first 4 months of life. Exclusive breastfeeding for 6 months has been found to reduce the risk of diarrhoea and respiratory illness compared with exclusive breastfeeding for 3 and 4 months respectively. If the breastfeeding technique is satisfactory, exclusive breastfeeding for the first 6 months of life meets the energy and nutrient needs of the vast majority of infants. No other foods or fluids are necessary. Several studies have shown that healthy infants do not need additional water during the first 6 months if they are exclusively breastfed, even in a hot climate. Breast milk itself is 88% water, and is enough to satisfy a baby’s thirst. Extra fluids displace breast milk, and do not increase overall intake. Water supplementation is unnecessary as it reduces the baby’s desire to suckle and could also be a potential source of contamination. Even in the hot summers, an infant does not need water

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Percentage of infants exclusively breastfed for the first six months of life

supplementation. Very often in newborn babies, water and teas are commonly given in the first week of life. This practice has also been associated with a two-fold increased risk of diarrhoea. For the mother, exclusive breastfeeding can delay the return of fertility and accelerate recovery of pre-pregnancy weight. Mothers who breastfeed exclusively and frequently have less than a 2% risk of becoming pregnant in the first 6 months postpartum, provided that they still have amenorrhoea [71]. Recent data from 64 countries covering 69% of births in the developing world suggest that there have been improvements in this situation. Between 1996 and 2006 the rate of exclusive breastfeeding at global level for the first 6 months of life increased from 33% to 37%. Significant increases were made in Sub-Saharan Africa, where rates increased from 22% to 30%; and Europe, with rates increasing from 10% to 19% (Figure 7.2). In Latin America and the Caribbean, excluding Brazil and Mexico, the percentage of infants exclusively breastfed increased from 30% in around 1996 to 45% in around 2006 [72]. Even though the global data over the last decade show that although exclusive breastfeeding rates have increased with time, worldwide, it is estimated that only 34.8% of infants are exclusively breastfed for the first 6 months of life and that the majority receiving some other food or fluid in the early months [71]. 1 00 90 80 70

A ro un d 19 96 A ro un d 20 06

60 50

44 45

40 30

30 19

20 10

30 26

27

32

37 33

22

10

0 C E E /C IS

S u b-sa ha ran S o uth A sia E a st M id dle A frica A sia /P a cific e ast/N o rth R e gion s (e xclu d ing A frica C h in a)

D e ve lo ping cou ntrie s (e xclu sin g C h in a)

7.2 Trends in exclusive breastfeeding rates in the first 6 months of life (1996–2006) [72].

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Box 7.7 Assessment and analysis of the situation reveals the following facts regarding why so many babies not breastfed exclusively ●

●

● ● ● ●

Mothers, health professionals, family and community members do not understand what exclusive breastfeeding is or that it makes a difference. They do not know enough about how breastfeeding works best, how to start it and what to do when a mother has difficulties. Therefore they are not able to provide the advice and support that is required. Mothers, health professionals, family and community members do not believe that exclusive breastfeeding for six months is possible, is convenient or that mothers have enough milk. They do not appreciate that any additional foods or fluids can actually be harmful to the baby. Mothers have to return to work before six months, either in or out of the home. Commercial advertising conveys the message that breast plus formula is even better than just breast milk. Mothers or caregivers “perceive” milk secreted is insufficient and introduce diluted animal milk. Water is introduced to quench thirst since mothers are not aware that no water is required to be given to exclusively breastfed infant.

Box 7.8 Exclusive breastfeeding in India The latest NFHS-3 figures indicate that less than half of the children are exclusively breastfed during the first six months of life. In most cases, along with mothers’ milk, foods such as water, cow/goats milk, honey, sugar water, ghutti, etc, are given to the baby. It is a well-established fact that introduction of other foods before six months displaces breastfeeding, which potentially marks the beginning of malnutrition and increased vulnerability to illnesses. In India, though infants are being breast-fed, only 69% babies are being exclusively breastfed at 2 months of life, between 2 and 3 months of age about half of the babies are being exclusively breastfed while at 3–4 months of age barely quarter of the babies in the country are being exclusively breast; indicating that exclusive breastfeeding is virtually nonexistent [73]. India is still far from achieving universal exclusive breastfeeding for the first six months of life which will help to achieve a substantial reduction in infant mortality indicators.

7.4

Integrating breastfeeding into public sector programmes

7.4.1

Global strategy for Infant and Young Child Feeding (IYCF)

Infant and young child feeding is a cornerstone of care for childhood development. In resource poor settings, improved feeding practices can lead to improved intakes of energy and nutrients, leading to better nutritional status. At present, there is ample amount of scientific data explaining the benefits of breastfeeding. Much has been learnt about effective interventions during the past few decades. These interventions

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Box 7.9 Breastfeeding patterns in India In India, breastfeeding is a traditional norm and is universal, yet there are many customs that are not conducive to health of the child. Systematic review of a large number of Indian studies indicate that usually, initiation of breast-feeding is often delayed being, nearly around 48–72 hours after birth while only a small proportion started within 24 hours. Early initiation of breastfeeding is relatively high among urban women, those with middle school education, from households with a high standard of living; women from several tribes have also been found to initiate timely breastfeeding. Circumstances surrounding child birth can have an important effect on early initiation of breastfeeding. Studies have noted that in rural and urban settings, cases where delivery was assisted by trained health professional or an institutional delivery, breastfeeding was initiated earlier than others. The policy on Infant and Young Child feeding (GoI) 2006 recommends that initiation of breastfeeding should begin immediately after childbirth, preferably within one hour. In India, only 23.4% newborns across the country are being breastfed in the first hour of birth. In other words, the early initiation of breastfeeding is not being practiced as desired. The NFHS data in the last 15 years indicates that there has been an improvement, but the rate has been extremely slow at nearly 1% per year [73]. Given the state of infant health and mortality indicators and the proven benefits of initiating breastfeeding in the first hour of life, timely initiation of breastfeeding surely needs to catch up pace [8]. The NFHS 3 data indicates that even in the better performing states, like the Northeastern states and the Southern states of the country, the early breastfeeding initiation rates are between 55% and 65%; the rates in the northern and central part of the country is between 4% and 19%, indicating that early breastfeeding initiation rates are far below the goal of universal follow up of this practice. Health care providers both at the facility and community level need to address this issue aggressively in order to make a substantial improvement [73]. Local customs/beliefs and socio-educational level of a population influence the feeding of prelacteals. Literature has indicated that the administration of prelacteals is quite rampant and has not changed much in the last four to five decades, especially among the low socio-economic groups. The infants are generally administered boiled water, tea, sugar, honey, jaggery or glucose with plain water or the diluted animal milk; the mode of feeding is often unhygienic and generally practiced by the illiterate women from lower socioeconomic background [74, 75] The latest NFHS – III data indicate that over half the mothers (57%) still gave their new born child prelacteals [73]. P r e s e n t l y, t h e b e n e f i t s o f c o l o s t r u m f e e d i n g h a v e b e e n g l o b a l l y acknowledged. Unfortunately in India, ancient physicians did not recommend colostrum feeding; instead honey with clarified butter and gold ash was recommended to facilitate the discharge of meconium [76] have pointed out that colostrum rejection too is a traditional practice as it was considered to be “dirty” / blocked milk that needed to be discarded before the “real/pure” milk was secreted [77]. Various researches carried out till the 1990s reveal that a majority of mothers discarded colostrum because of the traditional beliefs regarding colostrum; however, since the last three decades, the situation has noted to have improved considerably [77, 78]. Many studies carried out at this time reported that 30–40% of Indian mothers discard colostrum; however, it is not clear whether they totally discarded the breast milk continuously over 3 days or emptied out the breast once or merely

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discarded a few drops before initiating breastfeeding. Bhale et al (1999) noted that the amount of breast milk discarded for first two days varied largely from few drops to few spoons. In some communities, the mother’s breast fed their babies after two days without discarding the initial milk, which actually means that initiation of breast feed was delayed, but colostrum was not really discarded [79]. This indicates that a large majority of the neonates are deprived of the valuable immunoglobulins, vitamins and proteins which help to protect the baby from infections and support to adapt to the external environment.

indicate that mothers need support to initiate and sustain breastfeeding within the family, community, workplace and health system. Organizations like WHO and UNICEF have been pioneers in laying down infant feeding policies and creating supportive environments for mothers to breast feed [80, 81]. Evidence from a variety of countries indicates that marked improvements in exclusive breastfeeding are possible if supported by effective regulatory frameworks and guidelines and when comprehensive programmatic approaches are at scale [2]. The Global Strategy for Infant and Young Child Feeding, endorsed by WHO Member States and the UNICEF Executive Board in 2002, aims to revitalize efforts to protect, promote and support appropriate infant and young child feeding. The Strategy is a guiding framework to provide technical support to countries for implementation of child feeding programmes. According to the Global Strategy for Infant and Young Child Feeding, “Inappropriate feeding practices and their consequences is a major obstacle to sustainable socio-economic development and poverty reduction. Governments will be unsuccessful in the efforts to accelerate economic development in any significant long-term sense until optimal child growth and development, especially through appropriate feeding practices, is ensured.” According to WHO/UNICEF, supporting, protecting and promoting optimal breastfeeding practices is the single most effective intervention against child survival [8]. The strategy calls on the member states to act urgently. It urges all national policymakers, public health authorities, professional bodies, UN agencies, technical programme managers and NGOs to promote breastfeeding for the survival, growth and development of their children and societies. The strategy specifies not only responsibilities of governments, but also engages all relevant stakeholders and provides a framework for accelerated action, linking relevant intervention areas and using resources available in a variety of sectors [8]. At present, many countries need plans of action to protect, promote, and support exclusive breastfeeding at the national, health centre and community levels.

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At the national level, creation of appropriate structures that ensure the adoption and implementation of appropriate policies and legislation is vital. This includes the development and carrying out of national infant and young child feeding policies and strategy frameworks as well as the development and enforcement of legislation that relates to the International Code of Marketing of Breast-milk Substitutes and maternity protection. At the health systems level, this includes improving breastfeeding practices in maternity facilities, including through the implementation of the ‘Baby-Friendly Hospital Initiative’ (BFHI) as well as implementation of IYCF counseling and support at all relevant maternal and child health contacts, for which capacity-building and mentoring of health workers on topics such as breastfeeding counselling is essential. At the community level, mother support activities involving community health workers, lay counsellors and mother-to-mother support groups are crucial. Implementation of an evidence-based comprehensive communication strategy using multiple channels, which ties efforts at the three levels together, is also vital for the successful protection, promotion and support of breastfeeding. Governments are in fact obliged, under Article 24 of the Convention on the Rights of the Child, to ensure that all sectors of society know about the benefits of breastfeeding.

In the developed countries, programmes like the Baby Friendly Hospital Initiative (BFHI) have been instrumental in directing necessary resources to improve the care quality of feeding care in maternity services. These programmes contributed significantly towards not only increasing early breastfeeding initiation rates but also extended skilled services to the mother in case she encountered a problem. However, this initiative has helped to improve breastfeeding trends only in some countries. In addition, communities were also mobilized (i) to create breastfeeding friendly environments and (ii) community-based resource persons in providing this support to mothers. Although BFHI includes a community component, its implementation for instance in India, has been particularly weak. The initiative started off with a great amount of fervor in the early 1990s, however, towards the latter half of the decade it became weak. In many countries, the BFHI has not been implemented as a vertical project and has not been well institutionalized within the standard operating and quality assurance procedures for all maternity facilities. Even those institutions that received BFHI training, support was only available to the mothers during a short period before and after delivery. Post partum follow-ups to ensure that the mothers followed exclusive breastfeeding or counseling (in case the mothers encountered any problems) were virtually nonexistent.

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Box 7.10 Ten steps to successful breastfeeding [10, 86] 1.

Have a written breastfeeding policy that is routinely communicated to all health care staff. 2. Train all health care staff in skills necessary to implement this policy. 3. Inform all pregnant women about the benefits and management of breastfeeding. 4. Help mothers initiate breastfeeding within one half-hour of birth. 5. Show mothers how to breastfeed and maintain lactation, even if they should be separated from their infants. 6. Give newborn infants no food or drink other than breast milk, unless medically indicated. 7. Practice rooming in - that is, allow mothers and infants to remain together 24 hours a day. 8. Encourage breastfeeding on demand. 9. Give no artificial teats or pacifiers (also called dummies or soothers) to breastfeeding infants. 10. Foster the establishment of breastfeeding support groups and refer mothers to them on discharge from the hospital or clinic.

Since in many developing countries including India, a large number of women in rural areas still deliver at home, interventions at the community level continue to be extremely important for supporting and promoting early and exclusive breastfeeding. Much needs to be done to scale up promotion of and integrate breastfeeding into the national maternal and child health programmes at both health service and community level. Synthesis of lessons learnt, especially with reference to effective trials conducted in population-based programmes which promote timely initiation and exclusive breastfeeding is critical for effective programme designing and moving forward. The next step is to identify proficient and well proven interventions into child health programmes [87].

7.4.2

Scaling-up breastfeeding interventions into national programmes

The key processes required for exclusive breastfeeding scale-up are (1) An evidence-based policy and science-driven technical guidelines; and ● This includes political will, strong advocacy, enabling policies and legal framework that makes it possible for mothers to exclusively breast feed. ● Well-defined short- and long-term programme implementation strategy, sustained financial support, clear definition of roles of multiple stakeholders and emphasis on delivery at the community level. A set of approaches that ensure programmatic success include [82].

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Formative research for designing programmes, its interventions and delivery. Effective use of antenatal, birth and post-natal contacts at homes through community mobilization efforts. Strong communication strategy and support. Committed good quality trainers and training. Monitoring and evaluation with feedback systems that allow for periodic programme corrections and continued innovation. Legal framework such as maternity leave that facilitate mothers to exclusively breastfeed for at least 4 months. Strong national- and state-level leadership.

In addition to these it is essential for sustained programme efforts to achieve high coverage. Figure 7.3 highlights the components needed at the policy, health services and community level for a comprehensive breastfeeding programme. P OL IC Y

■ ■ ■ ■ ■ ■

N a tio n a l in fa n t a n d y o u n g ch ild fee d ing p olic y a nd stra te gy N atio na l B re a stfee d in g C o m m iss io n H ea lth s yste m n o rm s C od e of M a rke tin g of B re as t M ilk S u b stitute s W or ksite law s a n d re gu la tion s In for m a tio n , e d u ca tion a nd c om m un ic atio n

HE ALT H S E RVIC ES

■ ■ ■ ■

P re -s erv ic e c urricu lu m B a by F rie n d ly H o sp ita l In itia tive IY C F c ou n se lin g at a ll M C H co n ta cts In -s erv ic e tra in in g S u pp o rtiv e su pe rv isio n ■ ■ ■ ■

C O M M UN ITY

■ ■ ■

C o m m u nity p a rtic ipa tion , e .g . m o the r s up p o rt gro u ps Tra in in g an d s u pe rv isio n o f c ou n se lin g ne tw o rk C o m m u nity e d u ca tio n

In fo rm ation , e du ca tio n a n d co m m un ica tio n M o n itoring , re s ea rch a n d e va lu atio n H e a lth in for m a tion sys te m s R e fer ra l a n d co u n te r re fe rra l

7.3 Elements of a comprehensive breastfeeding programme.

(i) Policy framework Creation of a policy framework to promote the formation of supportive systems for exclusive breastfeeding is the first step towards designing an effective breastfeeding programme. These frameworks have started at have started at the international level and need to be adopted at the national, state and district till the village level. Breastfeeding can only be promoted and protected if the environment is conducive. In order to make the environment facilitating and supportive

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so that mothers are motivated to breastfeed their babies, a number of worldwide efforts are constantly being made by various governments, INGOs UN bodies to protect and promote breastfeeding (Box 7.10–7.12). Box 7.11 Breastfeeding promotion, protection and support The various global and Indian policies to promote, protect and support breastfeeding include: ●

●

●

●

●

●

International Code of Marketing of Breast Milk Substitutes (1981) aims to curb marketing practices of baby food manufacturers and protect the nursing mothers from misinformation. Infant Milk Substitutes, Feeding Bottles, and Infant Foods Regulation of Production, Supply and Distribution Amendment Bill, 2003 (IMSAB) bans all forms of promotion of infant feeding products, including offering benefits to any person. Funding of seminars, meetings, research or any sponsorship is also prohibited [83]. Innocenti Declaration (1990) aimed to create a global environment that protects, promotes and supports breastfeeding; empowers women to breastfeed exclusively for 4 – 6 months and continue to breastfeed for 2 years or more. Building on the previous one, the 2005 Innocenti Declaration highlights roles and responsibilities of key players to be met so that mothers, families and other caregivers can make informed decisions about optimal infant feeding. [84, 85]. Infant Milk Substitutes, Feeding Bottles and Infant Foods (Regulation of Production, Supply and Distribution) Act (IMS) indicates that in case of infants requiring artificially feeds, the feeding decisions should be untainted by commercial influences [83]. The Baby Friendly Hospital Initiative (BFHI) (1991, updated materials 2009) aims to encourage hospitals and maternity services to promote the health and well-being of babies born in hospitals by (i) increasing breast-feeding, (ii) counselling mothers, (iii) promoting early initiation of breast-feeding through rooming-in, and (iv) establishing support groups for mothers [86]. The World Health Assembly in May 2001 resolved the confusion on appropriate time of introducing complementary feeding and stated that exclusive breast-feeding for the first six months (180 days) is most appropriate. WHO/UNICEF’s Global Strategy on infant and young child feeding (2003) based on Innocenti Declaration is reflective of rights-based, lifecycle programming, recognition of gender needs, supportive of mother and family and directly improving early childhood survival, growth and development. It emphasizes that exclusive breastfeeding for first six months significantly reduces morbidity and mortality, while continued breastfeeding together with nutrient-dense complementary feeding into the 2nd year is advisable [8].

(ii) Making an effective implementation plan Once the decision to scale up a programme for exclusive breastfeeding is made in a region or state or country, the logical starting point is to review the relevant, existing national policies and to assess whether these address varying circumstances and are able to provide supporting environment(s) under which women deliver and live (such as urban or rural residence, working women and place of delivery).

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Box 7.12 Indian policy scenario on promoting breastfeeding programmes In the Indian context, the National Guidelines on Infant and Young Child Feeding (2006) recognize clearly that poor feeding practices in infancy and early childhood, result in malnutrition, contribute to impaired cognitive and social development, poor school performance and reduced productivity in later life. The Ministry of Women and Child Development and Ministry of Health and Family Welfare hold special responsibility to contribute to optimal infant and young child nutrition by making National Guidelines on infant and young child feeding an integral part of nation-wide Integrated Child Development services (ICDS) and Reproductive and Child Health (RCH) programme or National Rural Health Mission (NRHM). To effectively operationalise these guidelines, field functionaries of these ongoing programmes need to provide assistance to all mothers starting at antenatal stage for influencing feeding at the first hour of birth. These field functionaries need to have the training for providing regular skilled support for early initiation of breastfeeding, exclusive and continued breastfeeding as well as appropriate complementary feeding after six months. However, at present, the recommended patterns of breastfeeding are far from the optimal levels [73].

Subsequent to a national policy being in place, a policy framework for implementation needs to be developed prior to scale-up. This framework should include a vision, consensus on technical issues, on programme strategy, roles, relationships and responsibilities of implementing partners, measurable goals within defined time lines and predictable adequate funding to achieve these outcomes. The framework needs to also address the capacity of all implementing partners as well as emphasize breastfeeding promotion through community-based programmes. Further, political commitment and ownership by relevant government departments at national, state and district levels is critical for effective scale-up and any lacunae in the system needs to be addressed [88]. The next step is designing a potentially effective programme implementation strategy which would help in achieving high coverage, quality and sustaining service delivery combined with capacity building and effective programme management is good [88]. Breastfeeding scale-up programmes when integrated into ongoing activities are more likely to be more sustainable. Further, emphasis needs to be laid on delivery of interventions at the community level so that mothers have easy access to support. (iii) Programme delivery Following formulation of broad strategy for implementing the programme, attention must then shift to the operationalization of the strategy. Programmes can be delivered through existing health systems either through institutions or through communities based systems.

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Box 7.13 International code of marketing of breast-milk substitutes In 1981, Member States of the World Health Organization adopted the International Code of Marketing of Breast-milk Substitutes, with the aim to protect, promote and support appropriate infant and young child feeding practices. The adoption of the Code was a key milestone in global efforts to improve breastfeeding, and countries have taken action to implement and monitor the Code. In the 1970s, a general decline in breastfeeding was noted in many parts of world due to soc-cultural reasons and increased promotion of breast milk substitutes. It is recognized that the encouragement and protection of breastfeeding is an important part of the health and nutrition and other social measures are required to promote healthy growth and development of infants and young children; and that breastfeeding is an important aspect of primary health care. It is highlighted that the governments should develop social support systems to protect, facilitate and encourage breastfeeding, and that they should create an environment that fosters breast-feeding, provides appropriate family and community support, and protects mothers from factors that inhibit breast-feeding. The infant formula should not be marketed or distributed in ways that may interfere with the protection and promotion of breastfeeding and that improper practices in the marketing of breast-milk substitutes and related products can contribute to these major public health problems. In view of the vulnerability of infants in the early months of life and the risks involved in inappropriate feeding practices, including the unnecessary and improper use of breast-milk substitutes, the marketing of breast-milk substitutes requires special treatment, which makes usual marketing practices unsuitable for these products. Governments are called upon to take action appropriate to their social and legislative framework and their overall development objectives to give effect to the principles and aim of this Code, including the enactment of legislation, regulations or other suitable measures. The Code has 11 articles which highlight the aim of the code, specify the definition of breast milk substitutes, responsibility of the governments in the marketing of breast milk substitutes, increasing awareness and providing consistent information on infant and young child feeding through various medium. These articles also highlight quality specifications for production of the breast milk substitutes so that the health of infants is protected, advertisement, labelling of the product and marketing restrictions of breast milk substitutes. Role and responsibilities of health care systems, health workers at the community level has been specified. Lastly, for implementation and monitoring of the Code, social and legislative framework, regulations or other suitable measures to be undertaken by government to protect, promote and support breastfeeding has also been described [83].

Experiences from regions where hospital deliveries are the norm, scaleup efforts through BFHI has been successful and the strategy has helped increase rates of exclusive breastfeeding [89, 90]. However, in many countries, after initial years of enthusiasm, the scale-up effort seems to have reached a plateau. Programmatic experience has shown that in communities with higher number of hospital deliveries, the initial high rate of exclusive breastfeeding was not sustained after mothers were discharged from facilities [91]. The challenge, therefore, is to continue support that was available in institutes in the post-delivery phase at home

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and community levels and in all subsequent child health contacts. This could be given through public and private providers to sustain exclusive breastfeeding [92]. Countries have addressed this issue of home level support in different ways. In the last few decades, in most developed countries, a cadre of breastfeeding counsellors has been created. Developing countries, recognizing that facility-based interventions are insufficient, are expanding the community-based strategies. At the community level, multiple platforms can be used to give the same advice for a specific behavioural change. In some instances, routine activities in regular health programmes have been modified to incorporate exclusive breastfeeding counselling. In India, immunization sessions could be used as a platform for counseling in the presence of another local worker during the session. Another illustration is the adaptation of Integrated Management of Childhood Illness (IMCI) programme of the WHO/ UNICEF (2002) to the Integrated Management of Neonatal and Childhood Illness (IMNCI) by India. The IMNCI includes three home visits for all births in the first 7 days of life by an existing community worker, the Anganwadi worker to promote essential newborn care elements and one of these is promotion of exclusive breastfeeding. Further in regions where coverage through other channels is low or not feasible and a cadre of community workers exists, home visits are particularly important. Pilot programmes in India have shown that exclusive breastfeeding can be promoted through health worker’s home visits, at immunization clinics, growth monitoring sessions and at sickchild contacts [82]. Effectiveness trials with a variety of local workers such as peer counsellors (Bangladesh), lady health workers (Pakistan) and the ‘Accredited Social Health Activists’ (ASHA) worker (India) to promote exclusive breastfeeding by itself or as a part of essential newborn care have been tried and found to be effective before being scaled up and integrated in the national programmes. In addition, these peer counselors / lay counselors can be linked with the auxiliary nurse midwife (ANM) or other professional person in the existing primary health care system. This is because these frontline workers may not be able to resolve complex breastfeeding problems as the management of breastfeeding problems is too technical and beyond the capacity of a grassroots level functionary to solve. Another alternative to address this problem at the grassroots level could be to train frontline service providers and PHC staff for atleast 6– 8 days in addressing breastfeeding problems; however, this strategy is cost intensive [82]. Box 7.13 describes the various contact points to reach out to the community to promote breastfeeding.

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Box 7.14 Contact points that can be used for community outreach and support Potential contact points

IYCF topics for discussion

Maternity services, Health centres

Early initiation of breast feeding and exclusive breastfeeding Exclusive breastfeeding and complementary feeding

Growth monitoring and promotion programmes, immunization clinics or campaigns Mother support groups Women’s groups Home visits Workplaces, community meetings, Schools Health fairs, agricultural extension programmes, credit or micro-enterprise programmes Family planning programmes

Exclusive breastfeeding and complementary feeding Exclusive breastfeeding and complementary feeding Exclusive breastfeeding and complementary feeding Early initiation of breast feeding, Exclusive breastfeeding and complementary feeding Exclusive breastfeeding and complementary feeding Early initiation breast feeding and exclusive breast feeding

Channels that can be used for community outreach and support ● Health service personnel, home birth attendants, traditional healers, staff or volunteers from NGOs, lay or peer counselors, teachers, agricultural extension agents, family planning staff Some activities for infant and young child feeding community outreach and support ●

Individual counseling, group counseling, community education, cooking demonstrations, promotion of production of food that can fill gaps in the local diets, micronutrient campaigns mother-to-mother support, trials of new infant or young child feeding practices, baby shows or contests featuring infant and young child feeding, organization of workplace nurseries for breastfeeding infants, breastfeeding rooms or areas, social mobilization activities – planned actions that reach, influence and involve all relevant segments of society like world breastfeeding week activities, world walk for breastfeeding.

Community support strategies should focus on protection, promotion and support of both breastfeeding and complementary feeding [93].

Programmes that used multiple channels reported broader coverage [94, 95]. In India, formative research showed that immunization sessions and private providers were the channels to which a majority of infants and their mothers could be addressed. Following constitution of a breastfeeding-promotion programme, caregivers most often received exclusive breastfeeding counseling at immunization sessions (~40%), weighing sessions (~25%) and home visits (25–30%). In reality, through the government physicians or private providers were supposed to carry out periodic counseling, however in reality, despite being trained, these

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counseling sessions rarely (~2%) took place. When all the opportunities were considered together, 55–60% of caregivers had been counselled at least once, by at least one of the channels in the last 3 months, indicating that multiple channels reached more families [94]. The frequency of contact with caregivers or the intensity of counseling influences the cumulative benefit of the counselling; for example, six contacts with mothers resulted in higher adoption rates for exclusive breastfeeding as compared with three [96]. In India, the number of channels at which caregivers were counselled was positively associated with the rates of exclusive breastfeeding at 3 months of age [97]. There is a growing recognition that progammes which reach beyond the walls of health care facilities and which involve community as partners have a great potential for reducing child mortality rates at minimal cost. Community based health programmes have the potential to accelerate progress in reaching the MDGs in health [98]. Box 7.15 presents an overview of efforts made by various developing countries in improving exclusive breastfeeding rates through community based health workers and volunteers. (iv) Capacity building Prior to scale-up, it is critical that the training needs are assessed and defined for developing the training strategy. Use could be made of the extensive experiences such as the adapted versions of the UNICEF/WHO Breastfeeding Counseling Course for a wide range trainees including health workers, counselors etc [109, 110]. From global experience, it is evident that the duration of training is from 3 full days to 10 part days for different cadre of workers. Experience has shown that the training strategies were effective when designs were ‘concise and action oriented’ and aimed to equip trainers with practical skills and confidence to counsel appropriately. The recommended courses indicate a wide variation in focus e.g. for frontline workers training needs to be an integrated course on infant and young child counseling while for the midwives, the course content needs to address specific problems like feeding problems in young infants, feeding low birth weight babies etc. It is critical that health professionals, both from the private and government sector, are trained in infant and young child feeding so that there is uniform information on management of breastfeeding in community and institutional set up. Further, basic course in counseling could be organized for programme managers, trainers, supervisors, district managers and administrators using the WHO decision maker’s course module [8].

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Box 7.15 Experiences from other developing countries in improving breastfeeding rates through frontline workers Developing countries around the world have sought support from the community, peer counselors and have empowered primary care workers and health workers in hospitals in different ways to provide conducive environments that have helped more mothers to breastfeed exclusively. Findings from projects and community based studies indicate the following: ● In Gambia, Village Support Groups, for example parent-to-parent support groups were trained to give accurate information and help with correct breastfeeding technique. More mothers started to breastfeed within an hour of delivery, and 99.5% breastfed exclusively for 4 months instead of only 1.3% at baseline. Over 200 communities in the Gambia are now Baby-Friendly Communities [99]. ● In Ghana, several different methods of communication, workshops, and training were used to reach the wider community (including grandmothers, fathers, and the media) and mother support groups were formed. Within 2 years, the number of mother’s breastfeeding exclusively at 5 months had increased from 44% to 78% [100]. ● In Ghana, Village Banks made small loans to women to help them to become economically active. The women were also given education on health and child feeding. The average duration of exclusive breastfeeding increased from 1.7 months to 4.2 months, and the nutrition of the children at one year improved [101]. ● In India, health and nutrition workers learned to counsel mothers on breastfeeding while they were doing their other primary care work. At six months, 42% of mothers who were counselled breastfed exclusively, but only 4% of the mothers who were not counselled did so [97]. ● In Bangladesh, mothers from the community were trained as peer counsellors for breastfeeding. They visited women during pregnancy and for five months after delivery, making a total of 15 visits. Counselled mothers started breastfeeding earlier, and 70% of them breastfed exclusively for 5 months, compared with only 6% of the other mothers [102]. ● In Mexico, mothers from the community were trained to counsel about breastfeeding during home visits. 12% of mothers who were not visited breastfed exclusively; and the rate increased to 50% for mothers who were visited 3 times, and 67% for mothers who were visited six times (Morrow, 1999). ● In Belarus, 43% of the mothers who delivered in the 16 baby-friendly hospitals breastfed exclusively at three months, but only 6% of mothers who delivered in the 15 hospitals which are not baby-friendly [103]. ● In Bolivia, Guinea, India and Nicaragua, NGOs such as Save the Children and CARE mobilized the community by training health and community workers, involving grandmothers and fathers, men’s groups and mother support groups. Exclusive breastfeeding rates increased from 11% to 44% in Guinea; 41% to 71% in India and 10% to 50% in Nicaragua. In Bolivia, diarrhoea rates were halved and exclusive breastfeeding of infants under six months increased to over 75% when support groups were integrated into community activities in low-income neighborhoods in La Paz [104]. In India, Dular and MCHN programmes also indicated failure to promote exclusive breastfeeding despite counseling by community volunteers [105,106]. ● In Philippines baby-friendly crèches were formed to cater to working women. Mothers can drop in anytime to breastfeed, leave their expressed breastmilk, or avail themselves of the services of a wet nurse. Solid foods to complement breastmilk for babies above six months were made of natural and indigenous ingredients [107]. Successful strategy adopted in developed countries such as in Norway and Sweden, demonstrates that breastfeeding rates are much higher than in other parts of Europe. This is partly because health authorities consulted mothers’ organizations. Their advice and criticisms are listened to, respected and followed more than in most countries [108].

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(v) Behaviour change and communications approach A comprehensive communication strategy is critical for improving the breastfeeding behaviours of mothers. This would involve a mix of following communication channels which are directed to mothers as well as to family members, community leaders and other social, religious and political influences for influencing individual behaviours and social norms. These communication channels include ● ●

●

mass, electronic and print media (e.g., radio, TV, newspapers, flyers) community advocacy and events (e.g., theater, fairs, community gatherings, religious institutions) interpersonal communication (e.g., community groups, individual counseling, mother-to-mother support groups, home visits)

In addition to mass media, interpersonal and group counseling are two approaches which have the potential in bringing about the desired behavioural modifications. Effective counseling involves not only building on assessment of existing feeding practices, but also recognition of problems and negotiation with the mother in choosing improved “do-able” practices [110]. The messages and negotiation strategies with caregivers should be simple, action oriented and based on evidence of the context-specific barriers to optimal practices. Generic, empirical messages (e.g. “breast is best”; “breastfeeding your baby exclusively for six months gives a baby the best start in life” etc) usually don’t motivate behavior change. Both one-on-one counselling during opportunities in which more time is available such as home visits have been found to be effective. Group counselling can be carried out in communities where there are fewer opportunities for one to one communication and the health workers have lesser available time [94]. Peer counsellors can be employed for counseling mothers/caregivers during home visits [96, 102]. The more diverse the functions of the local worker, lesser will be the emphasis on a single component such as exclusive breastfeeding. Community mobilization programmes, such as street plays, rallies, radio programmes and songs, helped disseminate messages and increase community involvement [94, 95]. Figure 7.4 describes the direct/ proximate factors that influence infant feeding practices of mothers and caregivers. The intermediate determinants influence these direct factors while the underlying determinants have an influence on both intermediate and proximate determinants. Programmes seek to address all these factors to improve infant feeding behaviours through different communication channels or combination of different approaches.

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In fa nt fee d in g b eh aviou rs

P ro x im ate d ete rm in an ts

M atern al cho ices

O pp o rtun itie s to a ct on th ese c ho ic es

In te rm e d ia te d ete rm in an ts

In fa nt fee d in g inform atio n an d p hysical a nd socia l sup po rt d u rin g p re g n an cy, ch ild b irth a nd p ost pa rtu m

U n de rlyin g d ete rm in an ts

■ ■ ■ ■

F a m ilial, m e dica l an d cu ltu ral a ttitud e s a n d n or m s D e m o grap hic an d e c on om ic co nd ition s C o m m e rcia l p ress ure s N a tio na l a n d inte rn atio na l p olicie s an d no rm s

7.4 Model of determinants of breastfeeding behaviour [111].

Box 7.16 presents the stages through which an individual or communities undergo before there is a change in knowledge and attitudes. The change model also highlights the different communication approaches that need to be applied at each stage. The communication approach needs to be modified when the community/individual moves from one stage to another. Box 7.16 Stages of change and communication approaches [112] Stages of change

Level of knowledge and attitude toward or experience with the new practice

Purpose of appropriate communication interventions to move individual to next stage

Pre-awareness Awareness

Has not heard of new practice Has heard of new practice

Contemplation Intention

Considers the resources and tasks needed to actually perform the practice Intends to try new practice

Trial of new practice

Tries new practice to experience benefits and overcome obstacles

Adoption of new practice

Appreciates benefits and has overcome obstacles during the trial of new practice; adopts practice Decides to continue new practice Believes in new practice and wants to tell others

Provide information Provide more information and begin to focus on persuasion Provide encouragement that practice is “do-able” and introduce role playing, role modeling Focus on appreciating benefits and overcomeing obstacles; introduce negotiation of trying new practice; home visits are very appropriate Reinforce benefits and overcoming obstacles with family and community influentials; provide additional support mothers through home visits and support groups Continue to reinforce and support practice, including praise from influentials

Maintenance Telling others

Continue to reinforce and support practice, including praise from influentials Provide opportunities for practitioners to communicate their messages to other women widely (mass electronic and print media) or within the comm.-unity (comm.unity events and advocacy; interpersonal communication)

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(vi) Enhancing programme coverage In addition, to engaging workers from within the community, other interventions which mobilize and involve communities are also critical in improving child health. Interventions like participatory women’s groups for empowerment and education about maternal health and infant health issues, micro-credit programmes for women, conditional cash transfers to women (in which poor women receive cash transfers with the condition that they obtain certain health services) have found to be effective. Programmes with a strong community outreach component which include home visits to all households, involving the local leaders, programme managers and strong partnerships with the community have also appeared to be beneficial Experience has shown that stronger the community outreach services of a community based programme, it is more likely that such a programme will reach (i) those who need child survival interventions and (ii) those who belong to the lowest wealth quintile. (vii) Monitoring and evaluation Monitoring and evaluation is a critical area to support programme implementation. Designing of programme strategy needs to include systems for monitoring and evaluation of the programme implementation. A number of tools are already available for monitoring progress within the context of BFHI, IMCI and routine health reporting systems in some countries [112] Simple, valid and reliable indicators are crucial for tracking progress and guiding investment to improve nutrition and health during the first two years of life. These indicators have been issued by the WHO / UNICEF / AED / USAID, 2008 for assessing breastfeeding practices and have been valuable in informing programme efforts in many countries. Examples of facility based indicators include – percentage of children less than two years assessed for feeding problems, feeding counseling received by parents of malnourished children, percentage of pregnant women provided breastfeeding counseling in health facilities, percentage of mothers provided breastfeeding counseling post partum. The outcome indicators that can be used for both monitoring and evaluation are outlined in the table below [87] Evaluations need to be carried out periodically and ideally results of evaluation surveys would help to make programme adjustments for improving infant and young child feeding. This will help to maintain the effectiveness of the programme as the scale of implementation expands. The possible process indicators could include the availability of infant and young child feeding counseling, IYCF pre-service education for service providers and frontline workers, worker performance during programme intervention, referral and action etc. On the other hand, process indicators could include information on other indicators to be included are for national actions and adequacy of resources etc.

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Box 7.17 Indicators for monitoring and evaluation of breastfeeding practices Feeding practice

Requires that infants receive

Allows the infant to receive

Does not allow the infant to receive

Exclusive breastfeeding

Breast milk (including milk expressed or from a wet nurse) Breast milk (including milk expressed or from a wet nurse) as the predominant source of nourishment

ORS, drops, syrup (vitamins, minerals, medicines) Certain liquids (water and water-based drinks, fruit juice), ritual fluids and ORS, drops or syrups (vitamins, minerals, medicines) Anything else; any food or liquid including nonhuman milk and formula

Anything else

Predominant breastfeeding

Complementary feeding(a)

Breastfeeding

Bottle feeding

(a)

Breast milk (including milk expressed or from a wet nurse) and solid or semi-solid foods Breast milk (including milk expressed or from a wet nurse) Any liquid (including breast milk or semisolid food from a bottle with a nipple/teat)

Anything else (in particular, non-human milk, food based fluids) NA

Anything else; any food or liquid including non

NA

Anything else; any food or liquid including non

NA

The term complementary feeding, reserved to describe appropriate feeding in breast fed children 6 months of age or beyond, is no longer used in the indicators to assess infant and young child feeding practices. The previously used indicator “Timely complementary feeding rate” which combined continued breastfeeding with consumption of solid, semisolid or soft foods, was difficult to interpret. This indicator has therefore been replaced by the indicator “Introduction of solid, semi-solid or soft foods”, which is a measure of a single feeding practice. Nevertheless the term complementary feeding is still very useful to describe appropriate feeding practices in breastfed children 6–23 months of age and will continue to be used in programmatic efforts to improve infant and young child feeding as guided by the Global Strategy on Infant and Young Child Feeding. The timely complementary feeding rate can also be calculated using the data generated for measuring the new and updated indicators [4].

Monitoring and evaluation when integrated and built into the existing health programmes and system is more sustainable. Some ways in which monitoring and evaluation could be built into the system include ●

●

●

Recording information on infant and young child feeding practices in the mother child health cards that are kept by caregivers; Inclusion of infant and young child feeding indicators into the routine monitoring system; Incorporation of key infant and young child feeding activities in

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the monitoring system of other sectors (i.e., maternity entitlements in the Labour Ministry, adoption and compliance with the code and reference to Codex standards in food laws regulating trade and industry). The most important use of the monitoring and evaluation process is to ensure that the service providers who are stakeholders are fully involved in the analysis and/or interpretation of emerging information. Such efforts are critical for ongoing system strengthening and serve as a catalyst for improving programmes, workers skills and performance [112]. (viii) Programme management and working towards sustainability Programme management involves periodic assessment of barriers and revising programme strategy to address the barriers and improve the programme outcomes. It is crucial that with reference to breastfeeding programmes the assessment of programme barriers is undertaken at all levels through a good monitoring system i.e., from national right down to the district and village levels. Feedback at all levels from periodic assessments is essential for improving the programme implementation and interventions. Most developing countries are progressing towards this approach and are going through a process of decentralization with increasing responsibility for planning, implementation and evaluation being delegated to lower levels of the health-care system. This principle applies towards building long term sustainability into the various health programmes including promoting infant and young child feeding. However, building local capacity at the local level requires time, resources and patience [89].

7.5

Programme design – community based

7.5.1

Significance of community-based programmme approaches

For sustained improvements in child health, experience has shown that community-based programes are beneficial. There is growing scientific evidence that community based programmes can improve the health of children at scale at an affordable cost. This means that even the most impoverished societies have a powerful incentive to expand community based programs; however, high-quality field research and monitoring of mortality impact are fundamental. This will ensure progress in improving the health of children and the achievement of the Millennium Development Goal for children in the future. Community based systems can make its greatest contribution when

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health systems are weak and under-5 mortality is high. When health systems are strong (as in case of many developed countries), strengthening community based systems may not provide additional health benefits. In many developing countries where health systems are often weak, establishing a strong community based programme would prove to be beneficial. In addition, areas where primary health care facilities are burdened with more patients (than can be adequately managed at the facilities), strong community based activities can also support to reduce the patient load, thereby actually saving money for the health system as well as for the patient and their families. In other settings, community based programmes can also increase the utilization of services, making health care system more efficient and effective. To build strong community based activities, it is important to engage communities in programmes, build upon their trust and develop strong community participation and partnerships. Community-based services can be integrated at all levels of health services. It is crucial that community based programme models are designed with a vision of scale, as all too often they remain small-scale NGO-supported initiatives without national Government ownership that are never taken to scale and are not sustained beyond the life of the NGO project. Their design is often not amenable to scale-up and too resource and support intensive to be taken to scale. The processes required to develop and maintain effective partnerships between health intervention delivery systems and communities vary greatly, mainly, because of the marked variations in conditions encountered from one locale to another. Populations with the most limited access to formal health care are typically in the most un-reached areas/socially excluded areas where mortality is the highest and impact can be greatest. Training community health workers, promoting partnerships between communities and health programs, drawing on local resources for program support, and promoting community and women’s empowerment were common features of successful community based programs.

7.5.2

Community-based programme and IYCF

(1) Community-based approaches are particularly relevant for interventions which involve behavior change at the household level. Examples of such interventions are improving neonatal care practices, infant feeding practices, etc, all of which have great importance for child health. Many of these behaviors are based on ingrained cultural beliefs and practices, and health systems have been ineffective in changing them.

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Behaviour change communication interventions need active community involvement (in planning, implementation and assessment of the programme). Successful promotion of these kinds of behaviors requires stronger linkages between health systems and community than ‘simple’ outreach activities as is in the case of immunization or vitamin A coverage. (2) Promoting community empowerment can increase intervention effectiveness. Activities through which communities can contribute to improving effectiveness of child health interventions and at the same time can be sustained include ● Involving local leadership in mobilizing a partnership between communities and programme managers at the local level for planning and managing program activities and resources. ● Clarifying respective value systems to help both health care workers and community members develop joint understanding and respect as they work together for benefits that are effective and equitable. ● Involving women’s groups to provide peer-to-peer education and home-based care while also involving men and mothers-in-law in creative ways to encourage community action for healthy behavior and appropriate health care utilization. ● Adapting the health delivery system to local realities and culture, with integration of interventions and practices for maximizing acceptability and efficiency. ● Enabling communities to collaborate with the health system not just in the initial stages of implementation but in a continuing relationship so that families feel ownership of the process and together they can establish a long-term partnership for robust and sustainable improvements in child health. Registering vital events registration, identifying newborns who need to be enrolled in community based services and programs, and tracking under5 mortality rates at the local level. Community-based approaches necessary for facilitating the effectiveness of community-based programmes are summarized below (i) Trust in the health system – It is essential that the community trusts, respects and has confidence in the local health and community based system. Trust, respect, and confidence arise when people believe that the health system and community based system provides quality services and has basic medicines and supplies to solve some commonly occurring problems and health concerns. (ii) Strong outreach system – Some of the interventions required to improve child health and nutrition require technical expertise and equipments not available within the community. Health systems need

210

(iii)

(iv)

(v)

(vi)

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to provide these services for which coverage outreach sites readily available to the populations are required. These outreach service delivery points provide a key opportunity for strengthening other community-based services. Experience has shown that stronger the outreach services of a community based programme, more likely the programme will reach those who really need them, especially those in the lowest wealth quintile. Programmes which are facility based with poor outreach services are inherently inequitable for 2 main reasons (i) utilization of health facilities decreases exponentially as one’s distance from the facility increases (ii) health facility utilization involves pro-active decision that involves significant costs in terms of time, transport fees and other associated costs. As a result, the poorest household (those who are in greatest need of services) are less likely to use the facility based services. With a strong community outreach service component, these barriers are diminished. From this perspective, the community based approaches which provide services to all households can have a strongly positive equity impact. Community-based workers – In order to implement interventions and to reach out to populations who need these services appropriately trained community based workers are an essential element of the programme. These workers can be employed by the health / community based system or other local Government structure or can be volunteers. If they are unpaid volunteers, they must have a limited set of tasks and not be expected to work more than a few hours a week; otherwise they tend to abandon their responsibilities. Needs-based interventions – Programme interventions targeted at child health and nutrition should be designed such that they (i) address the priority health needs of children in a population and (ii) reach out to those at greatest risk. This is because such children in such populations are at a higher risk of death. For e.g. if poor infant feeding practices is one of the leading cause of malnutrition among children less than 2 years, then promoting optimal infant and young child feeding practices should be prioritized in the programme interventions from both the public health point of view as well as from equity point of view. Increasing programme coverage – A method of developing and maintaining contact with all homes and mothers is necessary in order to identify pregnant women and young children, to provide services in the home when possible, and to identify those in need of services which cannot be provided in the home. Routine systematic visitation of all homes by community-based workers is a common approach to achieving this. Maintaining a register of vital events, including births

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and deaths, and a register of all families facilitates tracking of children to ensure that all are reached with program services. Emphasizing expanded coverage of interventions that require a trained provider near the home to respond to serious and urgent childhood issues, improving childhood nutrition through promotion of exclusive breastfeeding and appropriate complementary feeding (for which there are available proven interventions is important). Though these interventions have great potential for reducing mortality, but in reality they have particularly low coverage in priority countries. Programme coverage can be improved through health programmes by making additional efforts to reach the unreached i.e., (i) the highly vulnerable groups (children <3 years; pregnant and lactating mothers); and (ii) reaching out to the geographically remote areas, (iii) the tribals, (iv) the socially excluded groups and (iv) the minorities. (3) Referral care – Finally, high-quality curative and referral care, which can address the local health care needs and problems like basic hospital care, lends credibility to the community-based work and the workers that provide it [98].

7.6

Large scale community-based programmes – lessons learned

Quinn et al (2005) examined the strategies and successes of large-scale community-level, communication-centred programmes designed to improve breastfeeding practices rapidly at scale in Bolivia, Ghana, and Madagascar through the Linkages project (1996 to 2006) using a multifaceted, communication-focused approach, tailored specifically to increase the timely initiation of breastfeeding (TIBF) – primarily among mothers with young infants in resource-poor settings. In each country programme, an overall monitoring and evaluation system was established to provide data to track progress and use in programme management [95]. Over 3–4 years, early breastfeeding initiation (within 1 hour of birth) increased from 56% to 74% (P < 0.001) in Bolivia, 32% to 40% (P < 0.05) in Ghana and 34% to 78% (P < 0.001) in Madagascar. Marked increases in exclusive breastfeeding of infants 0 to 6 months of age were also documented: from 54% to 65% (P < 0.001) in Bolivia, 68% to 79% (P <0.001) in Ghana, and 46% to 68% (P < 0.001) in Madagascar. In Ghana and Madagascar, significant results were seen within 1 year of community interventions. The strategies of these successful programmes were analysed to have been built on four core components: partnerships, training, behaviour change communication (BCC), and community activities.

212 ●

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●

●

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Partnership-building – collaborating with partners and carrying out participatory programme design, implementation, programme monitoring and evaluating activities. The partners were national government health workers collaborating with partner nongovernmental organizations (in Bolivia), local radio announcers, journalists, university staff, members of the Food and Nutrition Security Network (Ghana). The government and other local groups, including donors were assisted to disseminate nutrition messages and share experiences. Capacity-building – In all these three countries, training materials were developed to meet the specific, short-term, and practical needs of service providers and community volunteers. Apart from strengthening the counseling skills of the service providers, frontline workers and community volunteers, negotiation skills necessary to convince mothers to change their infant-feeding behaviours were also fostered. Behaviour change communication (BCC) – The intention of BCC was to change individual behaviour while educating and engaging fathers and/or grandmothers, who influence the mother’s choices. “Targeted, concise messages” were developed to promote “do-able” actions, and “edutainment” strategies dominated. These messages were disseminated through the mass media or at the local level. In some countries, the mass media was used to complement BCC change in the community level. Community activities – Women were reached through small- and large-group activities, one-on-one counselling in homes and at local health posts, breastfeeding promotion songs performed by women’s groups and musical troupes, and community mobilization events such as local theatre, health fairs, and festivals celebrating breastfeeding and child health days. Celebrations of success through village festivals, healthy baby contests, and “nutrition certificates” for families with optimally fed babies were drawn upon to fuel enthusiasm in the communities. A key communication strategy highlighted here is the value of peer group support and interaction.

It is evident that a mix of activities, such as interpersonal counselling, community mobilization, and mass media, contributes to behaviour change when these activities deliver consistent messages. Further, linking health workers and community health promoters (particularly for referral) are useful strategies for ensuring that mothers receive consistent messages. In addition to harmonizing approaches and messages through partnership and community involvement, it is also important to have a positive policy environment for exclusive breastfeeding promotion for improving nutrition.

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WHO/UNICEF/AED/USAID (2008) also conducted a ‘lesson learnt’ review of large scale community-based breastfeeding programmes in ten countries with diversity in the programmatic approaches and different rates of exclusive breastfeeding: Benin, Bolivia, Cambodia, Ethiopia, Ghana, Honduras, India, Madagascar, Mali and Nepal. These were large scale IYCF programmes (coverage of >1 million). In these countries, programme implementation was made effective by employing a combination of the following approaches: ●

●

●

●

●

●

●

●

●

●

Integrating the IYCF interventions with the child survival, reproductive health or maternal and child health initiatives. Implementing a range of programme interventions which included facility based to community owned and led initiatives through multiple partners. Creating strong political commitment, a well developed advocacy framework, clear programme implementation plan in collaboration with the state and district level stakeholders for implementation and scale-up. Creating/strengthening linkages with the health systems, communitybased services and also engaging communities. Developing and implementing a robust communication strategy with a clear-cut vision (engaging opinion leaders, policy makers and programme planners), simple, consistent, targeted messages which were delivered and reinforced through multiple and well-coordinated systems/platforms. Expanding nutrition contacts to multiple contact points during programme delivery with the help of community health workers and volunteers. Building capacity of service providers and nutritional promoters in inter personal communication (IPC) through single or cascade trainings and conducted periodic performance monitoring. Implementing proven interventions at the community level by local trained and well-supervised health workers so that coverage, impact, and equity were favorably affected. Mobilizing and engaging communities as well as supporting the building of strong community partnerships with the health delivery systems in improving the health of children. Monitoring, measuring progress and evaluating the interventions to identify successful and unsuccessful steps and making appropriate programme adjustments.

The story of their vision, innovations in programme delivery, partnerships, trials, errors and programmatic outcomes indicate that (1) The community offers indispensable resources for breastfeeding promotion

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and support, and these resources need continual mentoring and encouragement; (2) Multiple programme frameworks offer opportunities for community-based breastfeeding promotion and support; (3) Breastfeeding practices can change over a relatively short period and need continued reinforcement to be sustained; (4) Effective communication and advocacy are vital to set policy priorities, influence community norms, and improve household practices; (5) More attention needs to be given during training to interpersonal counselling skills; (6) Partnerships, leadership, proof of concept, and resources, facilitate programme scale up; and (7) Monitoring and evaluation is critical to measure progress, identify successful and unsuccessful strategies, and make appropriate programmes adjustments [87].

Conclusion It is a well-known fact that the 0–2 years period in a child’s life is critical for preventing malnutrition. Many developing countries are struggling to resolve this issue. Ensuring optimal infant and young child feeding during this period has its significant implications in reducing infant morbidity and mortality; but these practices need to be accelerated to achieve universal coverage before a noticeable improvement is seen in these indicators. To accomplish this, optimizing and improving breastfeeding practices has been identified to be the single most crucial indicator for improving child survival. At present, there is sufficient scientific evidence on effective interventions to improve breastfeeding indicators and practical solutions on how to incorporate the proven interventions into a comprehensive approach for scale-up. Leveraging scientific knowledge and previous programming wisdom along with a strong political will; national and local leadership; and efficient governance will make programme delivery more efficient in order to make IYCF programmes effective. Such programming is feasible when adequate policies and regulatory frameworks are backed by strong management and functioning service delivery systems, and sufficient resources – it is also imperative to achieve a high coverage of service delivery and to effect widespread change in community and household behaviours and practices. Over the past 5–10 years, 16 countries have recorded gains of 20 percentage points or more in exclusive breastfeeding rates. Many of these countries face serious development challenges as well as emergency situations. Experience has shown that the implementation of large scale programmes in these countries was based on national policies and often guided by the WHO–UNICEF Global Strategy for Infant and Young Child feeding. The country programmes included the adoption and

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implementation of national legislation on the International Code of marketing of breast-milk substitutes and subsequent World Health Assembly resolutions, as well as maternity protection for working women. Further actions included ensuring that breastfeeding was initiated in maternity facilities (and that no infant formulae were given in facilities). Community based strategies like strengthening of local capacity, building health worker capacity to offer counselling on infant and young child feeding, and mother-to-mother support groups in the community helped to provide integrated and effective package of key interventions. Further partnerships of health systems with communities were promoted for achieving sustainable health outcomes along with increasing the demand for health and nutrition, services at community level. These actions were also accompanied by communication strategies to promote breastfeeding using multiple channels and messages tailored to the local context [3].

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(2008). Maternal and child under nutrition: effective action at national level. The Lancet 371, no. 9611, pp. 510–526. ESTRIK PV (1995). Care and caregivers. Food and Nutrition Bulletin 16, no. 4, pp. 378–388. HURLEY W (2003). Lactation Biology. Department of Animal Sciences, University of Illinois, Urbana–Champaign: http://classes.aces.uiuc.edu/AnSci308/. JELLIFFE DB and JELLIFFE EFP (1978). The volume and composition of human milk in poorly nourished communities. A review. American Journal of Clinical Nutrition 31, pp. 492–497. American Academy of Pediatrics (AAP, 2005). AAP policy statement of breastfeeding and the use of human milk. Pediatrics 115, no. 2, pp. 496–506. RIORDAN J and AUERBACH KG (eds) (1993). Breastfeeding and Human Lactation, 2nd ed. Boston: Jones and Bartlett. SALAZAR H , TOBON H (1974). Morphologic changes of the mammary gland during development, pregnancy and lactation. In. Josimovich JB, Reynolds M, Cobo E (eds). Lactogenic Hormones, Fetal Nutrition, and Lactation. New York: John Wiley and Sons, pp. 221–77. HARTMANN PE , OWENS RA , COX DB and KENT JC (1996). Establishing lactation. Breast development and control of milk synthesis. Food and Nutrition Bulletin 17, no. 4, pp. 292–301. NEVILLE MC and MORTON J (2001). Physiology and Endocrine Changes Underlying Human Lactogenesis II. Symposium: Human Lactogenesis II: Mechanisms, Determinants and Consequences. Journal of Nutrition 131, pp. 3005S–3008S. MCNEILLY AS, GLASIER A , and HOWIE PW (1985). Endocrine control of lactational infertility. Maternal Nutrition and Lactational Infertility. Dobbing J (ed.). New York: Raven Press. HAYWARD AR (1983). The immunology of breast milk. Lactation: Physiology, Nutrition and Breast-Feeding. NEVILLE MC and NEIFERT MA (eds). New York: Plenum Press, pp. 249–272. TINDAL JS , KNAGGS GS , HART IC , BLAKE LA (1978). Release of growth hormone in lactating and non-lactating goats in relation to behaviour, stages of sleep, electroencephalograms, environmental stimuli and levels of prolactin, insulin, glucose and free fatty acids in the circulation. Journal of Endocrinology 76, no. 2, pp. 333–346. EDMOND KM, ZANDOH C, QUIGLEY MA, AMENGA -ETEGO S, OWUSU-AGYEI S, and KIRKWOOD BR (2006). Delayed breastfeeding initiation increases risk of neonatal mortality. Pediatrics 117, pp. 380–386. KULSKI JK , SMITH M, HARTMANN PE (1981). Normal and caesarean section delivery and the initiation of lactation in women. Australian Journal of Experimental Biology and Medical Science 59, pp. 405–412. MARTIN RH , GLASS MR , CHAPMAN C, WILSON GD , WOODS KL (1980). Human alphalactalbumin and hormonal factors in pregnancy and lactation. Clin Endocrinol 13, pp. 223–230. HARFOUCHE JK (1970). The importance of breast-feeding. Journal of Tropical Pediatrics 16, no. 3, pp. 133–169. NANTEL AJ (2002). Clostridium Botulinum. International Programme on Chemical Safety Poisons Information Monograph 858 Bacteria. WHO, pp. 1–32. KRELL R (1996). Value added products from bee-keeping. FAO Agricultural Services Bulletin no. 124: http://www.fao.org/docrep/w0076E/w0076e00.htm/

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(1978). Anti-microbial factors in human milk. Studies of concentration and transfer to the infant during the early stages of lactation. Acta Pediatrica Scandanavia 271, pp. S1–S20. DONANGELO CM , TRUGO NM , KOURY JC , BARRETO SILVA MI , FREITAS LA , FELDHEIM W, BARTH C (1989). Iron, zinc, folate and vitamin B 12 nutritional status and milk composition of low-income Brazilian mothers. Eur J Clin Nutr 43, no. 4, pp. 253 –266. LAMOUNIER JA , DANELLUZZI JC, VANNUCHI H (1989). Zinc concentrations in human milk during lactation: a 6-month longitudinal study in southern Brazil. Journal of Tropical Pediatrics 35, pp. 31–34. NAGRA SA . Longitudinal study in biochemical composition of human milk during the first year of lactation Journal of Tropical Pediatrics 35, pp. 126–128. LÖNNERDAL B, FORSUM E and HAMBRAEUS L (1976a). A longitudinal study of the protein, nitrogen and lactose content of human milk from Swedish wellnourished mothers. American Journal of Clinical Nutrition 29, no. 10, pp. 1127– 1133. LÖNNERDAL B , FORSUM E , GEBRE - MEDHIN M, HAMBRAEUS L (1976b). Breast milk composition in Ethiopian and Swedish mothers. II. Lactose, nitrogen and protein contents. American Journal of Clinical Nutrition 29, no. 10, pp. 1134–1141. NEVILLE MC , ALLEN JC , and WATTERS C (1991). The mechanisms of milk secretion. In: Lactation – Physiology, Nutrition and Breast-Feeding. NEVILLE MC and NIEFERT MR, eds (1983) NEVILLE MC , ALLEN JC , ARCHER P, SEACAT J , CASEY C, LUTES V , RASBACH J . AND NEIFERT M . STUDIES IN HUMAN LACTATION : Milk volume and nutrient composition during weaning and lactogenesis. American Journal of Clinical Nutrition 54, pp. 81–93. READ LC , UPTON FM , FRANCIS GL, WALLACE JC, DAHLENBERG GW and BALLARD FJ (1984). Changes in the growth-promoting activity of milk during lactation. Pediatric Research 18, no. 2, pp. 133–139. SOMMERBURG O , MEISSNER K , NELLE M , LENHARTZ H , LEICHSENRING M (2000). Carotenoid supply in breast fed and formula fed neonates. European Journal of Pediatrics 159, pp. 86–90. GARG M , THIRUPURAM S , SAHA K (1988). Colostrum composition, maternal diet and nutrition in North India. Journal of Tropical Pediatrics 34, pp. 79–87. CHANG SJ (1990). Anti-microbial proteins of maternal and cord sera and human milk in relation to maternal nutritional status. American Journal of Clinical Nutrition 51, pp. 183–187. HOUGHTON MR , GRACEY M, BURKE V , BOTTRELL C and SPARGO RM (1985). Breast milk lactoferrin levels in relation to maternal nutritional status. Journal of Pediatric Gastroenterology and Nutrition 4, pp. 230–233. MIRANDA R, SARAVIA NG, ACKERMAN R, MURPHY N, BERMAN S and MCMURRAY DN (1983). Effect of maternal nutritional status on immunological substances in human colostrum and milk. American Journal of Clinical Nutrition 37, pp. 632–640. AHMED L , NAZRUL ISLAM SK , KHAN MNI , HUQUE S and AHSANB M (2004). Antioxidant Micronutrient Profile (Vitamin E, C, A, Copper, Zinc and Iron) of Colostrum: Association with Maternal Characteristics. Journal of Tropical Pediatrics 50, no. 6, pp. 357–358. SAHA K and GARG M (1999). Studies on Colostrum – Nutrients and Immunologic Factors: http://www.nutritionfoundationin.org/ARCHIVES/OCT91C.HTM JENSEN RG , HAGERTY MM and MCMAHON KE (1978). Lipids of human milk and infant formulas. A Review. American Journal of Clinical Nutrition 31, pp. 990.

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Complementary feeding of infants and young children

8

Complementary feeding of infants and young children Veenu Seth and Aashima Garg

Veenu Seth, MSc, PhD, is an Associate Professor at the Department of Food and Nutrition, Lady Irwin College, University of Delhi. Dr. Seth has extensive research experience in the area of infant and young child feeding, specifically on complementary feeding. Aashima Garg is a Nutrition Specialist with UNICEF (India Country Office). Her PhD research is in the area of improving complementary feeding practices in rural Uttar Pradesh, India.

8.1

Complementary feeding practices – a critical determinant of undernutrition in young children

Appropriate infant and young child feeding practices constitute a critical determinant of child nutrition, survival, growth and development. The importance of nutrition as a foundation for optimal health is undisputable. On the other hand, poor nutrition leads to ill health and ill health can contribute to further deterioration of nutritional status. These effects are most evident in infants and young children, who bear the brunt of the onset of malnutrition [1]. Childhood malnutrition is a significant health problem in developing countries and one of the main causes of infant and young child morbidity and mortality [2]. Recent estimates on status of undernutrition in developing countries [3] report 112 million and 178 million children under 5 years to be underweight and stunted, respectively A vast majority of these malnourished children are from South-Central Asia and Sub-Saharan Africa. Of these, 90% (160 million) live in just 36 countries of the world, representing almost half (46%) of the 348 million children from these countries. India is home to 40% of the World’s malnourished children [4], where approximately about 50% of children under the age of 3 years are still malnourished and this figure has only marginally changed over the past almost 2 decades [5–8]. It has been documented that poor fetal growth or

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stunting in the first 2 years of life leads to irreversible damage, including shorter adult height, lower attained schooling, reduced adult income and decreased offspring birth weight [9]. In developing countries, the critical period when growth faltering occurs often with long term adverse consequences, has been shown to be around 6 months to 2 years, with the start of undernutrition at 6 months and peak between 18 and 24 months. This period of progressive increase in undernutrition coincides with inadequate breast milk to meet the growing child’s nutritional needs and concurrent unsatisfactory and inadequate introduction of semi-solid foods other than breast milk, or complementary foods [10].The complementary foods, when delivered inappropriately, results in growth retardation from mid infancy onwards. Scientific research identifies sub-optimal complementary feeding is as a significant determinant of stunting and urges to focus improvements in feeding frequency and energy density of complementary foods fed to infants and young children [3]. For India, this pattern of onset of malnutrition in infants and young children has been reported in all the three national surveys of 1992–93 [5], 1997–98 [6] and in 2005–06 [8]. Figure 8.1 presents the data of national survey of 2005–06 [8]. This period of complementary feeding is especially vulnerable, as infants are just learning to eat and must be fed appropriate and adequate foods, patiently and frequently, while continuing with breast milk. The nutrition provided in this phase of life, lays the foundation of health and healthy feeding habits. Stun ted U nde rw e igh t

70

% C h ildre n

60 50 40 30 20 10 0 < 6m

6-8m

9-11m 12-17 m 18-23 m 24-35 m 36-47 m 36-47 m A g e in m on ths

8.1 Pattern of onset of malnutrition in infants and young children in India [8].

This critical period between 6 and 24 months of age has thus, rightly been described as the ‘window of opportunity’ for prevention of malnutrition, since the extent of undernutrition reaches its maximum level during this early and critical phase of life. It is well known that poor nutrition during this period contributes to significant morbidity and

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mortality, some of the long term consequences being reduced work capacity, impaired intellectual performance and increased risk of chronic diseases. Increase in number of brain cells is almost complete before birth, but most of the neuronal connections are established before the age of 3 years. Therefore if malnutrition persists during this period, consequences on physical growth and mental development can be long term and not amenable to management. The rate of growth, at this stage, is incomparable to that in later life. Birth weight doubles by 6 months and triples by 1 year with body length increasing by 1.5 times by first year. Most of the organs of the body also grow rapidly, both structurally and functionally, during the early years with a slower growth rate later on. Most of the growth in the nervous system and brain is complete in the first 2 years of life. Thus to achieve optimum growth and development, there is an increased demand of energy and essential nutrients. Breastfeeding alone is not able to meet the increased requirements for nutrients and needs to be complemented with feeding of food other than breast milk. This additional food is referred as “complementary food”. Adequate complementary feeding from 6 months, with continued breastfeeding up to 2 years and beyond, is important for sustaining growth and development of the infant. Appropriate complementary feeding helps to promote growth, prevent stunting, and increase a child’s chances for a healthy, productive life as an adult. The quality of infant and young child feeding, comprising breastfeeding and complementary feeding, thus becomes fundamental for improved nutritional status, achieving optimal growth and development.

8.2

Optimal infant and young child feeding

The global strategy for Infant and Young Child Feeding (IYCF), developed by WHO/UNICEF [10], provides a comprehensive framework for promoting appropriate feeding practices and reducing malnutrition. The strategy has been adopted by many developing countries. The Indian National Guidelines on Infant and Young Child Feeding of the Ministry of Women and Child Development, Government of India [11] conform to the global recommendations, keeping in mind, the country’s socioeconomic and cultural framework, and existing feeding status of infants and young children. The strategy recommends exclusive breastfeeding for infants for the first 6 months of life and there after, safe and adequate complementary foods, while breastfeeding is continued for 2 years at least. The transition from exclusive breastfeeding to complementary feeding covers the period from 6 months to 2 years, the vulnerable period, when growth faltering begins in many children. Pioneering studies carried out in India, in the sixties and seventies clearly showed that exclusive breastfeeding for the first six months and continued

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breastfeeding thereafter, coupled with adequate and appropriate foods available at home, promotes growth and is associated with lowering morbidity. According to the Lancet [12] Child Survival Series, exclusive breastfeeding for the first 6 months and continued breastfeeding along with complementary feeding for the next 6 months could cut down all child deaths by 13% and prove as the single most effective prevention intervention. Adequate complementary feeding between 6 and 24 months could prevent an additional 6% of all such deaths. The recent Lancet Maternal and Undernutrition Series [13] has reported revised mortality reduction attributable to optimization of infant feeding practices with improved breastfeeding practices contributing to the reduction of about 8% and appropriate complementary feeding strategies contributing to mortality reduction of another 1%. The difference in the rates of mortality reduction in the two Lancet series have been due to the difference in the outcome indicator, which in 2003 series was increase in weight-for-age Z scores (underweight) and in 2008 series was height-for-age Z scores (stunting). This implies that extending coverage of exclusive breastfeeding to at least 2 years and introduction of appropriate complementary feeding at 6 months could save over 450,000 child deaths each year in India [14]. Thus, identifying approaches to reduce the prevalence of malnutrition particularly in the vulnerable first 2 years of life and focusing on infant feeding practices, is a priority for developing countries, appropriate Infant and Young Child Feeding (IYCF) could improve child survival, growth and development, with health benefits extending into adult years.

8.3

Complementary feeding – issues and guidelines

Complementary feeding refers to giving foods, in addition to breast milk or breast milk substitutes, in case of non breastfed infants. These complementary foods, of varying texture, locally prepared or manufactured, complement breast milk or infant formula, when either becomes insufficient to meet the needs of the baby. Historically, the period of transition from only breast milk to complementary foods for the infants has been referred to as weaning period and the foods other than breast milk are described as weaning foods [15]. The terminology “weaning” is discouraged since it is viewed to imply termination of breastmilk and weaning from breast. The term preferred is “complementary feeding”, i.e. complementing breast milk with introduction of semi-solid food. During the period of complementary feeding, a baby gradually becomes accustomed to eating family foods. By the end of this period,

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usually around 2 years, breast milk is entirely replaced by family foods, although some children may still be breastfed occasionally or allowed to suckle for comfort. The transition from exclusive breastfeeding to family and other foods, typically covering the period from 6 to 18–24 months of age, is critical, as eating patterns and habits developed in the first two years of life usually continue till later years [16]. Moreover infants during this period of accelerated growth also are increasingly exposed to infections such as diarrhea [17]. If this feeding is inappropriate, as discussed, malnutrition starts to set in many infants. It is not unexpected therefore, that infant and young child feeding has been the focus of attention of scientists and planners since long and Global and National Guidelines have been developed for complementary feeding, besides breastfeeding.

8.4

Initiating complementary feeding

Complementary feeding should be timely, i.e. all infants should start receiving foods in addition to breast milk from 6 months onwards (Box 8.1). It should be adequate, or the nutritional value of complementary foods should meet the nutrition gaps required to be filled in with reduction of breast milk. Foods should be prepared and given in a safe manner, implying that steps are taken to minimize the risk of contamination with pathogens. The food should be given in a way that is appropriate, which involves ensuring that foods are of appropriate texture, given in sufficient quantity and frequency. Box 8.1 Timely introduction of complementary foods Complementary foods should be introduced in infants’ diet when the need for energy and nutrients exceeds what can be provided through exclusive and frequent breastfeeding. WHO (2001) recommends the introduction of semi-solid/soft or solid foods in addition to breastfeeding at completion of 6 months of age, i.e. 180 days. The concept of introducing complementary foods around 6 months of age has been practiced traditionally since ages by the name of “Annaprashan Vidhi” in Hindu community. This ritual marks an infant’s intake of food other than milk. This ceremony is commonly referred to in English as “First Rice”.

The adequacy of complementary feeding depends not only on the availability of a variety of foods in the household, but also on the feeding practices of caregivers. Feeding young infants require active care and stimulation, where the caregiver is responsive to the child cues for hunger and also encourages the child to eat. This is also referred to as active or responsive feeding [1].

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8.5

Adequacy and frequency of complementary feeding

Access to adequate complementary foods is a necessary condition for improving infant and young child feeding. Complementary foods are needed to fill the gap between the total nutritional needs of the growing child and nutrients provided by breast milk. An energy gap which starts at 6 months and increases as the child grows (Table 8.1) can be minimized by gradually increasing the energy density of complementary foods with the age of child. Besides energy, gaps exist for other nutrients also, especially iron, zinc, vitamins A and C [18]. To meet the increased nutritional demands, WHO [19] recommends that infants start receiving complementary foods at 6 months of age in addition to breast milk/milk substitute, initially 2–3 times a day between 6 and 8 months, increasing to 3–4 times daily between 9 and 11 months, and 12–24 months with additional nutritious snacks offered 1–2 times per day, as desired. Table 8.1 Energy needs from complementary foods in infants and young children [19]

Total energy needs (kcal/day)

Energy from breast milk (kcal/day)

6–8

615

413

202

9–11

686

379

307

12–23

894

346

548

Age (months)

Energy from complementary food (kcal/day)

The amount of milk consumed by exclusively breast fed infants at 6 months ranges between 760 and 775 ml/day, with an energy density ranging from 74 to 67 kcal per 100 ml breast milk [20]. Based on the requirements of energy and other nutrients by infants and young children, the amount of these provided by breast milk, the energy and other nutrients that complementary foods need to provide can be estimated. Due to increased growth velocity during this period leading to age related increased energy and nutrient requirements of the infants and young children, age-specific recommendations for energy and nutrient from complementary foods are presented in Table 8.1 [21].

8.6

Energy and other nutrient intake from complementary foods

8.6.1

Energy intake

The recommended levels of energy intake from complementary foods for infants with average breast milk intake in developing countries are about

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200 kcal/d for infants 6–8 months of age, 300 kcal/d for infants 9–11 months of age, and 550 kcal/d for children 12–23 months of age [22]. The amount of energy required from complementary foods has been estimated by subtracting the amount of energy from breast milk from the age-specific total energy needs of infants and children (Table 8.1). These recommendations have been derived for developing countries on the basis of assuming good maternal nutritional status and adequate breast milk volume and composition. In industrialized countries, these estimates differ somewhat (130, 310 and 580 kcal/d at 6–8, 9–11 and 12–23 months, respectively) because of differences in average breast milk intake. The Indian Recommended Dietary Allowances (RDA) for infants aged 6–12 months give the net energy requirements as 98 kcal/kg body weight of the age group, but does not specify the amount of energy required from complementary foods for this age group [23]. Hence, for practical purpose, the WHO [19] energy requirements are used. To develop general feeding guidelines for children, information on children with low energy intake from breast milk was used, as these provide the most conservative assumptions regarding the minimum desirable number of meals or energy density of complementary foods needed to ensure adequate total energy intake. Based on these estimates, revised recommendations have been formulated. For an average healthy breastfed infant and young child with average energy density from complementary foods of at least 0.8 kcal/g, it is recommended that complementary foods be fed 2–3 times per day at 6–8 months of age, 3–4 times per day at 9–11 months of age, and 3–4times per day at 12–23 months of age [19]. Recommendations also state that older infants and young children should be provided additional nutritious snacks (such as a piece of fruit or bread or chapatti) offered 1–2 times per day, as desired. Snacks are defined as foods eaten between meals, usually self-fed, convenient, and easy to prepare. The calorific value of these snacks could be increased with addition of oil or fat to these. If energy density or amount of food per meal is low, or the child is no longer breastfed, more frequent meals may be required. The previous recommendations [21] for children 12–23 months of age were to feed complementary foods 4–5 times per day. It is currently believed, however, that high meal frequency may lead to excessive displacement of breast milk. For this reason, the revised recommendation limits the number of feedings to a maximum of four, even among children in their second year of life. It is thus important to confirm that energy density of the complementary food is 0.8 kcal/g or higher in this age group, to ensure that young children receive sufficient energy from complementary foods (Table 8.2).

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Table 8.2 Minimum number of complementary feeds/day to provide energy and nutrient needs of young children [19–22] Energy density (kcal/g complementary food)

No. of meals 6–8 months

9–11 months

12–23 months

0.6

3–4

4

5

0.8

3

3

3–4

1.0

2–3

2–3

3

These guidelines are based on theoretical estimates of the number of feedings required, calculated from the energy needs from complementary foods and assuming a gastric capacity of 30g/kg body weight per density and a minimum energy density of complementary foods of 0.8 kcal/g. Infants with low intakes of breast milk would require higher meal frequencies. Also, as indicated in Table 8.2 when energy density of the usual complementary foods is less than 0.8 kcal/g or infants typically consume amounts that are less than the assumed gastric capacity at each meal, meal frequency would again need to be higher than the values shown.

8.6.2

Other macro and micro-nutrient requirements

It is equally important to ensure that infants and young children in addition to their energy requirements meet their protein and other micronutrient requirements from a combination of complementary foods and breast milk. As indicated above, nutrient requirements from complementary foods have been estimated as the difference between infants and young children’s estimated total nutrient needs and the amounts transferred in breast milk to children of different age groups. With regards to fat content of complementary foods, WHO [19] recommends the amount of fat that should be present in complementary foods to assure that fats provide 30–45% of the total dietary energy together from both breast milk and other foods. The recommended protein and other micronutrient intakes from complementary foods were estimated by subtracting the amounts provided by human milk from the recommended nutrient intake for each age group. These have then been further expressed as recommended nutrient densities, which have been calculated by dividing the amount of nutrient required from complementary foods by the amount of energy needed from these foods for each age group [21]. In addition to WHO/UNICEF [21] recommendations on micronutrient densities, a revised vitamin and mineral requirements have been published by WHO/FAO [24]. Table 8.3 gives the recommended protein and micronutrient densities required from complementary foods as given by WHO/ UNICEF 1998 report [21] and WHO 2002 report [24] assuming average breast

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milk intake. As mentioned in case of energy requirements, Indian Recommended Dietary Allowances (RDAs) for infants give the recommended nutrient amounts per kg body weight per day and there are no recommendations available for specific amount required from complementary foods, which again poses a problem in using these RDAs for comparison purpose. The recommended protein, calcium and vitamin A densities are generally met in infants diet consisting of a mixture of cereals and milk or commercial infant formula along with breastfeeding since in developing countries, human milk, commercial infant milk formula, and cow’s milk are good sources of vitamin A. Poor vitamin A status during infancy is generally associated with low intake of milk and vitamin A rich food during infancy and occurrence of infectious diseases. This is the reason why vitamin A supplementation first dose is recommended as per the Government of India Policy to be administered to infants between 6 and 12 months though it is administered at the age of 9 months, along with measles vaccine, for using the contact opportunity of the National Immunization Schedule. As can be seen in the Tables 8.3 and 8.4, the requirements of iron are very high. Infant’s iron needs are acquired from two different sources, prenatal reserves and food sources. Before birth, the fetus accumulates iron in the last trimester of pregnancy. Premature infants have limited reserves that are quickly depleted. Healthy term infants are born with iron stores sufficient for the first 6 months of life. At birth, the total body iron content is approximately 75 mg/kg, twice that of an adult man in relation to weight. During the first 6 months of life, total iron body content increases slightly and exclusive breastfeeding is sufficient to maintain an optimal iron balance. Thereafter, with high growth rate, iron requirement increases substantially (Tables 8.3 and 8.4) The Indian RDA for 6–12 months is 1 mg/kg body weight per day (Table 8.4). After 6 months, an infant Table 8.3 Recommended nutrient densities of complementary food diets as per WHO/ UNICEF 1998 [21] and WHO 2002 [24] values Recommended nutrient densities 6–8 months

Nutrient

WHO/UNICE WHO F 1998 2002 Protein (g/100 kcal) 0.7 Vitamin A (ìg RE/100 kcal)) 5 Vitamin C (mg/100 kcal) 0 Iron (mg/100 kcal) 4.0 Calcium (mg/100 kcal) 125 Niacin (mg/100 kcal) 1.1 Riboflavin (mg/100 kcal) 0.07 Thiamine (mg/100 kcal) 0.04 Folate (ìg/100 kcal) 0 Zinc (mg/100 kcal) 0.8 Vitamin B6 (mg/100 kcal) 0.09

1.0 31 1.5 4.5 105 1.5 0.08 0.08 11 1.6 0.12

9–11 months WHO/UNICEF WHO 1998 2002 0.7 9 0 2.4 78 0.9 0.04 0.04 0 0.5 0.08

1 30 1.7 3 74 1 0.06 0.06 9 1.1 0.08

12–23 months WHO/UNICEF WHO 1998 2002 0.7 17 1.1 0.8 26 0.9 0.05 0.05 0 0.3 0.98

0.9 5 1.5 1 63 0.9 0.06 0.07 21 0.6 0.08

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becomes critically dependent on dietary source of iron, provided through complementary foods. A low amount and/or bioavailability of dietary iron provided through complementary feeding at the age of 6–12 months is one of the important factors contributing to nutritional iron deficiency in infancy. Table 8.4 Indian recommended dietary allowances for infants (6–12 months) and young children (13–24 months) [23] Nutrient

RDA 6–12 months

13–24 months

Protein (g/d)

1.65 g/kg body weight per density

22 g/d

Vitamin A (ìg RE/d) Vitamin C (mg/d) Iron (mg/d) Calcium (mg/d) Niacin (mg/d) Riboflavin (mg/d) Thiamine (mg/d) Folate (ìg/d) Vitamin B6 (mg/d)

350 25 1 mg/kg body wt/d 500 650 ìg/kg body wt/d 60 ìg/kg body wt/d 50 ìg/kg body wt/d 25 0.4

400 40 12 400 8 0.7 0.6 30 0.9

Box 8.2 Problem nutrients in complementary feeding diets As per WHO/UNICEF report 1998 [21], “problem nutrients” are defined as those for which there is greatest discrepancy between their content in complementary foods and the estimated amount required by the infant. They can be identified by comparing the estimates of desirable nutrient densities of complementary foods with actual densities of these nutrients in the diets of breastfed children in various populations. Table 8.6 gives the reported nutrient densities of complementary food diets consumed by infants as per different age groups from 4 developing countries: Bangladesh, Ghana, Guatemala and Peru. On comparing the nutrient densities of complementary foods diets consumed by infants in Table 8.5 with the desirable nutrient densities of complementary foods as recommended by WHO/UNICEF (1998) [21] and WHO (2002) [24] in Table 8.3, iron, zinc, vitamin B6 and vitamin A are problem nutrients in complementary feeding diets of developing countries. The same findings have also been reported by studies in other developing countries [25–27], signifying the urgent need to focus on nutrition programming for addressing the deficiencies of iron, zinc, vitamin A and vitamin B6 in developing countries.

8.7

Causes of faulty complementary feeding practices

Undernutrition in children is not simply the outcome of food insecurity but of inappropriate feeding practices, along with poor care practices, lack of safe drinking water and sanitation, resultant infections and mostly poor access to health care services.

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Table 8.5 Nutrient densities of complementary food diets consumed by infants in developing countries Nutrients Age group No. of infants Protein (g/100 kcal) Calcium (mg/100 kcal) Iron (mg/100 kcal) Vitamin C (mg/100 kcal) Vitamin A (RE/100 kcal) Zinc (mg/100 kcal) Vitamin B6 (mg/100 kcal) Age group No. of infants Protein (g/100 kcal) Calcium (mg/100 kcal) Iron (mg/100 kcal) Vitamin C (mg/100 kcal) Vitamin A (RE/100 kcal) Zinc (mg/100 kcal) Vitamin B6 (mg/100 kcal)

Bangladesh(a) 6–8 months 50 1.9 16 0.4 0.00 0 0.2 0.02 9–11 months 66 2.5 20 0.4 0.3 1 0.3 0.03

Ghana(b)

Guatemala(c)

Peru(d)

207 3.3 35 1.2 0.02 7 0.6 0

194 2.2 27 0.5 2.30 87 0.4 0.05

107 2.6 19 0.4 2.30 35 0.4 0

171 3.1 40 1.3 0.9 9 0.6 0

148 2.7 37 0.6 2.4 62 0.4 0.07

99 2.6 27 0.4 1.1 29 0.4 0

Kimmons et al 2005 [25] Lartey et al 1999 [28] (c) Brown et al 2000 [29] (d) Creed de Kanashiro et al 1990 [30] (a)

(b)

Inappropriate feeding practices are often a greater determinant of inadequate intakes and malnutrition, than the availability of foods in the households. Factors such as lack of awareness and knowledge about feeding amount, frequency and type of food contributes significantly to the poor nutritional status among children, even in families where adults meet their daily requirements [2, 31] . For example, in some cases complementary foods are introduced earlier than is desirable, in other cases their introduction is inappropriately delayed. The frequency and amounts of the foods that are offered may be less than required for normal growth, or their consistency or energy density may by inappropriate in relation to the child’s needs. Further, reports on prevalence of specific micronutrient deficiencies in early childhood suggests that the specific micronutrients content of these foods is either inadequate or nutrient absorption is impaired by other components of these foods. Frequent microbial contamination of complementary foods and the associated high rates of diarrhoeal disease indicate a need for introduction of measures for improved food safety. Finally, responsive feeding, maternal encouragement to eat, and other psychosocial aspects of care during feeding which again arise due to time constraints of mother and other caretakers and is important for ensuring adequate food and nutrient intake

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of the child, are generally not addressed [32]. Box 8.3 discusses the findings of a formative study on assessing complementary feeding practices from India. Box 8.3 Complementary feeding – a challenge to be addressed in rural Uttar Pradesh, India [34] In a formative study conducted in 6 villages of District Ghaziabad, Uttar Pradesh, India, it was observed that of the total sample only 6% infants were exclusively breastfed till 6 months of age and similarly only 6% were introduced semisolid foods along with breastfeeding at completion of 180 days of age. The age of introduction of complementary foods varied as per the family belief and mothers’ breast milk secretion. With regards to frequency of feeding complementary foods, majority (48%) of the mothers reported feeding 1–2 times/day, with only 16% and 5% infants in the age group of 6–8 and 9–12 months receiving recommended frequency of 2–3 t i m e s / d a y a n d 3 – 4 t i m e s / d a y, r e s p e c t i v e l y. T h e c o n s i s t e n c y o f complementary food fed was either very thin like pulse water, fruit juices etc, or solids like roti 1 , biscuits etc. Lack of awareness, ignorance and mothers’ lack of motivation emerged as prime factors responsible for these faulty feeding practices. The energy and nutrient intake from complementary food suggested monotony and inadequacy in diets fed to infants between 6 and 12 months of age, with no significant difference observed between the mean nutrient intake of 6–8 and 9– 12 months age group. Iron density from complementary food was found to be sub-optimal for all the three age groups, though protein and calcium densities were high when compared to standards [22]. Food group analysis showed that consumption of pulses, green leafy vegetable and other vegetables and fruits though present in adults’ diets but didn’t find place in infants’ diet due to age old beliefs and ignorance. The prevalence of diarrhoea, fever, cough and acute respiratory tract infection was 48, 42, 39 and 12% respectively. The prevalence of infants underweight, stunted and wasted was found to be 27.1%, 24.5% and 16.5%, respectively. Thus, lack of exclusive breastfeeding till 6 months of age, delayed initiation of complementary foods and inappropriate complementary feeding with respect to the quality, quantity and consistency were observed to be the major factors contributing to high morbidity and malnutrition amongst infants’ up till 12 months of age.

Food restrictions due to cultural beliefs are at times causative factors for poor nutritional status, especially in South East Asia, despite steady improvement in incomes and food availability [21]. Ignorance about the easy availability of complementary foods within economic means from the ‘family pot’, food fads and beliefs, are also major culprits. Urbanization and industrialization have to an extent compounded the problem, due to socio-cultural changes and breakdown of social support systems, with more urban and rural women working outside home, even before child is 3 months. These factors can have adverse effects on infant and young child feeding as summarized below in Box 8.4.

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Box 8.4 Determinants of inadequate food intakes and malnutrition in infants and young children ● ● ● ● ● ● ● ● ● ●

Lack of awareness and knowledge about feeding amount, frequency and type of food Local perceptions about the acceptability of specific foods for young children Cultural beliefs and perceptions on mode of feeding e.g. bottle feeding, feeding with hands Ignorance about the easy availability of complementary foods Inappropriate age of introduction of complementary foods Inappropriate energy density and frequency of feeding complementary foods Caregiver’s education Caretaker’s especially mother’s time commitments to other activities Feeding schedule and style Feeding environment of the infants

In India, according to NFHS-3 [8], 57 children per 1000 live births die every year. Inappropriate infant feeding practices which are mainly attributable to lack of nutrition awareness within the community, are primarily responsible for the high morbidity and mortality of infants and young children [33].

8.8

Desirable features of satisfactory complementary feeding

Within the framework of the global and national Infant and Young Child Feeding (IYCF) guidelines, the prime characteristic of satisfactory complementary feeding is that foods given should complement rather than replace breast milk, which should continue till at least 2 years age, to meet the nutrient needs of the young child. The guiding principles for complementary feeding given by WHO [1] and also by the Food and Nutrition Board of the Ministry of Women and Child Development (MWCD) [11], in their National Guidelines on Infant and Young Child feeding, focus on the following aspects: Duration of exclusive breastfeeding and age of introduction of complementary foods – Exclusive breastfeeding from birth to 6 months of age, with introduction of complementary foods at completion of 180 days of age, while continuing to breastfeed. Maintenance of breastfeeding – Continued frequent, on-demand breastfeeding until 2 years of age or beyond. Quantity of complementary foods – Starting at 6 months of age with small amounts of food, increase the quantity of complementary foods fed to the infants from 2 to 3 katori/day (katori is a small bowl of medium size with a volume of 150 cc) at 6–8 months of age to 3–4 katori/day and

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4–5 katori/day at 9–11 months and 12–23 months of age, while maintaining frequent breastfeeding. Food consistency, meal frequency and energy density – Gradual progression of food consistency and variety as the infant gets older, adapting to the infant’s requirements and abilities. Infants can eat pureed, mashed and semi-solid foods beginning at six months of age. By 9 months of age infants along with semi-solid foods can also eat “finger foods” or snacks. By 12 months, most infants can eat the same types of foods as consumed by the rest of the family but here nutrient density of the foods should be kept in mind and additional fat may be required. Addition of 0.5–1.0 tsp fat or oil in 1 katori of complementary food is recommended to increase density. Foods that may cause choking or items that have a shape and/or consistency that may cause them to become lodged in the trachea, such as nuts, grapes, and raw pieces of carrots must be avoided. There has to be an increase in the number of times that the child is fed complementary foods as he/she gets older in order to meet the recommended quantity of feeding. The appropriate number of feedings depends on the energy density of the local foods and the usual amounts consumed at each feeding. If energy density or amount of food per meal is low, or the child is no longer breastfed, more frequent meals may be required. Nutrient content of complementary foods – A variety of foods should be fed to ensure that the age –specific nutrient needs of the infants and young children are met. Meat, poultry, fish or eggs should be eaten daily, or as often as possible, if affordable and culturally acceptable. With vegetarian diets often it might be difficult to meet nutrient needs of infants and young children unless nutrient supplements or fortified products are used. Vitamin A and vitamin C rich fruits and vegetables and iron rich cereals, nuts and green leafy vegetables are recommended to be eaten frequently. Diets with adequate fat with incorporation of cereal-pulse combination should be provided, while avoiding drinks with low nutrient value, such as tea, coffee and sugary drinks such as aerated beverages, which are unnecessary foods as they are a poor source of nutrients and lead to malnutrition [35]. Several commercial complementary foods fortified with nutrients are available for fulfilling the nutrient requirements of the infants and young children, but these are within the reach of only the affluent class of people. The process of complementary feeding can be made economical, sustainable and practical for the masses, if based on local resources and home available foods. If complementary feeding of young children is to become universal, especially in developing

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countries, there is need to focus on children in low income settings, with consideration for the economic and environmental constraints, common in these countries [21]. Box 8.5 outlines the food based approaches to improve the iron and vitamin A content of complementary food diets. It is possible to develop appropriate and nutritious complementary foods using appropriate food combinations, in diverse cultural settings, which less privileged mothers can prepare and their children are able to eat. Box 8.5 Food-based approaches to improve iron and vitamin A content of complementary foods Dietary improvement ● ●

●

Increase the intake of iron and vitamin A rich foods (both carotene and retinol) In case of iron there is a need for improving meal pattern to enhance iron absorption with including enhancers of iron absorption like consumption of vitamin C rich foods, fermented and germinated foods and meat, fish and poultry especially after 9 months of age. Efforts have to be made to avoid giving the child milk and iron rich food together, as calcium acts as an inhibitor to absorption of iron from the diet. For vitamin A, there is a need to include both carotene (from plant-based diet) and retinol (milk, meat and fish diet) in complementary food

Food fortification ● ●

Consumption of iron and vitamin A fortified complementary foods Adding ‘home fortificants” such as micronutrient sprinkles to the complementary food

Use of vitamin–mineral supplements or fortified products for infant and mother – There should be need based use of fortified complementary foods or vitamin–mineral supplements for the infant. In some populations, breastfeeding mothers may also need vitamin– mineral supplements or fortified products, both for their own health and to ensure normal concentrations of certain nutrients particularly vitamins in their breast milk. Key micronutrients like iron, zinc, calcium, vitamin A and vitamin B12 are needed to be given if diets are plant-based or in non-breast fed infants. Safe preparation and storage of complementary foods – Practice good hygiene and proper food handling behaviors. Important behaviours include washing caregiver’s and children’s hands before food preparation and eating, storing foods by covering and keeping at an elevated place, serving foods immediately after preparation, using clean utensils to prepare and serve food, using clean cups and bowls when feeding children, and avoiding the use of feeding bottles which are difficult to keep clean. Responsive feeding – Practice responsive feeding applying the principles of psycho-social care. This involves feeding infants directly

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and assisting young children when they feed themselves; being sensitive to their hunger and satiety cues; feeding slowly and patiently, and encouraging children to eat but not forcing them; if children refuse many foods, experimenting with different food combinations, tastes, textures and methods of encouragement; minimizing distractions during meals if the child loses interest easily; remembering that feeding times are periods of learning and love; talking to children during feeding, with eye-to-eye contact. Feeding during and after illness – Increase fluid intake during illness, including more frequent breastfeeding, and encouraging the child to eat soft, varied, appetizing and their favorite foods. It is observed that the children are fed less amount of complementary foods or at times not fed complementary foods during illness especially during diarrhea due to the fear of them suffering with more diarrhoea episodes. This practice should be discouraged and the mothers and other caretakers should be encouraged to feed the child foods which he/she likes along with breastfeeding during illness. After illness, food should be given more often than usual and the child is encouraged to eat more.

8.9

Measuring the status of complementary feeding

Till recently, there was a lack of evidence and consensus on simple indicators of appropriate feeding practices in children 6–23 months of age which has hampered the progress in measuring and improving the infant feeding practices. In 2001, WHO recommended indicators on measurement of exclusively breastfeeding and complementary feeding practices, which have now been revised and released as definitions by WHO in 2008 [36]. These indicators focus on selected food related aspects of child feeding, amenable to population-level measurement. Table 8.6 gives the list of population-level indicators on IYCF practices which can be used primarily for assessment, targeting, monitoring and evaluation. Efforts have also been made to develop and use an Infant and Young Child feeding Index (ICFI) for measuring optimal IYCF practices [37]. The ICFI is a composite index of scores for breastfeeding, avoiding bottle feeding, 24-hour dietary diversity (measured by total number of food groups consumed), frequency of feeding of complementary foods and past 7 days food frequency score. The ICFI has been reported to be useful in identifying faulty feeding practices in a sample as well as for monitoring and evaluation of nutrition interventions [38]. Box 8.6 gives the indicators and the scoring system used in the complementary feeding index (CFI) developed by a study in India [39].

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Table 8.6 Core indicators of measuring IYCF practices at population level [36] 1

Early initiation of breastfeeding

2

5

Exclusive breastfeeding under 6 months Continued breastfeeding at 1 year Introduction of solid, semisolid or soft foods Minimum dietary diversity

6

Minimum meal frequency(a)

7

Minimum acceptable diet

8

Consumption of iron-rich or iron fortified foods

3 4

Note:

Proportion of children born in the last 24 months who were put to the breast within one hour of birth Proportion of infants 0–5 months of age who are fed exclusively with breast milk during the previous day Proportion of children 12–15 months of age who are fed breast milk during the previous day Proportion of infants 6–8 months of age who received solid, semi-solid or soft foods during the previous day Proportion of children 6–23 months of age who receive foods from 4 or more food groups during the previous day Proportion of breastfed and non-breastfed children 6–23 months of age who receive solid, semi-solid or soft foods (also including milk feeds for non-breastfed children) the minimum(a) number of times or more during the previous day Proportion of children 6–23 months of age who receive a minimum acceptable diet (minimum dietary diversity and minimum meal frequency) during the previous day Proportion of children 6–23months of age who receive an iron rich food or iron-fortified food that is specially designed for infants and young children

Minimum is defined as 2 times for breastfed infants 6–8 months, 3 times for breastfed children 9–23 months and 4 times for non-breastfed children 6–23 months.

(a)

Box 8.6 Variables and scoring pattern for Complementary Feeding Index (CFI) for infants aged 6–12 months in rural India [39] Indicator

Variable

Scoring

(a)

1. Continued BF Breastfeeding No Yes 02 2. Bottle feeding Uses bottles No Yes 10 CF were initiated on the completion of 6 months (180 days) No Yes 02 3. Timely Initiation of CF(b) 4. Dietary diversity For infants (6–8 months) (past 24 hours) Sum of cereals (grains/tubers) + pulses + milk (other than 0 1–2 3+ 012 breast milk)+ GLVs(c) and vitamin A rich fruits + egg + others(d) For infants (9–12 months) Sum of cereals (grains/tubers) + pulses + milk (other than 0 1–3 4+ 012 breast milk)+ GLVs and vitamin A rich fruits + egg + others 0 1–3 4+ 012 5. Food frequency Starchy staples (grains/ tubers) Pulses 0 1–3 4+ 012 (past 7 days) Milk (other than breast milk) 0 1–3 4+ 012 Meat/egg 0 1–3 4+ 012 Vitamin A rich fruits and vegetables 0 1–3 4+ 012 Other fruits/vegetables 0 1–3 4+ 012 Foods made with oil, fat or butter 0 1–3 4+ 012 Food frequency score = sum of scores for starchy staples + pulses + milk + meat/egg + vitamin A rich fruits/vegetables + foods made with fat 6. Meal frequency For infants (6–8 months) (past 24 hours) No. of times the child was fed in the past 24 hours 0 1 2+ 012 For infants (9–12 months) 0 1–2 3+ 012 No. of times the child was fed in the past 24 hours

CFI Score Range: Low: =6; Medium: 7–16; High: 17–23 (a) (d)

BF = Breastfeeding (b) CF=Complementary foods; (c) GLVs=green leafy vegetables; other category includes fruits, other seasonal vegetables, fat and sugar food groups.

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8.10

Complementary feeding status – global and India

The recent report of the State of World’s children [40], reports the following rates of appropriate complementary feeding amongst 6–9 months infants: SubSaharan Africa – 68%, Eastern and Southern Africa – 71%, West and Central Africa – 65%, Middle East and North Africa – 57%, South Asia – 53% and East Asia – 45%. These figures suggest that South Asian countries lag behind the other developing countries in appropriate complementary feeding practices. An analysis of the rates of complementary feeding in South Asian countries have been presented by State of World’s Breastfeeding report of South East Asian countries [35]. The rate of complementary feeding in South Asian Countries varies from 22% to 98% (Figure 8.2). In the report Pakistan has been reported to have lowest (22%) complementary feeding rates followed by Afghanistan (29%) and India (35%), while Sri Lanka with 98% has the excellent status regarding complementary feeding practices. In the recent World Breastfeeding Trend’s Initiative India report [41], India scored 69 out of 150 on IYCF indicators with complementary feeding rate (56.7%) getting a score of 3/10. In India, although breastfeeding is almost universal, poor rates of exclusive breastfeeding of only about 46% have been reported by the recent NFHS-3 [8] survey, with late introduction of complementary foods in a high proportion of infants. Timely introduction of complementary foods has been reported to be low, with only almost half of the infants’ population (53%) being given complementary foods in addition to breast milk between 6 and 8 months of age [8]. Trends in initiation of breastfeeding and complementary feeding show very minimal upward change over about the last 15–17 years, as reflected in comparison of the three National Family Health Surveys (NFHS) [5, 6, 8], held in 1992, 1998–1999 and 2005–2006. Box 8.7 discusses the state-wide scenario across India of the complementary feeding rates as reported by the State of World’s Breastfeeding, India Report [42]. C om p lem entary feedin g R ate (6-9 m o nths) 1 00 80 60 % 40 20 0 S

a ril

nk

a M

d al

iv

es

Ba

ng

d la

es

h N

ep

al

In

di

a

Af

g

n ha

is

ta

n k Pa

is

ta

n

8.2 Complementary feeding rates of infants (6–9 months) in South-Asian countries [35].

Complementary feeding of infants and young children

241

Box 8.7 India: State-wide scenario [41] As presented in the report of the ‘State of the World’s Breastfeeding India report’, India scored 5 or ‘poor’ amongst 8 South Asian Countries, for timely and appropriate complementary feeding . Differences have been reported across the states with wide variations in under nutrition rates and IYCF practices. Appropriate practices were followed most often in Sikkim and Kerala, where undernutrition figures are relatively lower, but in these states too, a large percentage of infants and young children were not fed appropriately. States which were a little better off were Goa, Manipur, Himachal Pradesh and Delhi. The lowest compliance was observed in states of Andhra Pradesh and Maharashtra. Rural data was even worse than urban. Factors exerting a positive influence on feeding practices were mother’s education and income status. Figure below presents the data emerging on complementary foods started between 6–9 months in two national surveys – NFHS 2 (1998-99) and NFHS 3 (2005-06) as well as the goal stated under the 10 th and 11 th Five Year Plan (FYP).

% C h ildre n

Initiation of com plementary Feeding-Status and G oals 90 1 00 75 80 5 5.8 60 40

3 3.5

20 0 1 0th P lan 11 th P la n G o als G o als C o m p le m en tary F oo ds Started b y 6 -9 m on th s NHFS 2

NHFS 3

8.3 Target goals for achieving complementary feeding rates as per 10th and 11 th five year plan of the government of India [14].

8.11

Low-cost complementary feeding

To provide nutritionally adequate and balanced complementary foods, it is important to have food mixtures or a variety of foods that fulfill all the nutrient and energy needs of the child. The young infant, although developmentally mature to start complementary foods, has a small stomach and can only consume small amounts of food at a time. Thus, energy and nutrient dense meals assume importance. A start made with cereals provides some energy, calcium, iron and zinc besides some other minerals and vitamins. Cereals however have phytates which are inhibitors of iron absorption. They also do not contain vitamins A and C and are not protein dense providing energy and good quality protein. Cereals therefore need to be given with added pulse or animal foods such as milk, meat, eggs etc, if these are unaffordable and culturally acceptable. Oil or nuts help to increase the energy density and further contribute to some of the protective nutrients. Addition of sugar/jaggery

242

Public health nutrition in developing countries

also increases nutrient density. In developing countries with cereal based high bulk diet, addition of fat or oil (0.5 to 1 tsp in 1 katori) is recommended with every meal to increase density. Seasonal and locally grown fresh or dehydrated vegetables/fruits are desirable to meet the requirements of micronutrients (especially vitamins A and C, iron and zinc) to ensure nutritional balance. This may sometimes prove a challenge. Foods prepared could be fresh, modified from the ‘family diet’, traditional foods or low cost ‘Ready to Eat’ (RTE) premixes or instant infant foods, requiring only reconstitution. Traditional practices and processes like multimixing, roasting, parching, puffing, fermenting and malting could be used, resulting in beneficial outcomes like improved nutritional balance, reduction in dietary bulk due to dextrinization of starch, reduction in the anti-nutrient and phytate content due to soaking of grains, reduced viscosity of starchy gruels due to amylase production, facilitating increased nutrient density and easy digestibility [40]. Appropriate low cost complementary foods therefore require consideration of traditional feeding practices and home based diets, within the economic means. Diverse food habits exist among various regions and communities of developing countries, although all diets are predominantly cereal or millet based. Thus, the basic component of the complementary food has to be the staple cereal/millet of the region. In fact, the first semi-solid food to be introduced into the child’s diet in India and other South Asian countries is usually a cereal based gruel or porridge made with addition of pulse or milk. The cereal use varies region wise. While this may help to initiate the child’s eating and swallowing of soft foods, the nutritional balance and quality of foods are important, as mostly small amounts and very thin gruels are given to infants and that also often irregularly. The use of very thin gruel, such as mere cooked cereal starch or watery portion of pulse is low in nutrients and is an in-appropriate practice which should be actively discouraged. Table 8.7 provides an example of a day’s sample diet for an infant.

8.12

Different ‘home based’ complementary foods

8.12.1 Traditional foods Most of the traditional foods are based on starchy gruels, cereals, cereals with pulse, cereals with milk or a soft seasonal fruit or tuber. Based on the region, there are several traditional foods like khichri, pongal, dalia, kheer, upma, idli, roti with dal/curd, ragi balls sattu, panjiri, etc, which are used for infant feeding [41].

Complementary feeding of infants and young children

243

However, these are usually not fed in adequate amounts or at the right time. In some countries, like India, ‘Annaprashan’ ceremony (Box 8.1) is held, when solid food/cereals are first introduced, between 6 months to 1 year of age. However, this is often not followed with continued active feeding of the child with right frequency and consistency. While some of these foods do provide energy and good quality protein, being based on cereal pulse combination, they lack important protective nutrients. Foods are often only carbohydrate rich and nutritionally unsuitable for the child. It becomes evident therefore, that traditional food and local and regional dietaries need to be identified with their good practices supported. Use of the desirable foods should be encouraged and sustained by focused, universalized nutrition education and awareness programs, emphasizing ways to make these traditional foods nutritionally dense and complete by addition of extra fat/nuts/oilseeds, sugar/jaggery to increase the energy density and fruits/yellow and orange coloured vegetables/green leafy vegetables (GLVs) to provide micronutrients. In vegetarian diet, iron and vitamin A availability of micronutrients is low and therefore use of micronutrient sprinkles has been tried with positive impact [32, 38]. Table 8.7 Sample diet for a day for an infant aged 12 months belonging to low socioeconomic group family in India Time

Feed

Feed content

Morning

Sweetened milk with chapatti or Milk bread sugar or jaggery chapatti or local bread Banana

1 medium Sized

Noon

Rice Pulse (Dal) (b) DGLV(b) Oil Chapatti Dal (b) DGLV(b) Oil

1 bowl (150 cc) 0.5 bowl (75 cc) 0.5 bowl 1 tsp 1.5 Chapatti 0.5 bowl 0.5 bowl 1 tsp

Milk Sugar or Jaggery Chapatti or local bread

3/4th cup 1 tsp 0.5 chapatti or 1 slice

Evening

Khichri–rice pulse mixture (modified from family pot)

Sweetened milk with Chapatti or bread

Or Dry take home ration (THR) with Milk milk THR Night

(b)

3/4th cup 1 tsp 0.5 chapatti or 1 slice

Mid-noon Banana or any other fruit

Or Chapatti/bread with dal and vegetable (can be mixed in one bowl)

(a)

Household measures(a)

Chapatti / bread / rice with Dal or vegetable

GLV: Green leafy vegetable Cooked

Chapatti / rice / bread Dal or Vegetable (GLV or yellow vegetable) Oil

3/4th cup 3 tsp 1 Chapatti or 1 bowl rice ½ bowl 1 tsp

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Public health nutrition in developing countries

8.12.2 Modified family foods In the less privileged sections of society, complementary foods are mostly home-made, based on the modified adult diet. However, as indicated by several studies, complementary feeding is delayed and the quantity of solid food given is meager. In fact, modifying the family diet can be the most economical, practical and effective means of ensuring complementary feeding of children, provided a suitable combination of foods is given with incorporation of additional oil or fat and variety gradually increased, to ensure nutritional adequacy and easy adaptation to the home diet. High requirements of iron through dietary source are difficult to meet unless food source is rich in heme iron or fortified food items or “home fortificants” such as sprinkles are incorporated in food (see chapter on child anaemia for details) Appropriate introduction of semi-solid food can also develop good eating patterns and habits which usually continue till later years. In this respect, the more economical home-based complementary foods have an edge over the high cost commercial foods with little variation in texture, consistency and flavor. Starting with mashed and smooth mixtures at 6 months, the mixtures can progressively be made thicker, with gradual transition to soft chopped and lumpy foods. By 1 year of age, most infants are ready to eat unmodified but ‘non-spicy’ adult or family diet. Personal hygiene in feeding the child, food safety aspects like well cooked food, fresh food, and food hygiene such as food kept covered are however some important aspects of complementary feeding that also need attention. One issue of concern that arises is that the underprivileged families often eat only 2 meals per day, while a young child needs to be fed 4–5 times a day or more, due to the limited stomach capacity and high nutrient requirements per unit body weight. Frequent feeding of the family diet, which being predominantly cereal based also tends to be bulky and may be impractical, as the food maybe subject to spoilage. Thus, processes like roasting and malting of cereals are beneficial to reduce dietary bulk. Between meal feedings, use of ready to eat (RTE) infant foods or nutritious snacks that can be stored, facilitate meeting the child’s dietary and nutrient needs. Soft seasonal, locally grown and easily available fruit may also be used for between meal feeding. Thus, awareness creation is needed regarding the ways and means of making the home based infant food as rich in nutrients as possible, within the constraints of time, cost, and other physical facilities. Simple one dish meals with different food groups need to be promoted. A study [45] to assess the amount of GLVs and carrot required to meet the vitamin A requirements of infants and young children, taking into account the contribution of breast milk at different ages between 6 months to 3 years,

Complementary feeding of infants and young children

245

quantified the amount of GLV needed as 10 g/day (1/4 medium katori raw and 1 tablespoon cooked) for the 6 month infant, 20 g/day at 9 months with reduction in breast milk, and 30 g/d from 1 to 3 years age. From the practical point of view, about 3 times the amount required daily or 1/4 katori cooked GLV could be given twice a week instead of GLV daily [45]. This addition of GLV contributes to the iron and vitamin C content of the complementary food also. Carrot required to provide the same amount of vitamin A is approximately 3 times the quantity of GLV needed at a particular age group.

8.12.3 Ready-to-eat (RTE) infant premixes or instant infant foods Low cost RTE infant foods, made from grains available in the home, have a major role to play in supporting complementary feeding and its sustainability for the common man, especially in view of the increasing workforce of women outside home and changing social networks affecting the practicality of using only freshly prepared foods. RTE infant foods only require reconstitution with boiled warm water. Other fluids like milk, lassi/buttermilk, coconut milk could also be used, if available and affordable, to increase nutrient density. These RTE premixes, can be easily prepared at home by taking about 3 parts of the staple cereal or millet like atta, suji, ragi, rice, bajra or jowar and combining with 1 part of a locally available dehusked pulse such as arhar, chana dal, besan or moong, with addition of 0.25 or 0.50 part of some nut or oilseed to increase the energy density. These food items need to be roasted separately, ground finely and mixed well and stored in a clean airtight container for good shelf life. At the time of feeding, 2–4 tablespoons of the mixture can be mixed with boiled water or any other liquid, and sugar/jaggery and a teaspoon of oil added, and fed to the infant. Powdered millets may need sifting initially to reduce the husk content. Seasonal dehydrated GLV or carrot (1–2 g) may also be added to this premix to provide important micronutrients. The consistency of the reconstituted premix can vary depending on the age of the child and if available, some soft seasonal fruit could be chopped or mashed and added. In fact, such a premix could also be used to prepare the already mentioned mid meal snacks for the older child. Although roasted starchy grains swell less in water as compared to unroasted, the viscosity of the premix gruel or a starchy gruel could be further reduced by using a small amount of amylase rich flour (ARF), which then enables the child to have a higher intake. The efficacy of such foods has been amply shown by the early studies from Gujarat [46] to several more recent field and research studies (Chapter on ARF presents details).

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Public health nutrition in developing countries

It must also be kept in mind that mothers from the low income group may sometimes find it difficult to prepare even a simple RTE food due to physical and monetary constraints. Therefore community based enterprise to produce RTE foods with an element of income generation, especially for women, assumes significance. For community-based production at low cost, involvement of ‘panchayats’, (local governance) women’s groups and adolescent girls with NGO’s and Government linkages, for training in safe preparation, packaging and marketing to local shops or young child feeding programs, can go a long way in improving complementary feeding of infants and young children. Small scale production units could be attached to rural health centers, fulfilling the need of complementary foods and income generation for the women. Several such successful models are reported. However, an important prerequisite of any such venture is again widespread generation of nutrition awareness resulting in a realization for the need and demand for such foods.

8.13

Promoting improved complementary feeding practices – programs, strategies and challenge ahead

It is evident that appropriate complementary feeding requires a combination of strategies. Establishing appropriate universal and timely introduction of complementary foods has emerged as one major strategy to combat this ‘avoidable’ undernutrition in young children and could be one of the most economic means of reducing childhood malnutrition. Often, it is not the food insecurity with respect to the child’s diet but lack of awareness which results in inadequate intake and undernutrition. What is required is focused and aggressive awareness generation on issues related to complementary feeding such as time of introduction, the foods, texture, frequency and amount, and method of feeding complementary foods including active feeding and feeding during illness. Food fads found interfering with intake of nutritious foods need to be dispelled. From the point of view of custom, practice, feasibility and cost also, it has been recognized since long that it would be most convenient for mothers to feed their infants and toddlers, an easily modifiable family or home cooked food or traditional foods. Expensive commercial foods as well as biscuits, snacks are not essential and mostly, special foods may not be required to be produced for very young child in situations where family uses appropriate principles of complementary feeding [43].

Complementary feeding of infants and young children

247

Ensuring sustainability of improved complementary feeding in addition requires adequate advocacy and awareness among all stakeholders, community participation, encouragement to families and women’s self help groups to make low cost infant foods as well as public private partnership for production of the RTE. Production of RTE at community and large scale level from a variety of raw materials available in the household needs to be encouraged along with appropriate marketing strategies of reasonably priced convenient sized packs of complementary foods [47]. Fortification with micronutrients is another strategy which may need to be considered to improve nutrient balance of low cost infant foods, prepared on a large scale. Mixing of micronutrient sprinkles1 or nutrient-rich pastes has been successfully promoted in some settings, and requires further research. A review of the working group on breastfeeding and complementary feeding of Standing Committee for Nutrition (SCN) [45] of various intervention strategies to improve IYCF, such as nutrition education on energy rich complementary foods, food with education, fortification of complementary foods and increased energy density and/or nutrient bioavailability of complementary foods via simple technologies, concluded that educational approaches can be effective, but in many situations a greater impact may be seen when they are combined with home-fortification or provision of fortified foods. The biggest challenge for complementary feeding interventions is going to scale with a combination of the most cost-effective components, while assuring adequate delivery and sustainability. Targeted interventions are thus the need of the hour and interventions maybe at following different levels: ●

●

●

●

Interventions at the household level (with a focus on domestically produced foods). Interventions at the village or community level (focusing on low volume, community production units and local distribution). Interventions at the intermediate level (focusing on intermediatevolume production units and regional distribution). Interventions at the central, industrial level (focusing on large volume, industrial production units and widespread distribution).

There is need to identify local feeding practices, common problems associated with feeding appropriate complementary foods and adapt to the feeding recommendations based on guidelines given by WHO [10]. 1. Sprinkles is a dry, tasteless, single-serving packet to be ‘sprinkled’ onto food. It includes a mix of iron, vitamins C, D and A, and zinc. Contrary to many other supplements it doesn’t change the taste or appearance when mixed into children’s food, making it more acceptable to use.

248

Public health nutrition in developing countries

Improvement of complementary feeding has received insufficient attention as a public health intervention and poor feeding practices continue as a major threat to social and economic development in our country. Development of successful interventions to improve child feeding practices, in particular are necessary to begin to overcome earlier insults to child’s nutrition status and to mitigate the effects of poverty. Some of the successful models, used across the country, by Government, NGOs, research groups, public nutritionists, for improving infant feeding practices have been based on community participation, active feeding counseling, mobilization of community based voluntary workers, positive deviance approach2 or advocating what works, nutrition education and counseling of mothers, and frontline workers, involvement of grandmothers and mobilization of self-help groups. It must be borne in mind that approaches to improving the availability of adequate complementary foods include simple technologies that can be applied in the home or community, and larger-scale industrial production of fortified processed foods that can involve both the public and the private sector. In conclusion, 10 messages for successful complementary feeding are 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Age of introduction of complementary foods Safe preparation and storage of complementary foods Foods of appropriate consistency for age and development stage Fat and carbohydrate content of complementary foods Energy density of food-addition of fat or oil. Amount of complementary foods needed Appropriate meal frequency Protein and micronutrient content of complementary food Use of supplements or fortified products Continuation of breastfeeding Responsive feeding

The global strategy on IYCF gives due weightage not only to infancy and young child feeding but mother and child dyad and advocates that improved IYCF begins with ensuring the health and nutritional status of women, in their own right, throughout all stages of life [10]. Thus, focusing on improving the complementary feeding is an intervention requiring urgent attention as improved feeding practices during the first 2 years of life is an important key to bridge the gap in the health and nutrition continuum of care. 2. Positive Deviance is a process of inquiry and action that looks for children who are well-nourished in spite of the forces working against their nutritional status, and examines the behaviors, beliefs, and practices which enable that child to cope and thrive.

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References 1. WHO (2001). ‘Complementary Feeding’, Report of the Global Consultation and Summary of Guiding Principles for Complementary Feeding of Breastfed Infants. WHO, Geneva. 2. MURRAY CJ, LOPEZ AD (1997). ‘Mortality by cause for 8 regions of the world: Global Burden of Disease Study’, Lancet, 349, pp. 1269–1276. 3. BLACK RE, ALLEN LH, BHUTTA ZA, CAUFIELD LE, DE ONIS M, EZZATI M, MATHERS C , RIVERA J (2008). Maternal and child undernutrition: global and regional exposures and health consequences. Lancet 371, pp. 243–260. 4. BRAUN VJ, RUEL M, GULATI A (2008). Accelerating progress towards reducing Child Malnutrition in India: A Concept for Action, IFPRI. 5. NFHS 1 (1991–1992). National Family Health Survey, IIPS, Mumbai, India (1993). 6. NFHS 2 (1998–1999). National family Health Survey, India, International Institute for Population Sciences. Mumbai, India (2000). 7. DLHS (2002). District Level Household Survey: Phase 1 Round II, 2002. Department of Family Welfare, GOI, January 2004. 8. NFHS-3 (2005–2006), National Family Health Survey. Volume I. IIPS, Mumbai, India: 2007. 9. VICTORA CG, ADAIR L, HALLAL PC, MARTORELL R , RITCHER L, SACHDEV HS (2008). Maternal and child undernutrition: consequences for adult health and human capital. Lancet, 371, pp. 340–57. 10. WHO (2003). Infant and Young Child feeding. A Tool for Assessing National Practice, Policies and Program. Geneva. 11. Ministry of Women and Child (MWCD) (2006). National Guidelines on Infant and Young Child Feeding. Food and Nutrition Board, MWCD, GOI 2006. 12. JONES G, STEKETEE RW , BLACK RE, BHUTTA ZA, MORRIS SS and the Bellagio Child Survival Study group (2003). How many child deaths can we prevent this year? Lancet, 362, pp. 65–71. 13. BHUTTA ZA, AHMED T, BLACK RE, COUSENS S, DEWEY K, GLUGLIANI E, et al (2008). What works? Interventions for maternal and child undernutrition and survival. Lancet, 371, pp. 417–440. 14. MWCD (2006). Report of the Working Group on Integrating Nutrition with Health- 11 th 5 Year Plan: 2007–2012. MWCD, GOI Nov 2006. 15. LANIGAN JA, BISHOP JA, KIMBER AC, MORGAN J (2001). Systematic review concerning the age of introduction of complementary foods to the healthy full term infant. Eur J Clin Nutr, 55, pp. 309–20. 16. BUTTE N, COBB K, DWYER J, GRANEY L, HEIRD W, RICKARD K (2004). The healthy feeding guidelines for infants and toddlers. Journal of the American Dietetic Association, 104, no. 3, pp. 42–54. 17. BROWN KH, BLACK RE, LOPEZ DE ROMANA G, CREED DE KANASHIRO H (1989). Infant feeding practices and their relationship with diarrhoeal and other diseases. Pediatrics, 83, pp. 31–40. 18. WHO (2002). ‘Global Consultation on Complementary Feeding. Report of WHO Expert Consultation. WHO. 19. PAHO/WHO (2003). Guiding principles for Complementary Feeding of Breastfed Child. Washington D, Pan American Health Organisation, WHO. 20. RAMJI S (2006). ‘Appropriate Feeding: 6–24 months. Nutrition in Late Infancy and Early Childhood (6–24 months), Nutrition Foundation of India, New Delhi, pp. 32–34.

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21. WHO (1998). Complementary Feeding of Young Children in Developing Countries: A Review of Current Scientific Knowledge, Geneva. 22. DEWEY KG and BROWN KH (2003). Update on Technical Issues Concerning Complementary Feeding of Young Children in Developing Countries and Implications for Intervention Programs, Food and Nutrition Bulletin, 24, pp. 5–28. 23. Indian Council of Medical Research (ICMR) (1990). Nutritive Value of Indian Foods. NIN, Hyderabad. 24. WHO (2002). Joint FAO/WHO Expert Consultation. Vitamin and mineral requirements in human nutrition. World Health Organization, Geneva. 25. KIMMONS JE , DEWEY KG, HAQUE E, CHAKRABORTY J , OSENDARP SJM and BROWN KH (2004). Behaviour-change trials to assess the feasibility of improving complementary feeding practices and micronutrient intake of infants in rural Bangladesh. Food and Nutrition Bulletin, 25, no. 3, pp. 228–237. 26. HOTZ C and GIBSON RS (2001). Complementary feeding practices and dietary intakes from complementary foods amongst weanlings in rural Malawi. Eur J Clin Nutr, 55, pp. 841–849. 27. HUFFMAN SL, GREEN CP, CAUFIELD LE and PIWOZ EG (2000). Improving infant feeding practices: Programs can be effective! Mal J Nutr, 6, no. 2, pp. 139–146. 28. LARTEY A, MANU A , BROWN KH, PEERSON JM, DEWEY KG (1999). A randomised, community-based trial of the effects of improved, centrally processed complementary foods on growth and micronutrient status of Ghanaian infants from 6–12 months of age. Am J Clin Nutr, 70, pp. 391–404. 29. BROWN KH, SANTIZO MC, BEGIN F , TORUN B (2000). University of California, Davis and Instituto Nutricional de Centro America y Panama, unpublished data. 30. CREED DE KANASHIRO H, BROWN KH, LOPEZ DE ROMANA G, LOPEZ T, BLACK RE (1990). Consumption of food and nutrients by infants in Huascar (Lima), Peru. Am J Clin Nutr, 52, pp. 995–1004. 31. GHOSH S (2007). Viewpoint: National family Health Survey 3, 2007. Indian Pediatrics 44, p. 619. 32. R U E L M T , B R O W N K H and C A U L F I E L D L E (2003). Moving Forward with Complementary Feeding, IFPRI, FCND. Discussion Paper No. 146. 33. DEWEY KG (2001). The challenges of promoting optimal infant growth. J Nutr, 131, pp. 1879–1880. 34. Complementary Feeding practices – a challenge to be addressed in rural India (2009). Pak J Nutr 8, no. 4, pp. 505–506. 35. IBFAN Asia (2007). The State of World Breastfeeding South Asia Report. 36. WHO (2008). Indicator for assessing infant and young child feeding practices, Part 1. Definitions. WHO 2008. 37. ARIMOND M and RUEL MT (2002). ‘Progress in developing an infant and child feeding index: an example using the Ethiopia Demographic and Health Survey 2000. Food Consumption and Nutrition Division Discussion Paper 143, International Food Policy Research Institute, Washington, DC. 38. ARIMOND M and RUEL MT (2004). ‘Dietary Diversity is associated with child nutritional status, ‘Evidence from 11 Demographic and Health Surveys, J Nutr., 134, pp. 2579–85. 39. UNICEF, The State of World’s Children (2009). Maternal and Newborn health, New York. 40. BPNI/IBFAN Asia (2008). ‘World Breastfeeding Trend’s Initiative’, India Report. BPNI/IBFAN–Asia. 41. BPNI/IBFAN Asia Pacific (2005). State of Implementation of the Global Strategy for Infant and Young Child Feeding 2005.

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42. WHO (2000). ‘Department of Child and Adolescent Health and Development. Complementary Feeding Family Foods for Breast Fed Children’, WHO/NDH, Geneva. 43. SETH V (2006). ‘Appropriate Feeding: 6-24 months. Nutrition in Late Infancy and Early Childhood (6–24 months), Nutrition Foundation of India, New Delhi, pp. 35–43. 44. SHARMA S and SETH V (1994). ‘Quantification of Food Needs of Infants, Preschoolers and Pregnant Mothers, towards meeting their Energy and Vitamin A Requirements’, Project Report: Department of Food and Nutrition, Lady Irwin College, New Delhi India (Sponsored by UNICEF). 45. GOPALDAS T (1983). ‘Complementary and supplementary foods for young child feeding at household, community, programme and industrial levels’, Workshop on Weaning Foods: A Report, College of Home Science. Andhra Pradesh Agricultural University. Hyderabad, India. Pub: UNICEF. July, 1983. 46. GHOSH S (1995). ‘Preventing malnutrition: The critical period is 6 months -2 years’, Indian Pediatrics, 32, pp. 1057–1058. 47. SCN (2007). ‘The Working Group on Breastfeeding and Complementary Feeding’, 34 th Session of SCN, February 2007, Rome.

Options and strategies to reach under-two children ...

9

Options and strategies to reach under-two children through complementary feeding with ARF in the South Asian countries Tara Gopaldas

Tara Gopaldas is Director at Tara Consultancy Services, Bangalore. She was dean and senior professor at Faculty of Family & Community Sciences at M S University, Baroda (1978–1993); Honorary Director of the WHO Collaborating Centre (1989–1993); Senior Adviser, Planning Commission (1976–1978); Nutrition Adviser & Project Director, CARE-India (1970–1976); Research Executive, Hindustan Levers (1960–1965). Dr. Gopaldas holds a PhD Degree from University of Illinois, Ch-Urbana, USA (1958), MSc in Biochemistry from Indian Institute of Science, Bangalore and BSc in Home Science from Madras University. She is a member of Nutrition Mission of India since 2003 and was President of Indian Dietetic Association of India (1982–1986) and was a UGC National Lecturer (1984–1985).

9.1

Introduction

Most of the ‘malnutrition drama’ is already over by the time a South Asian child is of two years of age [1]. More than half the world’s underweight children live in South Asia [2, 3, 4]. India has about 45 million infants/ toddlers (6–24 months) per annum. As against India’s 45 million under two; Bangladesh would have about 6 million; Nepal about 1 million; and Sri Lanka about 1 million. The target population for complementary foods in just these four South Asian countries is a staggering 53 million per annum. This chapter consists of the following sections: ●

Section 9.2:

●

Section 9.3:

252

Nutritional needs, deficiencies and the role of complementary foods in the age group of under two Options for providing nutrition to overcome deficiencies

Options and strategies to reach under-two children ... ●

Section 9.4:

●

Section 9.5:

9.2

253

Technology for development of premixes/ complementary foods Delivery channels and mechanisms to improve outreach

Nutritional needs, deficiencies and the role of complementary foods in the age group of under twos

Section 9.2 focuses on the following three components: nutritional status of children under two in South Asia; nutritional requirements for the under two in South Asia; and role of complementary foods for the under two.

9.2.1

Nutritional status of children under two in South Asia

It is now well recognized that most of the children in Asia under-2 years of age, especially children 6–18 months old are extremely undernourished, underweight and stunted. Generally, data on nutritional status is available for the ‘Under Fives’ and “Under Threes” and not for the ‘Under Twos’. From Table 9.1, it can be noticed that underweight, stunting and wasting is very high in India, Bangladesh and Nepal. The picture is slightly better in Sri Lanka. In South Asia there are several factors operating synergistically to hasten the ‘Below Twos’ rapid decline into undernutrition, especially so, from his/her sixth month of life. These are as follows: ●

● ● ● ● ●

● ●

the child may have been low birth weight (LBW), i.e. below 2500 g at birth; lack of and/or total unsuitability of complementary foods; repeated episodes of diarrhoeal and respiratory infections; unhygienic personal, maternal and environmental status; unsafe drinking water and poor sanitation; limited, distant, slow and non-affordable access to preventive and curative health services; poor income levels, illiterate, and working parents; ignorance of simple and doable caring practices and large families with narrow or no birth spacing.

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Table 9.1 Selected indicators of the nutritional profile of the “under fives” in India, Bangladesh, Nepal and Sri Lanka in 1990 [7] Indicator Children underweight Children stunted Children wasted LBW babies (<2500 g) Prevalence of vitamin A deficiency

India (%)

Bangladesh (%)

Nepal (%)

Sri Lanka (%)

50 63 17 30 0.70 Night blindness 56

56 51 15 50 0.78 Night blindness 73

31 16 NA 18 0.6 Bitot’s Spots 45 School children 14 School children 24 60 66

Prevalence of iodine deficiency disorder

23–65

50

Exclusively breast fed up to 3rd month Breast fed with complementary food (6–9 month) Breast feeding until 20–23rd month

51 31

54 30

49 51 9 33 0.33 Bitot’s Spots 78 School children 40 School children 36 80

87

67

NA

Prevalence of iron deficiency – Anemia

India – India’s National Family Health Survey (1992–93) found the prevalence of undernutrition to be very high in the Under Twos. The Survey found more than half (53%) of all children under the age of four to be underweight and a similar proportion (63%) to be stunted. 21–29% of children were severely undernourished according to weight-for-age and height-forage measures. One in every six children was found to be excessively thin (wasted). It further documented that undernutrition varied substantially by the age of the child, being highest after first six months. Undernutrition was particularly high in Bihar and Uttar Pradesh, while the problem of wasting was most evident in Bihar and Orissa, which also have among the highest infant mortality rates in the country [5]. Recent NFHS-3 data on under-3 children also reveals 40.4% underweight, 44.9% stunted and 22.9% wasted [5a]. A study by Gopalan and coworkers nearly three decades ago, clearly showed that the greatest increase in height in a preschool child (1–5 years) was between the age of 1 and 2 years. It was much less thereafter [6]. Bangladesh [7] – Improper weaning practices were observed and labeled as a cause of early childhood malnutrition in Bangladesh. Too early commencement of complementary feeding (within a month of the child’s birth) was also a problem. Semi-solid and solid food (mostly boiled rice) was given to all children by the time they were a year old – but in tiny amounts. The urban and rural poor were similar as regards prolonged breast feeding. But the urban poor gave more snacks, earlier supplements such as rice, extra milk, fish, egg and vegetables to the infant. More complementary food and a better level of hygiene improved their growth even under impoverished conditions. Apparently IEC alone did reduce malnutrition to some extent [8].

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Nepal [7] – A Nepal nutrition survey clearly showed that the most critical age in the Nepali child’s life was 12–23 months, when 80% were undernourished (weight for age), and 48% had a less than normal height for age [2]. Another study indicated that the prevalence of undernutrition in the under 2 was very high [9]. Sri Lanka [7] – In Sri Lanka about 25% of mothers in urban areas begin giving semisolid food after the fourth month as compared to 6% in rural areas. Solids such as “rusks” and “biscuits” are offered in significant amounts only after the child is six months old [10]. Malnutrition prevalence in children is lower in Sri Lanka than in other South Asian countries. Rural children have a better exclusive breastfeeding pattern compared to their urban counterparts. The “Thriposha” project which promotes a high protein fortified food began in 1972, in collaboration with CARE. Wheat from the PL480 programme was diverted to prepare a weaning food. “Thriposha” is a cereal-based weaning food for the undernourished preschool children, undernourished children in primary grades, anaemic, pregnant and lactating women and ward patients. “Thriposha” contains wheat-based products such as flour and wheat protein concentrate, defatted soy flour, refined soy oil, vitamins and minerals, a percentage of pre-cooked local cereal-based flour. The promotion and intensive coverage of the supplement could be a major task for health planners of Sri Lanka. It can be seen from Table 9.2 that the child 1–3 years of age is most deficient in vitamin A, vitamin C, riboflavin, calcium, niacin, thiamine, energy protein of high biological value, and iron. Since the nutrients are available to the child from the staple cereal, much of the iron would not be available to the child [11]. Recent studies indicate that most South Asian children are deficient in zinc. The requirement is 5 mg/day [12]. Table 9.2 Average nutrient intake in Indian under-3 in India versus their RDA [6] Age (years)

Energy (kcal)

1–3 908 RDA 1–3 1242 % of RDA 73% 1–3

Prot (g) Ca (mg) Fe (mg)

Vitamin A Thaimin (µg) (mg)

B2 (mg) Niacin (mg)

Vitamin C (mg)

23.7 22.0 108%

117 400 29%

0.37 0.70 53%

14 40 35%

256 400 64%

10.2 12.0 85%

0.52 0.60 87%

5.55 8.00 69%

In sum the child needs all the micronutrients (both micro and macro) to be provided in his complementary food.

9.2.2

Nutritional requirements for the under twos in South Asia

Recommended daily allowances (RDA) for the Indian child is viewed to be the most applicable for South Asia. The nutrient requirements for the infant (6–12 months) and children (1–3 years) as recommended by the Indian Council of Medical Research (ICMR), 1992 [13] is set out in Table 9.3.

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The Dietary Guidelines for the infant (6–12 months) and the 1–3 year age group as per the National Institute of Nutrition (NIN), 1998, is reproduced in Table 9.4 [14]. It is evident from Table 9.4 that most of our rural, tribal and urban children aged 6–24 months are in no way fortunate enough to receive the balanced diet recommended by the National Institute of Nutrition (NIN). In North and West India the children under two receive miniscule amounts of dal–roti (pulse and wheat bread), while in South and East India they receive rice–sambhar or dal (pulse). The child, fortunately, is on breastmilk right into his third year. The National Family Health Survey found breastfeeding to be universal in India, with 95% of all children born in the 4 years preceding the survey having been breast fed. However, among children aged 6–9 months, less than one-third were receiving solid or mushy food (amount not specified) in addition to breast milk. Table 9.3 Recommended daily allowances for the infant (6–12 months) and the child (1–3 years) [14] Group

Infants

Children

Particulars Body weight (kg) Net energy (kcal/d) Protein (g/d) Fat (g/d) Calcium (mg/d) Iron (mg/d) Zinc (mg/d) Vitamin A (µg/d) β-Carotene (µg/d) Thiamine (mg/d) Riboflavin (mg/d) Nicotinic acid (mg/d) Pyridoxine (mg/d) Ascorbic acid (mg/d) Folic acid (µg/d) Vitamin B12 (µg/d)

6–12 (months) 8.6 843 14 25 500 12 5 350 1200 0.6 0.7 8.0 0.4 25 25 0.2

1–3 (years) 12.2 1240 22 25 400 12 5 400 1600 0.6 0.7 8.0 0.9 40 30 0.2–1.0

Table 9.4 Balanced diet for infants and children [14] Food groups

Infants (6–12 months) Amount per day (g)

Children (1–3 years) Amount per day (g)

Cereals and millets Pulses Milk (ml) Roots and tubers Green leafy vegetables Other vegetables Fruits Sugar Fats/Oils (visible)

45 15 500 50 25 25 100 25 10

120 30 500 50 50 50 100 25 20

Note: Top milk of 200 ml has to be given even in case of breastfed infants.

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Items listed in the National Institute of Nutrition (NIN), balanced diet for infants and young children such as top milk, roots and tubers, green leafy vegetables, fruits, fats and oils and sugar are luxuries beyond the means or comprehension of any typical rural or urban, poor Indian household. These expensive items of fruits, vegetables, milk and pluses are the dietary avenue to supply vitamins and minerals to the young child which almost all the low income group (LIG), or even middle-income group (MIG), urban or rural households cannot afford.

9.2.3

Role of complementary foods for the under 2

(i) Importance of complementary feeding for the under 2 – Complementary nutrition is a nutritional intervention, which aims to make up for the deficit in the child’s diet. The supplement provides the child with energy, proteins and micronutrients. Various nutritional programs have demonstrated the importance of complementary nutrition and the difference it has made to the nutritional status of the vulnerable age group. Data from CARE-India’s Project Poshak [15] revealed that ●

●

●

●

The experimental group (6–11 months, 12–23 months, and 24–36 months), which received instant corn–soya–milk fully fortified with vitamins and minerals, significantly improved their nutrient intake status versus a matched control group. However, one could see glaring deficits in the control group relating to calories, vitamin C, calcium and iron in the infant (6– 11 months). The deficit got accentuated with respect to calories, vitamin A and C, calcium and iron in the 12–23 month old child. This is because the volume of breast milk drops and the amount of complementary home diet is very meagre. Data show that the 2–3 year old child is able to fend for himself/herself better than the younger age groups as he/she is practically on the home diet. Great deficiencies in vitamin A and C persist [15]. Consequently most infants have to depend on fortified supplementary food to obtain their RDA of vitamins and minerals, at least partially. Every attempt should be made therefore to see that the complementary or supplementary food is fortified with 80–100% of the child’s RDA, especially that of vitamin A, B–complex, vitamin C, iron, zinc; is low-bulk (soupy) yet high in nutrient density, so that the child can consume all or at least almost all of his/her ration in one sitting. Portion size is very important, especially for the intake of the micronutrients.

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and that the ration gets to the home of most children under two, through delivery channels such as take-home rations (THR) or take home delivery systems (THDS). (a) These three important conditions need to converge if children are to benefit from complementary food. (b) It is of utmost importance that policy makers, implementers and the public health and nutrition community recognize these facts. (c) It is unfortunate that not even nutritionists and dieticians have sufficiently realized that the consistency, nutrient-density and the amounts and infant can consume at a sitting vary enormously for a 6–9 months old; a 9–12 months old; a 12– 15 months old infant till the child reaches his/her second birthday. More operational research and field-testing need to be done in this area. (ii) Timely complementary feeding rates in India – The Indian National Family Health Survey (1992–93) revealed a wide range among the Indian states as to when food (liquid, semi solid or solid) was first introduced into the diet of an infant, 6–9 months of age. It ranged from a mere 9% in Rajasthan to relatively high 69% in Kerala. Recent NFHS-3 data also shows similar pattern with 31% 6–9 months introduced to semi-solids (Table 9.5). However, no nation-wide survey has been able to quantify the amount of complementary food given to the infant. Such a survey is urgently required to be conducted. (The results of the above survey are shown in Table 9.5). ●

Table 9.5 Timely complementary feeding rates (%) in Indian states [4]

State

Rate (%)

Rajasthan Assam Bihar Orissa West Bengal Andhra Pradesh Karnataka Kerala Tamil Nadu Gujarat Maharashtra Uttar Pradesh Madhya Pradesh All India

9 39 18 30 54 48 38 69 57 23 25 19 28 31

Note: Amount of complementary food given is not stated.

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9.3

259

Options for providing nutrition to overcome deficiencies

To restate from Section 9.2, it is seen that a complementary food for the under 2 has to be fully fortified; liquefied or drinkable in consistency; and readily available and affordable. This section will address the importance of consistency of the complementary food under the following headings: (1) Problem of feeding the under-2 (2) Concept of amylase-rich-food (ARF) (3) Advantages of a fully micronutrient-fortified ready-to-eat (RTE) complementary food with ARF

9.3.1

Feeding the under-2

The vast majority of older infants (7–12 months) and young toddlers (13–24 months) in the developing world are chronically undernourished. Most of the undernutrition is associated with growth faltering that occurs in the so-called weaning period (6–24 months) [16]. This condition is associated with a high bulk, low energy diet [17], accompanied with bouts of diarrhoea contributed in large measure by the intake of contaminated left over foods [18]. The most common and first complementary foods to breast milk, which is fortunately one of the most energy and nutrient dense foods [19] are small amounts of soft boiled rice or mashed chapatti or bread or most commonly, viscous cereal gruels or preparations made from rice (Asia), sorghum, finger millet, maize, cassava and plantain (Africa); rice, wheat, millets, tapioca, potato (India) or sweet potato (Papua New Guinea) [20]. The problem is that most poor mothers make a 5% gruel (5 g of a staple cereal flour cooked in 100 ml of water), which becomes thick and voluminous on cooking due to gelatinization and water-binding capacity of the long chain carbohydrate component in the cereal flours. Such gruel would contribute a mere 20 cal/100 g gruel or it would have an extremely poor nutrient density whilst having a high dietary bulk [21]. Further, at 6 months, a child has a poor swallowing reflex and can consume only small portions of semi-solid preparations. Hence, the dilemma is how to feed enough of the traditional gruel with a high energy density? How can one modify the form and texture of a solid or semisolid complementary preparation to a pour batter consistency? In fact, how can one literally ‘thin’ an extremely thick preparation and make it swallowable yet energy rich for the weaning child?

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Table 9.6 Reduction in viscosity of 20% hot paste slurries with the addition of 0.8 g wheat ARF [24] Hot paste slurries

Viscosity in centipoise units

prepared with

Control gruel

Soya-fortified bulger wheat Low-fat Marie biscuits Medium-fat glucose biscuits High-fat biscuits (salty) Bread Khichdi Chapatti

22400 8100 15200 3800 9200 18000 14800

Experimental gruel 1210 2460 5000 2520 2360 10700 3600

Note: In all cases 20 g of the powdered material was cooked to boiling in 100 ml water. When ARF was added it was at the expense of the substrate powder.

9.3.2

Concept of amylase-rich-food (ARF)

The concept of amylase-rich-food or ARF [22] directly addresses the twin problems of dietary bulk and poor energy density of most weaning gruels of the poor. ARF is nothing but germinated cereal flours which are extremely rich in the enzyme alpha-amylase. Just tiny or catalytic amounts of any germinated cereal flour can instantly liquefy or reduce the dietary bulk of any viscous multimix gruel in which cereal flour is the main ingredient. The alpha-amylase cleaves the long carbohydrate chains in the cereal flour into shorter dextrins. However, for enzymatic action three conditions are required in the gruel or porridge, namely, it must be homogenous, it must be moist, and it must be hot (at least 70°C). Just half a flat teaspoon of any ARF can reduce even a very high solid concentration of 45 g made up of 25 g flour, 15 g sugar and 5 g oil cooked in 100 ml of water to soupy consistency. This remarkable property makes it possible to offer the child being introduced to semi solid food, a low viscosity yet high energy dense preparation from habitual ingredients that are used for young child feeding even in poor homes. ARF will act equally well on any gruel prepared from homogenized khichidi, or from chapatti, biscuit or bread powder, or soya-fortified bulgar–wheat powder. The single and unique contribution of ARF is that it can permit the mother to mix in much more flour into the gruel and consequently makes it high in energy density, yet low in viscosity and dietary bulk. Germination of pulses and cereals are part and parcel of the culinary culture of Asia and Africa. ARF preparation is relatively simple as it is broadly based on germination. A small amount of any whole cereal grain (100 g or so) is steeped overnight in 2–3 times its volume of water, the excess water drained, and the moist swollen seeds germinated in a moist dark environment for 24–48 hours till the sprouts are evident. The further steps are sun-drying for 5–8 hours and lightly toasting the grains on a flat

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skillet to remove any surface moisture. The sprouts and the grains are milled or powdered. This is stored in an air-tight bottle or plastic container. This small amount of ARF for a cost of about 20–40 US cents, will suffice for one child’s gruel for one month. It needs to be made also only once a month [23–27]. Summing up the advantages of ARF preparations are ● ● ● ●

cheap cost; widely known and practiced household technology; small amounts to be made only intermittently, and; adaptability of making at the household, the community or even at the scaled-up commercial level.

In fact a barley malt, which sells from Rs. 30–40 per kg at current rates, can be directly purchased from beer breweries, and be milled and packaged into 5 g packets with or without the micronutrients, which the mother can buy [28–33]. However, individual packaging will increase costs. Germinated sorghum flour has been used for the same purpose in Tanzania.

9.3.3

Advantages of a fully micronutrient-fortified readyto-eat (RTE) complementary food with ARF

As explained above, the transformation from a thick or pasty complementary food to a ‘drinkable consistency’ is the miracle of ARF. An infant/toddler (6–24 months) can easily consume 3–5 times of an isocaloric yet nutrient dense complementary food with ARF versus one without ARF (34–37). It stands to reason that unless the child consumes his/her entire ration of the complementary food, the vitamin and mineral fortificants will also go waste. The liquefied yet nutrient-dense complementary food, therefore becomes the conduit or channel to deliver the entire RDA of micronutrients to the infant and toddler.

9.4

Technology for development of premixes and complementary foods

The following four sub-sections address the issue of technology. 1. India’s experience with making complementary foods in the seventies 2. India’s expertise in the commercialization of these technologies at the present time 3. Major findings of the Baroda group (1980–1993) on the ARF technology 4. Baroda group’s findings can be applied to move forward to the commercial production of appropriate RTE complementary foods and/ or sprinklers/sachets that include micronutrients and ARF.

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9.4.1

India’s experience with making complementary foods in the seventies

In India the technology for preparing simple roasted mixtures from cereals, pulses, oilseeds and jaggery (brown sugar) or sugar has been formulated by many research groups for decades. Almost all have been field tested and were found to promote growth in the child. Many have found their way into community level or state level programmes (Table 9.7). However, the great lacunae in these early attempts at formulating these RTEs for infants, toddlers and preschool children were— ● ●

●

The concept of ARF the ‘liquefier’ was not known. The mixes were solid. Hence, the most vulnerable under-1 could consume very little of his/her ration. None of them were fortified with vitamin–mineral premixes.

Table 9.7 Protein-enriched RTEs for infants, toddlers and preschool children at the community and industrial level [15]

Reference

Product

Ingredients

No. Community level 1 2

3

4 5

Pasricha et al (1973)

60 g cereal (wheat, bajri or ragi) 15 g pulse (roasted Bengal gram), an oilseed and 40 g sugar/jaggery. Devadas et al (1974) Weaning mix Cereal (cholam, ragi or maize), pulse (roasted green gram or Bengal gram dal), oil seed (roasted groundnut) and jaggery. Gopaldas et al (1975) Poshak (a) Cereal (wheat, maize, rice or jowar), pulse (chana dal or mung dal), an oil seed (groundnut) and jaggery in the proportion of 4:2::1:2 Poshak (b) Same ingredients as Poshak (a) but in the proportion of 60:17:14:9 as per linear programming. Chandrashekhara et al Kerala indigenous Tapioca rava, soya fortified bulgar wheat food (KIF) (SFBW) rava and groundnut flour. (1975) ICMR (1975) Ready-to-consume Roasted cereal (cholam, maize, ragi or mixture bajra). Pulse (roasted or sprouted Bengal gram, green gram or fox gram), oil seed (groundnut, groundnut / sesame cake flour).

9.4.2

Ready-to-mix powder

India’s expertise in the commercialization of these technologies at the present time

In the last 10 years, India and other countries have advanced tremendously. Linear programming is used routinely for evolving nutritious low-cost complementary foods. It has the state-of-the art plants or factories in both

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the private and public sector with large capacities for making complementary or weaning foods. There are technologies such as extrusion; roller/drum drying; spray drying; addition of the entire or a large proportion of the RDA of vitamins–minerals requirements; and the ARF technology (Table 9.8). In additional, the technique of linear programming to obtain least cost multimixes to deliver a stated amount of energy and protein is also possible. Table 9.8 Weaning food formulations developed in various countries [42] Product

Country

Primary ingredients

Balanced malt food Bal-ahar (dry-blend)

India (CFTRI) India (FCI formulated by CFTRI) India (CFTRI) India (CFTRI)

Cereal, malt, pulses, and skim milk powder Wheat flour, groundnut flour, Bengal gram flour and skim milk powder Edible groundnut cake flour, Bengal gram flour, green gram flour, wheat flour Cereal flours, pulses and oilseed cakes

India (NDDB formulated by CFTRI)

Cereal flours, pulses, soya flour, skim milk powder

India India (Glaxo) India (Nestle) Columbia

Soyabean flour, milk powder Cereals and milk powder Wheat flour, milk Maize flour, cottonseed flour, soyabean flour, vitamin A, calcium cabonate Maize flour, soya, groundnut wheat germ, skim milk powder, fish flour Precooked maize, defatted soya flour, skim milk powder, CaCO3 , Vitamins De-germinated maize flour, wheat flour, soya flour, skim milk powder, CaCO3 , vitamins Hard wheat flour, chick-pea lentil flour, skim milk powder, vitamins Wheat flour, field pea flour, skim milk powder, chick-pea lentil Defatted soya flour, high lysine corn flour, corn starch, milk powder, vitamins, minerals Cottonseed flour, Quinoa flour, skim milk powder, sugar, spices, vitamins Wheat, chick-pea, and skim milk powder

Flakes (Macaroni process) Precooked weaning food of different formulae (Roller dried) Bal-Amul and Bal-Amul cereal with milk (Roller dried) Nestum Farex Lactogen Incaparina Pronutro

S. Africa

Corn soya milk

USA

Caplapro

USA

Superasmine

Algeria and Turkey

Faffa

Ethiopia

Duryea

Colombia

Peruvita

Peru

Laubina

Beirut

9.4.3

Major findings of the Baroda University group (1980–1993) on the ARF technology

Between 1980 and 1993, Baroda University established the following: ●

Toddlers consumed significantly greater amounts of fully malted mixes of wheat flour, chickpea flour and powdered groundnut flour than equivalent amount of roasted mixes. However, the task of germinating, drying and powdering large quantities of cereal and pulses was cumbersome and laborious [31].

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264 ●

●

●

●

●

●

●

Catalytic amounts of any germinated cereal grain (malt) powder, such as wheat, millet and barley, can liquefy virtually any cereal based viscous gruel. This is because of their high content of alpha-amylase, which has the power to break down starches into smaller units almost instantly at boiling temperatures. These malt powders were named Amylase-Rich-Food (ARF). By virtue of the drinkable consistency, a child could consume three to five times more of the treated food per sitting. Hence, the child received more food energy/nutrients [38, 22]. Traditional gruels were made more energy dense by cooking 40 g of staple flour +5 g of ARF +200 ml water. Toddlers were easily able to consume this amount, so obtaining 180 calories from a typical traditional gruel. Addition of oil and sugar raised the calorie intake to 200–250 Kcal / 200 ml [34]. The addition of ARF to donated foods such as soya-fortified bulger– wheat powder significantly increased calorie density and intake in infants/toddlers 6–24 months old [26]. Mothers in urban slums in the eighties were taught to make wheat ARF. They found the germination process laborious. However, they were more than willing to buy 5 g of ready-made ARF as an additive, even at Rs. 2/- per packet or Rs. 60/- per month. Nevertheless, they preferred to buy ARF – treated “fullfeed” packets of 50 g or 100 g for Rs. 3/- or Rs. 5/- each, respectively [39]. The cost would have doubled or tripled by 2009–10. ARF was found to liquefy khichadi (a boiled rice/lentil food), chapatti pieces soaked in water, corn–soya mix and soya-fortified bulger– wheat powders [40]. In a controlled six month trial of infants and toddlers fed a highenergy, low-bulk gruel (with ARF) or an isocaloric high energy, highbulk gruel (without ARF) in addition to their habitual home diet, intakes of the low-bulk gruel were significantly higher (91 ± 28 ml or 148 ± 46 kcal per ad-lib feed) than intakes of the high bulk gruel (26 ± 11 ml or 42 ± 18 kcal) [35]. Children on the low-bulk gruels also grew faster [36] (Figures 9.1 and 9.2). The ARF technology was very successful in nutritional rehabilitation [41]. A major breakthrough was achieved when commercial barley malt (CBM) powder was shown to have the most powerful ARF activity [42].

9.4.4

Application of Baroda University group’s findings to commercial production of appropriate RTE complementary foods and/or sprinklers/sachets that include micronutrients and ARF

Liquefaction of complementary foods with ARF promises to be a

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valuable technology to reduce the burden of malnutrition in infants and toddlers in developing countries. In India, for example, parents from an enormous pool of increasingly mobile, low to middle income families are looking for moderately priced foods that they can buy on a regular and sustained basis. They currently buy expensive brands but feed them in very small quantities. There is a strong habit among most Indians to buy food commodities such as milk and condiments in small amounts for the day. Preliminary participatory research assessments in 2003 have shown that even low-income couples are earnings total incomes of Rs. 4000–5000 per month. They are more than prepared to pay Rs. 3–5 for a single feed of 50 g right through a child’s weaning period (6–24 months). The concept of “sachets or sprinklers of CBM + the entire RDA of micronutrients” also appealed to them very much. CBM can be sourced like any of the other ingredients in complementary foods in the open market or from the local liquor or malt food industry. In India, a good grade CBM costs about Rs. 30 per kg in 2003. In fact the fuel costs of extrusion can be greatly reduced if ARF is added to the slurry prior to extrusion as shown by Buffa in 1971 [43]. CBM sells at only 20 US cents per kg in USA; so USAID, CARE and WFP should seriously consider sourcing this food commodity in addition to soya oil, CSB and SFBW. The government-run ICDS weaning food plants would only require 2000 tonnes of CBM for the 100,000 tonnes of complementary food they produce per annum. The ARF can be blended or mixed into the complementary food with the vitamin–mineral mix at the last stage of processing. The question might be posed as to why more research with commercial barley malt ARF is needed? There are cogent reasons for large multicountry operational research studies in South Asia as under: ●

●

●

●

●

Commercial barley malt is by far the most powerful ARF that has been tested. Just 5% CBM can liquefy a ready-to-eat ration (50 g in 100 ml boiling water) which wheat ARF cannot do. Hence, a 50 g complementary food in 100 ml of water can delivery an extra 200 kcal + 6 g protein. An infant or toddler can easily consume about 100 ml of ARF – treated complementary feed at one sitting. A low-bulk or “drinkable” feed fortified with the child’s entire RDA of micronutrients (Table 9.9) would also improve the child’s micronutrient and nutritional status. The concept of a measurable and adequate amount of complementary feed could be introduced through the concept of a daily 50 g packet per day. The concept of “protein size” and hygiene could be introduced through the “daily packed ration”. Since the entire amount can be consumed at one sitting, much of the problem of microbial contamination will not arise. Extrusion and individual packing are recommended to ensure a shelf

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●

●

life of more than a year. Simple roasted mixes have a shelf-life of only 3–4 months. Rice and green gram are accepted all over South Asia as being the most digestible cereals for the infant. The economic position of the low-income group is much better now. Their expectations are higher. They are prepared to pay for their child’s nutrition and health, provided such complementary food packets or sachets are affordable and easily available.

The concept could be extended to any population or condition requiring a high-energy, low-bulk food (e.g. geriatrics, tubal feeding, refugee, burn cases, HIV/AIDS, feedings, pregnancy, etc). What is now needed is an organization or company that is ready to take this initiative and bring the technology to a level that will allow this complementary food to be produced commercially.

9.5

Mechanisms to improve acceptability, palatability, utilization and outreach of the donated complementary food in the public sector

Corn–Soya–Blend (CSB) is a food that is widely donated in all the four countries under review to the public sector. Based on a review by CARE – India [45], the following issues are addressed. (1) Improving acceptability of CSB which is fully fortified with the micronutrients; (2) Improving palatability of cooked CSB rations; (3) Improving utilization of CSB; (4) and Improving outreach of donated foods.

9.5.1

Improving acceptability of CSB

CARE – India in the past supplies corn–soya–blend (CSB) and soya oil (SO) to India’s Integrated Child Development Services (ICDS) programme. Table 9.9 depicts the percentage contribution of a single ration of 65 g CSB + 8 g soya oil to the RDA of a child under-2 years of age. Assuming the child 6–24 months consumes his/her entire ration, this would satisfy the Government of India’s (GoI) requirements of delivering 300 kcal and 12 g protein per child per feeding day and address the nutrient gap of calories in their usual diet. However, the nutritional gap in vitamins and minerals remains. 1. CSB + soya oil are excellent complementary foods. The only problem with the CSB is that it is gritty or grainy in texture. When cooked –

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Table 9.9 Nutrient value of CSB and oil [45] 65 g ration of CSB + 8 g of oil

Nutrient value

Percentage RDA

Food energy Protein Vitamin A Riboflavin Folic acid Vitamin C Calcium Iron Zinc Iodine

319 kcal 11.7 g 1105 IU 0.33 mg 13.00 mg 26.00 mg 520.00 mg 11.70 mg 1.95 mg 32.50 ppm

26 53 69 47 43 65 130 98 39 108

it becomes pasty and non-homogenous to the touch and taste. It is not appropriate for the early infant or even the late infant. Due to its bulk and pastiness, the ‘Below 2’ cannot eat his full ration. Further, children upto one year of age, and evens upto two, have a poor swallowing reflex and are slow feeders. Hence, feeds that are nutrient dense but ‘liquidy’ go down faster, without spillage or waste. There are many options to enhance its acceptability. ● Fine grind it. ● Extrude CSB rather than roast it. Extrusion will powder the product and will thoroughly cook it. ● Blend in Soya oil, extra vitamins, minerals and 5% CBM. This should be done at the final stage. All these processing actions can be done at the manufacturing end and the specially processed food can be separately bagged and demarcated for children under-2. 2. If this not possible, the composition of the RTE complementary food, which is usually sweetened with sugar (25%), can be slightly modified as under. Five percent of the sugar can be replaced by 5% of CBM. The entire micronutrient RDA of a 1-year-old Indian child [13] or 80% of it should also be incorporated into the RTE. 3. Project Poshak [15] noted that most Indians like a fried/roasted/ caramelized smell and flavour. If within manufacturing and/or processing costs, the addition of a synthetic smell/flavour could be considered. 4. Another study reports that about half the mothers in Uttar Pradesh, India felt that the CSB-RTE was not suitable for the ‘Below Two’. The RTE had to be made semi-solid with milk or water. They felt the dry RTE choked the young child. However, the CSB – RTE in a semi solid gruel, halwa or dalia form was suitable [44]. 5. The concept of ‘hot’ and ‘cold’ foods are firmly entrenched in most rural and tribal populations. For instance, especially in Madhya Pradesh and Uttar Pradesh home diets made out of wheat, ghee, milk, jaggery and pulses, all considered ‘hot’ would be appropriate for the

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cold and rainy seasons. Whereas rice, curd, lassi, groundnuts and sugar (cold foods) could be fed to the child in summer. CSB/oil recipes and ingredients likewise could be adapted to the seasons [45].

9.5.2

Improving the palatability of the cooked CSB rations

1. The Regional Profile for ‘Malnutrition in South Asia’, UNICEF, 1997 strongly recommends the use of the ARF technology as a manageable, practical and traditional technology to increase the energy intake of traditional low energy-gruels [7]. We would go a step further and strongly endorse the adoption of the ‘ARF Technology’ for the immediate improvement of the CSB–THR ration [46]. CSB–THR rations without ARF are extremely bulky and pasty. Hence, the THR with ARF becomes smooth and semi liquid while retaining all its good nutrition. 2. For the ‘Below Twos’, especially the ‘Below Ones’, it is the consistency and texture of the complementary food that are of paramount importance. Most Indian mothers like a caramelized or roasted taste and flavouring. Both the mothers and the babies like it sweet. Intakes by children definitely are better with a sweet tasting preparation. 3. Sweet tasting or ‘liquidy’ dalia, rabadi or kheer recipes would be most suitable for the early-infant in Madhya Pradesh and Uttar Pradesh. It would be the payasam (milky sweet porridge) counterpart in Andhra Pradesh. 4. The older child (1–2 years) may like laddu (solid sweet made from gram flour ghee, sugar and special spices) which the mother can make by roasting the grainy CSB in the Soya-oil, add some jaggery and fashioning into laddus, halwa, sattu or prashad. Salty preparations would be chappati, paratha, dosai or uppumav. Our interactions with the mothers in Uttar Pradesh (particularly in Uttar Pradesh), Madhya Pradesh & Andhra Pradesh showed that most of the mothers generally wanted to cook only twice (morning and evening) perhaps due to fuel and time constraints. They usually chose to make the same dish that was most convenient for them to make, for instance, chapatti (unleavened bread) in Uttar Pradesh and Madhya Pradesh and uppumav (snack made from broken rice) in Andhra Pradesh. Even sweetening the CSM with jaggery or sugar was a special treat. In short, the mothers were not enterprising about varying the CBM–oil recipes for the ‘Below Twos’.

9.5.3 Improving the palatability of cooked CSB rations Although there is clear evidence that the THR has reached the homes of the ‘Below Twos’, it is still a question mark as to how much of the THR gets into the stomachs of the ‘Below Two’. This is the current problem. There is a lack of sufficient appreciation among all concerned, namely,

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the policy makers, the bureaucrats, the community and the mothers, that unless a major portion of the THR s fed to the intended ‘Below Two’, he/ she will not improve in weight or health. At the moment, about a fourth to a third of the ration may be consumed by the ‘Below Two’, while the rest is consumed by other siblings and the family. Possible solutions are 1. The concept of a full THR for the ‘Below Two’ has to be actively promoted by the implementing staff, health staff, panchayat, village health practitioners, village school teachers, change agents and adolescent girls and boys. 2. Change Agents, and adolescent girls/boys can advice and ensure that the THR is given to the ‘Below Two’, when the ‘Above Two’ is at the aanganwadi. This will greatly minimize sharing. 3. On the nutrition health days, repeated cooking demonstration or ‘demos’ of the cooked up THR may be done. A single demonstration ‘baby’ of 6, 9, 12 months can be fed in front of the mother group. They will then learn two important facts: (a) The amount that can be consumed by the infant; (b) The amount consumed per sitting will increase with age. Even a few months difference in age would make a big difference in consumption. Probably by 18 months, the entire THR ration would be consumed by the child at a sitting. 4. Mothers can be requested to bring their own small bowls or tumblers. These can be calibrated for CSB and oil single rations.

9.5.4

Improve the outreach of supplementary foods for under twos

The Planning Evaluation Organization (PEO), 1976, [47] and the Integrated Child Development Services (ICDS) National Evaluation in 1992 [48], pointed out that children under three could not reach the ICDS or aganwadi centre (AWC). Project Poshak in MP, 1975 [15], also showed that the children below three could not be transported every day to a feeding center for spot feeding. The problem is even more accentuated for the ‘Under Two’ especially in scattered tribal hamlets, hilly areas or even within a village. CARE – India’s baseline survey, 1997 reported that 40% children under-2 years of age were brought to the AWC in the past one week for spot feeding, a figure often grossly over-reported by the AWC workers [49]. Possible solutions are 1. The product should be ‘THR’ especially for the ‘Below Twos’. THR has to be appropriate and demarcated for the ‘Below Twos’.

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2. THR product should be made attractive and meaningful to the mothers in order that they come regularly to collect the THR for the ‘Below Twos’. 3. CARE – India has shown the way by organizing Integrated Nutrition Health Programme (INHP) Days, where both the functionaries of the ICDS (AWW and Supervisors) and Health (ANM) are present. The ‘Below Twos’ are weighed and the THRs distributed. Mothers willingly help and participate. This is an excellent mechanism and strategy that can be taken up by the entire National ICDS. 4. Possible areas that can be strengthened are counseling on the child’s weight 6–9 m, 9–12 m, 12–15 m and so on. The Nutrition and Health staff as well as the mothers will realize how much a cooked portion of a single ration will be and how much of this an infant of a specific age group can consume over a reasonable period of time (say 20 minutes). This is the kind of practical and visual education that will immediately communicate to both ICDS staff and mothers. 5. It would be useful if the NH days are held every 15 days rather than every month. One of the NH days should be exclusively for the ‘Below Twos’ and one exclusively for her mothers (P & L). The village elders and members of the village panchayat should be encouraged to participate and get actively involved. 6. The strategy of change agents to ensure that the services of ICDS are understood by all; and to roundup all the ‘Below Twos’, and their mothers is an excellent strategy for outreach. It could be universalized in the ICDS. 7. The setting up of ‘seasonal crèches’ and enhancing the THR may be considered for both mothers and child beneficiaries. Since, mothers will have to stay back on NH day(s), some monetary compensation for doing so may be considered by the village panchayat. 1 80 1 58

1 60

1 46

M ILLILITR E S

1 40

1 22

1 20 1 00

91

80 60 40

41 26

31

25

20 0 6 -12 m on th s

1 2-1 8 m o nths 1 9-2 4 m o nths A ge gro ups (m o nths ) C o ntr ol G rue l

O v era ll

E x pt. G ru el

9.1 Mean intake of control and experimental gruels by different age groups for a feeding trial period of 180 days [35].

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0 .4

V E LO CITY

0 .3

E xpe rim e nta l

0 .2 C o ntrol 0 .1

0 6 -12

1 3-1 8 A g e in M on th s

1 9-2 4

III.2

9.2 Growth velocity of children on control and experimental gruels by different age groups for a feeding trial period of 180 days [36].

References 1. Nutrition and Poverty: Papers from the ACC/SCN, 24th Session symposium, Kathmandu, Nepal, March 1997. 2. Nutrition in South East Asia: World Health Organization Regional Office for South-East Asia, New Delhi, 1999. 3. Malnutrition in South Asia: A Regional Profile. UNICEF Regional Office for South Asia, 1997. 4. Complementary Feeding of Young Children in Developing Countries: a review of current scientific knowledge WHO, Geneva, 1998. 5. The National Family Health Survey (MCH and Family Planning), India: Report of the International Institute for Population Science, Bombay, India, 1992–93. 6. G O PA L A N C , S WA M I N AT H A N M C , K R I S H N A K U M A R I V K , H A N U M A N TA R A O D ., VIJAYARAGHAVAN K (1973). Effect of calorie supplementation on growth of undernourished children. Am J Clin Nutr vol. 26, pp. 563–566. 7. ROY SK (1997). Complementary feeding in South Asia, in malnutrition in South Asia: A regional profile, pp. 51–73. 8. BROWN LV et al (1992). Evaluation of the impact of weaning food messages on infants feeding practices and child growth in rural Bangladesh. Am J Clin Nutr vol. 56, pp. 994–1003. 9. MORTORELL R , LESLIE J, MOOK PR (1984). Characteristics and determinants of child nutritional status in Nepal. Am J Clin Nutr vol. 39, pp. 74–86. 10. SOYSA P and SENNAYEKE M (1985). The Introduction of a low-cost weaning food, its acceptability and effectiveness in a well-baby clinic. Ceylon J (ed). Child Health vol. 14, pp. 21–26. 11. National Nutrition Monitoring Bureau: Report on the Repeat Survey (1988– 90). National Institute of Nutrition, Indian Council of Medical Research, Hyderabad, 1991.

272 12. 13. 14. 15.

16. 17. 18. 19. 20.

21.

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25. 26.

27.

28.

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et al (1998). Zinc supplementation in young children with acute diorrehea in India. New England Journal of Medicine vol. 333, pp. 839–844. Nutrient requirements and recommended dietary allowances for Indians (1992). The Indian Council of Medical Research, New Delhi. Dietary Guidelines for Indians – A Manual: The National Institute of Nutrition, Indian Council of Medical Research, 1998. GOPALDAS T , SRINIVASAN N , VARADARAJAN I , SHINGWEKAR AG , SETH R , MATHUR RS , BHARGAVA V : Project Poshak, pp. 73, vol. 1, printed by CARE-India, New Delhi, 1975. WATERLOW J and PAYNE PR (1985). The protein gap. Nature vol. 258, pp. 113– 117. NICOL BM (1971). Protein and calorie concentration. Nutr Rev vol. 129, pp. 83– 88. ROWLAND MGM , BARRELL R, W HITEHEAD RG (1978). Bacterial contamination in traditional Gambian weaning foods. Lancet vol. 1, pp. 136–138. CAMERON M , HOFVANDER Y (1971). Manual on feeding infants and young children. New York: United Nations, p. 73. ALNWICK D , MOSES S , SCHMIDT OG (1987). Improving young child feeding in Eastern and Southern Africa. Canada International Development Research Center, pp. 1–380. MELLANDER O , SWANBERG U (1984). Compact calories, malting and young child feeding. In: Advances in International, Maternal and Child Health. Jelliffe DB, Jelliffe EEP (eds). Oxford: Clarendan Press, pp. 84–85. GOPALDAS T , MEHTA P, PATIL A , GANDHI H (1986). Studies on reduction in viscosity of thick rice gruels with small quantities of an amylase rich cereal malt. UNU Food Nutr Bull vol. 8, pp. 42–47. GOPALDAS T , MEHTA P, JOHN C (1987). Bulk reduction of traditional gruels in: Improving Young Child Feeding in Eastern and Southern Africa. Alnwick D, Moses S, Schmidt OG (eds). Canada: International Development Research Centre, vol. 1987, pp. 330–339. GOPALDAS T (1988). Simple traditional methods for reducing the dietary bulk of cereal based diets in rural homes. Proceedings of the 20th Annual Meeting of the Nutrition Society of India, pp. 73–84. GOPALDAS T , DESHPANDE S , JOHN C (1988). Studies on a wheat amylase-rich-food (ARF), UNU Food Nutr Bull vol. 10, pp. 50–54. JOHN C , GOPALDAS T (1988). Studies on reduction in dietary bulk of soya fortified bulger wheat gruels with amylase rich food. UNU Food Nutr Bull vol. 10, pp. 1–7. DESHPANDE S , NISAR SR , GOPALDAS T (1990). A technology to improve the viscosity, texture and energy density of commercial weaning foods. Abstracts 27th National Conference of Indian Academy of Pediatrics, 1990. MOSHA AC and SVANBERG U (1983). Preparation of weaning foods with high nutrient density using flour of germinated cereals. UNU Foods Nutr Bull vol. 5, pp. 10– 14. DESIKACHAR HSR (1980). Development of weaning foods with high calorie density and low hot paste viscosity using traditional technologies. UNU Foods Nutr Bull vol. 2, pp. 21–23. BRANDTZAEG B , MALLESHI NG , SVANBERG U , DESIKACHAR HSR , MELLANDER O (1981). Dietary bulk as a limiting factor for nutrient intake in pre-school children. III

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32. 33. 34. 35.

36.

37. 38.

39.

40. 41. 42. 43.

44.

45. 46. 47. 48. 49.

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Studies of malted flour from ragi, sorghum and green gram. J Trop Pediatr vol. 27, pp. 184–189. GOPALDAS T , INAMDAR F, PATEL JB (1982). Malted versus roasted young child mixes: viscosity, storage and acceptability trials. Indian J Nutr Dietet vol. 19, pp. 327– 336. GOPALDAS T (1990). The ARF story. A compendium of research of amylase-richfood. National/International Workshop on ARF Technology, Baroda, p. 12. GOPALDAS T (1998). Fighting Infant Malnutrition with amylase complementary foods. Nutriview Issue vol. 2, pp. 2–4. GOPALDAS T (1991). Technologies to improve weaning food in developing countries. Editorial, Indian Paediatrics vol. 28, p. 217. GOPALDAS T and JOHN C (1993). Evaluation of a controlled six months feeding trial on intake by infants and toddlers fed a high-energy, low bulk gruel. J Trop Paediatr vol. 38, pp. 278–283. JOHN C and GOPALDAS T (1993). Evaluation of the impact on growth of a controlled six months feeding trial on children (6–24 months) fed a complementary food of a high energy, low bulk gruel in addition to their habitual home diet. J Trop Paediatr vol. 39, pp. 16–22. GOPALDAS T (1992). Amylase reactive foods in the Improvement of Young Child. Diets Proc Nutr Soc, India. GOPALDAS T (1984). Malted versus roasted weaning mixes. Development, storage, acceptability and growth trials. In: Interfaces between Agriculture, Nutrition and Food Science. KT Acharya (ed). UNU Food Nutr Bull Suppl vol. 9, pp. 293–307. GOPALDAS T , DESHPANDE S, VAISHNAV U et al (1991). The transfer of a simple dietary bulk reduction technology of weaning gruels by amylase-rich foods (ARFs) from laboratory to urban slum. UNU Food Nutr Bull vol. 13, pp. 318–321. GOPALDAS T (1988). Simple traditional methods for reducing dietary bulk of cereal based diets in rural homes. Proc Nutr Soc India vol. 34, pp. 73–84. TAJJUDDIN KM (1990). Studies on nutritional rehabilitation with ARF. Unpublished PhD results. MUJOO R (1993). Studies on commercial barley malt. Unpublished PhD results, 1993. BUFFA A (1971). Food Technology and Development, Part I. Processing lowcost nutritious foods for the world’s hungry children. Factors, formulas, processes. Food Engineering, pp. 79–106. Consultancy Report by IESSCO Pvt. Ltd., on Uttar Pradesh, India’s RTE, Cited as an Appendix in Reference; Pillai G, CARE – India’s Integrated Nutrition and Health Programme, 1995–2000. GOPALDAS T and SUNDER G (1998). Addressing Nutritional gaps in Children Under Two in Rural India. Working Paper for CARE – India, 1998. PILLAI G . CARE – India’s Integrated Nutrition and Health Programme 1995– 2000. Planning Commission Evaluation Report on the ICDSA 1976–78: New Delhi, Planning Evaluation Organization, New Delhi, 1982. National Evaluation of the ICDS: National Institute of Public Cooperation and Child Development, New Delhi, 1992. JOHRI N (1998). CARE – India’s INHP Results Reports. Achievements versus plans (FY 1997 Vs FY 1996).

Diarrhea and undernutrition

10 Diarrhea and undernutrition Shariqua Yunus

Shariqua Yunus, MBBS, MD, is currently working as Program Officer (Health and Nutrition) at the United Nation World Food Program (WFP). Prior to this, Dr. Yunus was working with WHO as their focal point for nutrition in India (2006–2009). Her areas of interest include role of nutrition in HIV and AIDS, nutrition in emergencies, community-based management of malnutrition and nutrition in relation to non-communicable disease.

10.1

Introduction

Diarrheal diseases and malnutrition are common in children of developing countries and an interaction between diarrhea and undernutrition has been well established. Undernutrition is the underlying cause of thirty-five percent of global childhood deaths [1]. Diarrhea is one of the primary cause of poor nutrition in the under five children. It is estimated that “the total number of deaths caused directly and indirectly by malnutrition induced by safe water, inadequate sanitation and insufficient hygiene is therefore 860,000 deaths per year in children under five years of age” [1]. Globally improving water, sanitation and hygiene could prevent at least 9.1% of the DALYs (disability adjusted life years – a weighted measure of deaths and disability) or disease burden or 6.3% of all deaths. In developing countries the consequences of unsafe water, inadequate sanitation or insufficient hygiene impact on nutritional status of children.

10.2

Definition of diarrhea

Diarrhea is defined as the passage of loose, liquid or watery stools. However, it is the recent change in consistency and character of stools rather than the number of stools that is more important. Infants, particularly those who are on breast feeds, during the initial 2–3 months of life may pass many “pasty” or semi-formed stools daily; if they are gaining adequate weight, this should not be considered diarrhea. Again, a recent change in character of stools is more important.

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Mothers usually know when their children have diarrhea and often have a local word for diarrhea. In developing countries, diarrhea is common during infancy – the period of accelerated growth. For e.g. in India, the highest prevalence of 18.1% is reported in the age group of 6–11 months [2].

10.3

Types of diarrhea

Acute diarrhea – it is an attack of sudden onset, which usually lasts 3–7 days, but may last up to 10–14 days. It is caused by an infection of the bowel. Only 3–12 percent of acute diarrhea episodes last beyond two weeks. For the purposes of this chapter, we will be considering diarrhea as acute diarrhea. Chronic/persistent – A diarrheal episode which lasts for more than 14 days is a chronic episode. The delineation of persistent diarrhea as a sub group distinct from acute diarrhea is, as such, arbitrary as the duration of acute diarrhea forms a continuum. Though the cut-off of 14 days for defining persistent diarrhea is illogical but is supported by observations of a significantly high case fatality rate when diarrhoea extends for two or more weeks. A proportion of persistent episodes are associated with growth failure. The persistent episodes with inadequate weight gain or loss of weight are termed prolonged ‘malnourishing diarrhea’. It is these cases that have the greatest clinical significance and require careful management. Acute diarrheal episodes may become chronic because of (i) persistent colonization of upper small intestines by microbes; (ii) dietary allergies; (iii) carbohydrate intolerance because of damage to the brush border of intestinal mucosa, resulting in low levels of disaccharidases; (iv) infants and children with decreased host immunity such as after an attack of measles or delayed repair of intestinal damage due to associated protein –energy malnutrition with increase in being prone to retracted diarrhea (younger infants who are weaned very early develop intolerance to food proteins such as cow’s milk or even soya milk); (v) poor personal hygiene and environmental or food contamination may lead to recurrent intestinal infections before the infant recovers from a previous episode; (vi) protozoal infections Giardia lamblia or Entamoeba histolytica; and (vii) inadequate treatment of acute diarrhea is another important cause. Dysentery – The clinical syndrome of dysentery is characterized by the presence of blood and pus in the stools, abdominal cramps and fever. Gross blood in stools is the most reliable sign; its presence facilitates early recognition by the mother and the health worker and identifies a clinically severe form of the disease.

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10.4

Causes of diarrhea

Agent factors – In developing countries, diarrhea is almost universally infectious in origin. A wide assortment of organisms cause acute diarrhea and many of them have been discovered only in recent years (Table 10.1). The rotavirus has emerged as the single most important cause of diarrhea in infants and children. Nearly all children are infected with rotavirus once before the age of 2 years. Viruses are probably responsible for about one-half of all diarrheal diseases in children aged up to 2 years. Table 10.1 Pathogens frequently identified in children with acute diarrhea in treatment centers in developing countries [3] Pathogen Viruses Bacteria

Protozoans No pathogen found

% of cases Rotavirus Enterotoxigenic • Escherichia coli Shigella • Campylobacter Jejuni • Vibrio cholerae • Salmonella (non-typhoid) Enteropathogenic • Escherichia coli Crytosporidium

15–25 10–20 5–15 10–15 5–10 1–5 1–5 5–15 20–30

Environmental factors – Environmental factors is the major contributory cause of the disease (Figure 10.1) and pertains to mainly ingestion of pathogens, especially in unsafe drinking water, in contaminated food or from unclean hands (Figure 10.1). Inadequate sanitation and insufficient hygiene promote the transmission of these pathogens. Unsafe water, inadequate sanitation or insufficient hygiene contributes to 88% of cases of diarrhea worldwide [1, 4]. These cases results in 1.5 million deaths each year, most being deaths of children. In India, 0.4 million deaths and 13.6 million DALYS lost on account of diarrhea are attributable to lack of safe water, sanitation and hygiene [1]. The category ‘diarrhea’ includes some more diseases, such as cholera, typhoid and dysentery-all of which have related ‘faecal-oral’ transmission pathways.

10.5

Diarrhea, morbidity, malnutrition and mortality

Diarrhea is a major public health problem and also a leading cause of morbidity, malnutrition and mortality in the developing countries. Diarrheal

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277

diseases contribute the highest fraction of the total global burden of disease in DALYs among diseases with the largest water, sanitation and hygiene contribution (Figure 10.2). Contribution of diarrheal diseases is 39 percent to the water sanitation hygiene related disease burden (Figure 10.3). N o n w a te r b o rn e s ew a ge

H ands

F lie s

F ish a nd s he llfis h

S o il

F o o d in g e n e ra l

H um an e xc re ta

H um an s W a te r b o rn e s ew a ge

L a trin e s

S u rfa ce w a te r

D rin k in g w a te r

G ro u n d w a te r

F ru its a nd v eg eta b le s

A n im a l e xc re ta A n im a l p ro d uc ts (e g g s)

10.1 Faecal–Oral Transmission Pathways [1]. DISEASES WITH T HE L ARGEST WATE R, SANITATION AND HYG IEN E CO NTRIBUTION, YEAR 2 002 F ra ctio n of to ta l g lob al bu rd e n o f d is ea se in D A LY s 2% 0% 3% 4% 1%

5%

D ia rrh o e a l d is ea se s C o n s eq u e n ce s o f m a lnu tritio n M a laria D ro w nin g s M a lnu tritio n (on ly P EM ) Ly m ph a tic fila ria sis In te stin a l n e m a to de in fe ctio ns Tra ch o m a S ch is to s o m ia sis E n viro n m en ta l N o n -e n v iron m e n ta l fra c tio n D A LY: d is a b ility-a d jus te d life ye a r (w hich m e as u re s th e ye ars o f life los t to p re m a ture m o rtality a n d th e ye ar lo st to d is a b ility ); P E M : p ro te in-e ne rg y m a lnu tritio n (w hich is m a ln utritio n th a t d ev e lop s in a d ults a n d ch ild ren w h o s e co ns u m p tion o f p ro te in a n d e n e rg y is in su ffic ie nt to s atis fy th e b o d y's nu tritio na l n e e d s).

10.2 Diseases with the largest water, sanitation and hygiene contribution, year 2002 [1].

278

Public health nutrition in developing countries D IS E AS ES CO NTR IB U TIN G TO THE WATER -, SA N ITAT IO N -A ND H YG IEN E R EL ATE D D ISEA S E B U RD E N O thers 7 % D row ning s 6% D iarrh oe al disease s 39 % C onseq uen ce of m alutrition 21%

M alnu trition (only P EM ) 5% Lym phatic filariasis 3% Schistoso miasis 1% Trachom a 2%

M alaria 14% In testinal nem atode infections 2%

PE M : protein-en er gy m alnutrition In disability-a djusted life years, or D A LYs.

10.3 Diseases contributing to the water, sanitation and hygiene related disease burden [1].

Children belonging to the age group of 0–59 months are most susceptible to diarrhea and other kinds of infections. In India, 9 percent of under-5 year children are found to suffer from diarrhea. A child in India suffers, on an average, 10–15 episodes of diarrhea in the first five years of life. Of these, three to five episodes occur in the first two years of life. Overall, children are ill with diarrhea for 10–20 percent of their first 3 years of life. About 12.1 percent of children under the age of three years suffer from diarrhea in the two weeks preceding the survey [2]. National Health Survey of India indicates a decrease in the prevalence of diarrhea in under-5 years between 1998–99 and 2005–06; about 19.2 percent in 1998–99 [5] and 9 percent in 2005–06 [2]. National Commission on Macroeconomics and Health (2005) estimates the disease burden due to diarrhea to be about 760 cases per 100, 000 population per year in the age group of 1–4 years [6]. About 17% of all under-5 child mortality worldwide is contributed by diarrhea [7] (Figure 10.4). As per the WHO Report on World Health Statistics, 20.3% of child mortality in India is attributable to diarrhea [8]. M alaria 8%

P n eu m on ia 1 9%

M ea s les 4%

Causes of neonatal deaths

In ju rie s 3%

O th er 7% Teta nu s 7% D ia rrh oe a 3% S e ps is / P n eu m on ia 26 %

D ia rrh oe a 1 7%

O th er 1 0% A s ph yxia 23 %

H IV /A ID S 3%

C o ng e n ita l 8 % P re te rm 28 % N e on a ta l 3 7%

10.4 Causes of under-5 child mortality [7].

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A meta-analysis review of child morality due to diarrhea in the developing countries placed global deaths from diarrhea in children under five years of age at 1.87 million; which is 19% of the total child deaths [9]. WHO African and South East Asia regions account for 78% of all diarrhea deaths occurring among children in the developing world; 73% of these are concentrated in just 15 developing countries (Figure 10.5).

W HO region

Th e A m ericas

W este rn P a cific E a stern M ed iterra ne an S o uth-e ast A sia

A frica 1 0% 2 0% 5 0% 3 0% 4 0% Percentage of diarrhoea deaths in all low -and m iddle income regions

10.5 Distribution of deaths due to diarrhea in five WHO low- and middleincome regions [9].

The two main dangers of diarrhea are malnutrition and death. The more common cause of diarrhea related deaths is dehydration but a substantial proportion of such deaths occur as a result of malnutrition consequent to a series of diarrheal episodes of varying length and severity. Equally important causes of death are dysentery and prolonged malnourishing diarrhea resulting in malnutrition. Diarrhea is rightly referred to as a nutritional disease, because malnutrition is associated with nearly twothirds of diarrhea-related deaths. Acute diarrheal diseases contribute to growth retardation in patients. Persistent Diarrhea (PD) exists in 3–20 percent of the total episodes of diarrhea [10]. It leads to worsening of malnutrition and is associated with a high risk of morbidity and mortality. Role of diarrhea in malnutrition – Diarrhea has been shown to have a significant impact on nutrition. Most field studies identify diarrhea as the major determining factor leading to malnutrition in developing countries. A child with multiple episodes of diarrhea suffers most severely from protein–energy malnutrition. Infection per se causes excessive catabolism and increases energy requirements above the normal. In addition, diarrhea is further associated with continuous losses of nutrients from the body in the form of stools. Even a brief episode of diarrhea leads to loss of 1–2 percent of body

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Public health nutrition in developing countries

weight per day. Infants and young children in developing countries are sick for about 10 percent of the time (or nearly 30 days per year) with diarrheal illnesses. Thus, over the time, even the slow and continuous deficit associated with mild illness can accumulate to become a major nutritional deficiency. Atrophy of the intestinal epithelium in cases of malnutrition causes malabsorption and accentuates malnutrition. A vicious cycle of diarrheamalnutrition-diarrhea sets in. Since, malnourished children are more prone to suffer from other infections as well; diarrhea malnutrition symptom complex contributes to the large majority of early childhood deaths either directly or indirectly. It would be prudent to mention that despite malabsorption of macronutrients during diarrhea, 80–90% of carbohydrates, 70% of fats and 75% of proteins are absorbed from diets based on common foods. Recent studies have indicated that enteral feeding may result in faster recovery with shorter hospitalization compared to parenteral nutrition [10]. Diarrhea results in impairment of appetite. Additionally, during diarrhea food is often withheld from the child by the mother due to erroneous belief that starvation rests the bowel and promotes early recovery from diarrhea. The practice of withholding of food in fact delays repair of the damaged intestinal lining and return of the ability to produce digestive enzymes. Many a times, the need for continued feeding during diarrhea or on correcting faulty feeding practice prior to illness is not appreciated by medical practitioners and not advised.

10.6

Management of diarrhea

There are three essential elements in the management of diarrhea in children namely, rehydration therapy, zinc supplementation and continued feeding.

10.6.1 Rehydration therapy During diarrhea, there is an increased loss of water and electrolytes in the liquid stool. Dehydration occurs when these losses are not adequately replaced and a deficit of water and electrolytes develops. The degree of dehydration is graded according to symptoms and signs that reflect the amount of fluid lost. Oral Rehydration Therapy (ORT) is at the core of management of diarrhea. The term ORT includes complete oral rehydration salts (ORS) solution with composition within the WHO recommended range (Table 10.2), as well as solutions made from sugar and salt, food based solutions and home available fluids (HAF) without insisting on inclusion of both

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glucose precursor and salt or their presence in specified amounts. It is imperative to stress upon the use of safe and clean water for purposes of preparing the oral rehydration solution. Table 10.2 Composition of the new ORS formulation [11]

New ORS

grams/litre

Sodium chloride Glucose, anhydrous Potassium chloride Trisodium citrate, dehydrate Total

Percentage

2.6 13.5 1.5

12.683 65.854 7.317

2.9

14.416

20.5

New ORS

mmol/litre

Sodium Chloride Glucose, anhydrous Potassium

75 65 75

Citrate Total Osmolarity

100.00

20 10 245

In India, it is reported that only 26% of children (less than 3 years of age) received ORS supplementation when suffering from diarrhea in contrast of 57% of children who receive neither Oral Rehydration Therapy (ORT) nor fluids in increased amounts when they are sick with diarrhea [1] – see Box 10.1. As presented in Table 10.3, only two infants out of ten in the age group of 6–11 months received ORT or increased fluids and continued feeding despite the fact the diarrhea management policy of Government of India clearly states the various actions to be taken (Box 10.1). Table 10.3 Percentage of children under age five who had diarrhea in the two weeks preceding the survey, the food offered compared to normal practices and percentage given ORT or increased fluids and continued feeding [1] Age (in months)

<6 6–11 12–23 24–35 36–47 48–59 (a)

Any diarrhea(a)

10.6 18.1 13.8 8.3 5.0 3.9

Amount of food offered (%) More food offered 1.7 1.9 1.7 2.3 1.9 3.2

Much less offered 6.9 7.4 13.6 11.7 11.6 11.1

Same as usual amount of food offered 23.3 30.3 39.7 43.3 45.4 41.5

ORT or increased fluids and continued feeding (%) 8.9 22.3 39.6 37.1 41.0 43.2

Diarrhea in the two weeks preceding the survey [1]

10.6.2 Zinc supplementation Zinc is an important micronutrient for a child’s overall health and development. Zinc is lost in greater quantity during diarrhea. Replacing the lost zinc is important to help recover and to keep the child healthy in the coming months

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A large body of evidence from India and other developing countries shows important therapeutic benefits with zinc administration during and after diarrhea, and some studies also reported reduction in diarrhea morbidity in the subsequent 2–3 months without further supplementation. Apart from reducing the duration and severity of the treated episode of acute diarrhea, zinc treatment in programmatic condition has the potential to decrease hospital admission rates by 15–20%, decrease child mortality by 3–5% and decrease the subsequent episodes of diarrhea and possibly pneumonia over the ensuing 3 months [15]. While ORS remains the mainstay of therapy during acute diarrhea, zinc has an additional benefit in reducing duration and severity of diarrhea. Addition of zinc supplements to ORS for treatment of diarrhea has been shown to substantially reduce use of unwarranted drugs during acute diarrhea [15]. This is likely to reduce emergence of drug resistant entero-bacteria, a major public health problem. The therapeutic benefits of zinc supplementation in acute diarrhea may be attributed to effects of zinc on various components of the immune system and its direct gastrointestinal effects. Government of India Policy on diarrhea Management and zinc supplementation is presented in Box 10.1. Box 10.1 National programmes for management of diarrhea in India [12, 13] The Diarrhea Disease Control Programme in India was launched in 1978. The main objective of the programme was to prevent death due to dehydration caused by diarrheal diseases among children less than 5 years of age due to dehydration. Since 1985–86, with the inception of the National Oral Rehydration Therapy Programme, the focus of activities has been on strengthening case management of diarrhea for children under the age of five years and improving maternal knowledge related to use of home available fluids, use of ORS and continued feeding. From 1992–93, the programme became a part of the Child Survival and Safe Motherhood (CSSM) Programme and all activities were integrated with those of the CSSM programme. CSSM was further merged with the Reproductive and Child Health (RCH) program in India following its launch in 1997–98. The second phase of the RCH in 2005 was accompanied by the introduction of the “Integrated Management of Neonatal and Childhood Illnesses (IMNCI)” which was based on the understanding that a child presenting with an illness may require follow up for other related issues as well. The IMNCI guidelines and training package is based on a logical framework of assessment, classification and management of illnesses. The Government of India has recognized that IMNCI is a superior approach to newborn and child survival and health. IMNCI does not imply that the health workers will not treat individual diseases. Rather, it implies that the workers will broaden their approach to consider and respond to the child and manage the different factors that could be contributing to child’s sickness. These guidelines recommend standardized case management procedures based on two age categories: (i) upto 2 months and (ii) 2 months to 5 years. In IMNCI, only a limited number of carefully selected clinical signs are considered, based on their sensitivity and specificity, to detect the disease. A combination of these signs helps in arriving at the child’s classification, rather than a diagnosis.

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Classification(s) also indicates the severity of the condition. The classifications are color coded: “pink” suggests hospital referral or admission, “yellow” indicates initiation of treatment, and “green” calls for home treatment. A sick young infant up to 2 months of age is assessed for possible bacterial infection, jaundice, and diarrhea. A sick child aged 2 months to 5 years is assessed for general danger signs and major symptoms like cough or difficult breathing, diarrhea, fever, and ear problems. All the children are also routinely assessed for nutritional and immunization status, feeding problems, and other potential problems. The IMNCI strategy provides for home-based care for newborns and young infants. IMNCI strategy promotes the accurate identification of childhood illnesses in outpatient setting and ensures appropriate combined treatment of all major illnesses, strengthens counseling of caretakers, and speeds up the referral of severely ill children. At a referral facility, the strategy aims to improve the quality of care provided to sick children. In the home setting, it promotes appropriate care-seeking behaviors, improved nutrition and preventive care, and the correct implementation of recommended care. The assessment, classification and management of diarrhea remain the same, though the approach proposed under IMNCI reflects a more integrated pattern. For further details, kindly refer to the IMNIC guidelines. In November, 2006, the Government of India after examining the evidence on the use of zinc in the management of diarrhea among children in the country issued a policy note to the effect. The salient features of the policy note [14] are as: Zinc (20 mg/day for 14 days) is to be used in the national programme as an adjunct to ORS in the management of diarrhea in children older than 6 months. For children less than six months, zinc in doses of 10 mg/day is dissolved in breast milk to be used for 14 days. ● ● ●

Zinc is a very safe drug. A stable formulation is available. It is well accepted by children and mothers.

Apart from reducing duration and severity of the treated episode of acute diarrhea, zinc treatment in the programmatic condition has the potential to decrease hospital admission rates by 15–20 percent, decrease child mortality by 3–5 percent and decrease the incidence of subsequent episodes of diarrhea. To ensure timely intervention and avoid expenditure of parents on unnecessary drugs Government of India has decided to supply zinc along with ORS under Reproductive child Health II/National Rural Health Mission. The critical issue is that zinc tablets must be freely available and accessible round the year in every village. All health personnel including private practitioners and ICDS workers must be included in the network of zinc distribution. In this context, it has been decided that all health personnel including AWW and ASHA will promote use zinc in addition to ORS for diarrhea management and make zinc supplement available at the ICDS centres.

10.6.3 Feeding Continuation of nutrition feeding is an important element in the management of diarrhea. Feeding of infants and children during diarrhea may be considered under-3 heads:

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Breast-fed babies – The infants should continue to be breastfed during an attack of diarrhea. Breastfeeding should be allowed as often as the infant desires it. Stimulation of the receptors of the nipple by continued suckling helps maintain milk production. Breastfeeding reduces severity and complications of acute diarrhea. Withdrawal of breastfeeding during diarrhea, apart from its deleterious effect on nutritional status, is also associated with a higher risk of dehydration compared with continuation of breastfeeding. Non-breastfed infants – Once the dehydration has been corrected, feeding can be done with full strength milk as there is increasing evidence available on not using diluted milk during any phase of acute diarrhea. Milk cereal mixtures can be used. Older infants who are receiving both solid and liquid diet including either breast milk or animal milk – The diet should contain adequate amount of calorie dense foods, so that enough nutrients are absorbed from a small quantity of food. Diet practices – The nutritional management of diarrhea diseases is challenging and should ideally evolve around diets based on low cost, practical and easily available foods acceptable to children of the specific age groups. Milled cereals are preferred to whole cereals. A well-cooked porridge or gruel of rice and lentil is usually well tolerated. Mashed bananas are also good. The diet should be iso-osmolar. These foods should be started 4–6 hours of starting the treatment. Soft drinks and fruit juices with high sugar content should preferably be avoided during diarrhea. Food should be easily digestible and can be given in smaller quantities at shorter intervals. Culture-specific beliefs influence feeding during diarrhea. The source of ideas is both folklore and existing philosophy of medical community. The medical community needs to upgrade its understanding based on recent carefully done research. Behavioral studies show that in India, some mothers offer less than usual amount of food to infants during diarrhea and often receive endorsement from physicians to do so. More often food intake is already low, prior to illness, due to use of dilute hypocaloric semi-solid complementary foods and less than required frequency of feeding. Children who need care for diarrhea are usually the children in a community whose feeding behaviour is likely to have been faulty. Diarrhea is therefore a great opportunity to introduce and influence proper complementary feeding practices. Details of dietary management of acute diarrhea are presented in Box 10.2. The dietary management of persistent diarrhea is not discussed as it is outside the scope of this chapter.

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Box 10.2 Recommendations for dietary management of acute diarrhea [15] ●

● ●

●

● ●

●

●

●

Children should continue to be fed during acute diarrhea because feeding is physiologically sound and prevents or minimizes the deterioration of nutritional status that normally accompanies such illness. In acute diarrhea, breastfeeding should be continued uninterrupted even during rehydration with ORS. Optimally energy dense foods with the least bulk that are recommended for routine feeding and available in the household should be offered during diarrhea, in small quantities but frequently, at least once every 2–3 hours. Staple foods do not provide optimal calories per unit weight and these should be enriched with fats and oils or sugar, e.g. khichri with oil, rice with milk or curd and sugar, mashed banana with milk or curd, mashed potatoes with oil and lentil. Foods with high fibre content, e.g. coarse fruits and vegetables should be avoided. In non-breast fed infants, cow or buffalo milk can be given undiluted after correction of dehydration together with semisolid foods. Milk should not be diluted with water during any phase of acute diarrhea. Alternatively, milk cereal mixtures, e.g. dalia, sago, milk–rice mixture, can be used. Routine lactose-free feeding, e.g. soy formula is not required during acute diarrhea even when reducing substances are detected in the stools. Lactose malabsorption meriting dietary modification is very uncommon in acute diarrhea. It may be required in very few infants in whom diarrhea persists beyond 8–10 days with progressive weight loss and >1 percent reducing substances in stools. During recovery, an intake of at least 125% of the normal diet eaten by the child should be attempted with nutrient dense foods. Such feeding should continue until the child reaches pre-illness weight and ideally until the child achieves normal nutritional status, as measured by expected weight for height or weight for age. This might take several weeks or longer, depending on the degree of deficit. The child must be offered an extra meal after an episode of diarrhea. Caution must be exercised to avoid hyper-osmolar foods like heavily sweetened juices, soft drinks and bottled or canned sweet drinks as they are hyper-osmolar and might aggravate diarrhea.

10.7

Prevention of diarrhea

Proper treatment of diarrheal diseases is highly effective in preventing death, but has limited impact on the incidence of diarrhea. Health staff working in treatment facilities is well placed to teach family members and motivate them to adopt preventive measures. Mothers of children being treated for diarrhea are likely to be particularly receptive to such messages. Overloading mothers with information should be avoided, only one or two of the following points most appropriate for the particular mother and child should be selected and need to emphasized. The basic diarrhea prevention strategies are presented in Box 10.3.

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Box 10.3 Basic diarrhea prevention strategies ● ● ● ● ● ● ●

The babies under 6 months of age should be exclusively breastfed. Complementary feeding practices should be improved. Clean water for drinking and washing should be used. Hand washing should be encouraged. Latrines should be used. There should be quick and sanitary disposal of babies’ stools. Children should be given measles immunization.

(i) Breastfeeding – During the first 6 months of life, infants should be exclusively breastfed. This means that the healthy baby should receive breastmilk and no other foods or fluids, such as water, tea, juice, cereal drinks, animal milk or formula. Exclusively breastfed babies are much less likely to get diarrhea or to die from it than are babies who are not breastfed or are partially breastfed. Breastfeeding should continue until at least 2 years of age. The baby should be put to the breast immediately after birth and should not be given any other fluids including water. The advantages of breastfeeding should be explained to mothers using simple language. If breastfeeding is not possible, cow’s milk (modified if given to infants younger than 6 months) (see Box 10.4) or milk formula should be given from a cup. This is possible even with very young infants. Feeding bottles and teats should not be used because they are very difficult to clean and easily carry the organisms that cause diarrhea. Careful instructions should be given on the correct hygienic preparation of milk formula using water that has been boiled briefly before use. Box 10.4 The modification required for cow’s milk [15] Dilution is recommended during the first two months of infancy to reduce the solute load on the kidney. The dilution recommended is as below:

|------------------+ ----------------- + ------- + ----------- +------- | |------------------| Infant's -------- | -------- | ------------ |-------- | |------------------| weight (kg)--- | -------- | ------------ |-------- | |------------------+ ----------------- + ------- + ----------- +------- -| |------------------|3----------------- |4 ------ |5 ---------- |6 ------ | |------------------+ ----------------- + ------- + ----------- +------- | |Cow's milk ---|70 --------------- |100 --- |150 ------- |180--- | |(ml)------------- | ------------------ | -------- | ------------ |-------- | |------------------+ ----------------- + ------- + ----------- +------- | |Sugar (g) ----- |5----------------- |10----- |10--------- |10 ---- | |------------------+ ----------------- + ------- + ----------- +------- | |Water(ml) ----|20 --------------- |20----- |0 ---------- |0 ------ | |------------------+ ----------------- + ------- + ----------- +------- | |Energy -------- |64 --------------- |103 --- |135 ------- |153--- | |------------------+ ----------------- + ------- + ----------- +------- | |Protein -------- |2.1 -------------- |3.0---- |4.5 ------- 5.4 ---- | |------------------+ ----------------- + ------- + ----------- +------- |

Instructions ● Place milk, water and sugar in a pan ● Bring to boil and then cool ● Pour into feeding vessel

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(ii) Use of safe water – To reduce the risk of diarrhea the cleanest available water should be used and it should be protected from contamination. Box 10.5 presents the details. Box 10.5 Use of safe water ● ● ● ● ● ● ● ● ●

Water should be collected from the cleanest available source. Bathing, washing, or defecation should not be allowed near the source. Latrines should be located more than 10 m away and downhill. Animals should be kept away from protected water sources. Animals should be kept away from protected water sources. Water should be collected and stored in clean containers. The container should be emptied and rinsed every day. The storage container should be covered and children or animals should not be allowed to drink from it. Water should be collected and stored in clean containers. The container should be emptied and rinsed every day. The storage container should be covered and children or animals should not be allowed to drink from it. Water should be removed from the storage container with a long handled dipper that is kept especially for the purpose so that hands do not touch the water.

There are numerous things mothers should do to decrease the chances of someone in her family getting sick with diarrhea. Listing these for the mother may not be the best way to get her to remember all of them. Instead, the health care workers should find out how much the mother knows and what she is already doing and then add to her knowledge. Health care workers should ensure that mothers or care givers know about the basic diarrhea prevention strategies. If fuel is available, water should be boiled for making food or drinks for young children. Water needs only to be brought to a rolling boil, i.e. when water has just started boiling Vigorous or prolonged boiling is unnecessary and also result in fuel wastage. The amount of water available to families has as much impact on the incidence of diarrheal diseases as the quality of water. This is because larger amounts of water facilitate improved hygiene. If two water sources of water are available, the better quality water should be stored separately and used for drinking and preparing food. (iii) Hand washing – All diarrheal disease agents can be spread by hands that have been contaminated by faecal material. The risk of diarrhea is substantially reduced when family members practice regular hand washing. All family members should wash their hands thoroughly after defecation, after cleaning a child who has defecated, after disposing of a child’s stool, before preparing food, and before eating/ feeding the child. Good hand washing requires the use of soap or a local substitute, such as ashes or soil, and enough water to rinse the hands thoroughly.

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(iv) Food safety – Food can be contaminated by diarrheal agents at all stages of production and preparation, including: during the growing period (by use of human fertilizers), in public places such as markets, during preparation at home or in restaurants, and when kept without refrigeration after being prepared. Individual food safety practices should also be emphasized. Health education for the general population should stress the following key messages concerning the preparation and consumption of food: ● Raw food should not be eaten except undamaged fruits and vegetables that are peeled and eaten immediately; ● Hands should be hashed thoroughly with soap after defecation and before preparing or eating food; ● Food should be cooked until it is hot throughout; ● Food should be eaten while it is still hot, or reheated thoroughly before eating; ● All cooking and serving utensils should be washed and thoroughly dried after use; ● Cooked food and clean utensils should be kept separately from uncooked food and potentially contaminated utensils; ● It should be ensured that the food cooked is consumed the same day; and ● Food should be protected from flies by means of fly screens. (v) Use of latrines and safe disposal of stools – An unsanitary environment contributes to the spread of diarrheal agents. Because the pathogens that cause diarrhea are excreted in the stools of an infected person or animal, proper disposal of faeces can help to interrupt the spread of infection. Faecal matter can contaminate water where children play, where mothers wash clothes, and where they collect water for home use. Every family needs access to a clean, functioning latrine. If one is not available, the family should defecate in a designated place and bury the faeces immediately. Stools of young children are especially likely to contain diarrheal pathogens; they should be collected soon after defecation and disposed of in a latrine or buried. The launch of “Total Sanitation Campaign” in India and efforts to address to sanitation through the National Rural Health Mission (NRHM) are the concentrated efforts to improve the sanitation situation in India (Box 10.6). (vi) Measles immunization – Measles immunization can substantially reduce the incidence and severity of diarrheal diseases. Every infant should be immunized against measles at the recommended age.

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A meta-analysis on impacts of diarrheal disease reduction by intervention/area revealed 25–37% reduction in diarrhea frequency by each of the intervention. Water, sanitation and hygiene interventions interact with one another and impact of each intervention may vary widely according to local circumstances. Based on local conditions, interventions need to be prioritized. Table 10.4 Impact on diarrheal disease reduction by intervention area [18] Intervention area

Reduction in diarrhea frequency (%)

Hygiene Sanitation Water supply Water quality Multiple

37 32 25 31 33

Box 10.6 Initiatives of the Government of India for improving sanitation situation (a) Total sanitation campaign [16] – Individual health and hygiene is largely dependent on adequate availability of drinking water and proper sanitation. There is, therefore, a direct relationship between water, sanitation and health. Consumption of unsafe drinking water, improper disposal of human excreta, improper environmental sanitation and lack of personal and food hygiene have been major causes of many diseases in developing countries. India is no exception to this. Prevailing high infant mortality rate is also largely attributed to poor sanitation. It was in this context that the Central Rural Sanitation Programme (CRSP) was launched in India in 1986 primarily with the objective of improving the quality of life of the rural people and also to provide privacy and dignity to women. Later CRSP strategy was modified with a “Demand driven approach” and the revised approach in the programme was titled as “Total Sanitation Campaign” (TSC). The TSC programme emphasizes more on information, education and communication (IEC), human resource development and capacity development activities to increase awareness amongst the rural people and generation of demand for sanitary facilities. The programme is being implemented with a focus on community led and people centered initiatives. The objectives of TSC are as follows: ● Bring about an improvement in the general quality of life in the rural areas. ● Accelerate sanitation coverage in rural areas. ● Generate felt demand for sanitation facilities through awareness creation and health education. ● Cover schools/anganwadis in rural areas with sanitation facilities and promote hygiene education and sanitary habits among students. ● Encourage cost effective and appropriate technologies in sanitation. ● Eliminate open defecation to minimize risk of contamination of drinking water sources and food. ● Convert dry latrines to pour flush latrines, and eliminate manual scavenging practice, wherever in existence in rural areas. The strategy is to make the Programme ‘community led’ and ‘people centered’. A “demand driven approach” is being adopted with increased emphasis on

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awareness creation and demand generation for establishing and usage of sanitary facilities in houses, schools and for cleaner environment. Alternate delivery mechanisms are being adopted to meet the needs.

(b) Formation of Village Health and Sanitation Committees (VHSC) [17] – Sanitation is considered as an important determinant of health under NRHM: Under the National Rural Health Mission, for institutionalizing community led action for health “Village Health and Sanitation Committees” are being formed at the village level. Of the various roles assigned to the committee. VHSC is also responsible for Participatory Rapid Assessment : to ascertain the major health problems and health related issues in the village. Estimation of the annual expenditure incurred for management of all the morbidities is also being encouraged. Mapping of health resources and the unhealthy influences within village boundaries is being done through participatory methods with involvement of all strata of people. The health mapping exercise aims to provide quantitative and qualitative data to understand the health profile of the village. The database includes information on number of households – caste, religion and income ranking, geographical distribution, access to drinking water sources, status of household and village sanitation, physical approach to village, nearest health facility for primary care, emergency obstetric care, transport system as well as morbidity pattern.

References 1.

2. 3. 4. 5. 6. 7. 8. 9.

10. 11. 12. 13.

14.

PRUS- USTUN A , BOS R, GORE F, BARTRAM H

(2008). Safe water, better health: costs, benefits and sustainability of interventions to protect and promote health. World Health Organization, Geneva. International Institute for Population Sciences. National India Fact Sheet. National Family Health Survey 3; 2005–06. FRICKER J (1993). Children in the Tropics. No. 204. UNICEF (2006). Progress for Children: A Report Card on Water and Sanitation. No. 5, September 2006. International Institute for Population Sciences. National Family Health Survey 2; 1998–99. Burden of Disease in India (2005). National Commission on Macroeconomics and Health. Ministry of Health and Family Welfare. BRYCE et al (2005). WHO estimates of the causes of death in under five children. Lancet vol. 365, no. 1147–1152. Report of World Health Statistics. World Health Organization, Geneva, 2008. CB PINTO , VELEBIT L , SHIBUYO K (2008). Estimating child mortality due to diarrhea in developing countries: a meta-analysis review. Bulletin of the World Health Organization vol. 86, no. 710–717. MEHTA M (1996). Nutritional management of diarrheal diseases. Indian Pediatrics vol. 33, pp. 149–157. Oral Rehydration Salts: Production of the new ORS, WHO/FCH/CAH/06.1 PARK K (2009). Intestinal Infections. Park’s Textbook of Preventive and Social Medicine 20th edition. Jabalpur: M/S Banarsidas Bhanot, p. 200. INGLE GK , MALHOTRA C . Integrated management of neonatal and childhood illnesses: an overview. Indian Journal of Community Medicine vol. 32, no. 2 (2007-04-2007-06). Government of India. Ministry of Health and Family Welfare, Department of

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15. 16.

17. 18.

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Family Welfare, Child Health Division. Use of Zinc as an alternate therapy in the treatment of diarrhea, 2006, no. Z 28020/06/2005-CH. Draft Guidelines for Management of Diarrhea in Children for Medical Officers and Health Workers. India, August 2007. Guidelines on Central Rural Sanitation Programme (2004). Total Sanitation Campaign. Department of drinking water supply, Ministry of Rural Development, Government of India. Framework for implementation of the National Rural Health Mission. Ministry of health and family welfare, Government of India. Nirman Bhavan, New Delhi. FEWTRELL L , KAUFMANN RB , KOY D , ENANARIA W , HALLER L , COLFORD JM JR (2005). Water, sanitation and hygiene interventions to reduce diarrhea in less developed countries: a systematic review and meta-analysis. The Lancet vol. 5, no. 1, pp. 45–52.

Prevention and management of protein energy malnutrition

11

Prevention and management of protein energy malnutrition Siddarth Ramji

Siddarth Ramji, MD, is professor in the Department of Pediatrics, Maulana Azad Medical College, New Delhi. His research interest include neonatal and child health, particularly nutrition amongst the low birth weight babies. He has been a member of several task forces of government and scientifice bodies.

11.1

Introduction

The most recent estimates of the global burden of malnutrition in under 5 children are that 178 million (one-third of all children) are stunted, 112 million are underweight, 55 million are wasted (19 million having severe acute malnutrition) and 13 million children are born each year with intrauterine growth retardation [1]. Together they account for 21% of all under-5 deaths. Besides increased risk of mortality and morbidity, recent reviews have also provided compelling evidence for links between stunting and reduced cognition and economic productivity, and for transgenerational effects resulting in small babies and increased risk of childhood under-nutrition, when accompanied by rapid weight gain with chronic diseases such as high blood pressure, metabolic and cardiovascular disorders. There is therefore sufficient reason to both prevent and appropriately manage malnutrition in early childhood if both the shortand long-term consequences are to be avoided.

11.2

Clinical syndromes of malnutrition

The classification of protein energy malnutrition (PEM) is primarily clinical (anthropometry and other clinical changes). Traditionally three syndromes have been described amongst severely malnourished children – kwashiorkor, marasmus and marasmic-kwashiorkor. Kwashiorkor is characterized by a weight for age between 60% and 80% of reference median with edema. These children are usually apathetic, irritable and inactive; usually have hepatomegaly, skin changes (desquamating hyperpigmented patches exposing raw areas of skin, fissures at flexures) and

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depigmented hair. Anorexia, intermittent diarrhea and vomiting after feeds are frequent complaints. Decreased serum albumin, anemia and signs of vitamin A deficiency are commonly associated in these children. Marasmic children are grossly emaciated due to wasting of muscles and subcutaneous fat, having weight for age < 60% of reference median and may be stunted and have no edema. These children are often irritable and unlike children with kwashiorkor may have good appetite for food. The skin and hair are usually dry and depigmented, and the hair is usually sparse. When children with features of marasmus have edema they are classified as marasmic-kwashiorkor. Children are classified as underweight (below –2 z-score from the median for weight-for-age), stunted (below –2 z-score from median for length/height for age), wasted (below –2 z-score from the median for weight-for length/height) and severly stunted (below 3 z-score from the median for length/height for age) based on the WHO standards. Severe malnutrition includes children who are severly wasted or severly stunted.

11.3

Prevention of malnutrition

Malnutrition in childhood is the result of a complex interplay of sociocultural, economic, health and biological factors, the details of which are presented elsewhere in this book. Eliminating and preventing malnutrition requires a change in economic and socio-cultural environment. However, these are beyond the realms of interventions that public health specialists or nutritionists can do. We therefore need to identify interventions that can be applied at scale without adding to the economic burden of nations.

11.3.1 Evidence-based interventions to improve child nutrition Critical evaluation of evidence-based literature would help in identifying such interventions that could be applied to scale for improving childhood nutritional status. This section provides an overview of strategies that could potentially prevent malnutrition. Table 11.1 summarizes the interventions that have evidence for affecting child undernutrition.

11.3.2 Low birth weight and fetal-growth restriction The NFHS-3 survey for India reports a low birth weight incidence of about 21.5%. Though exact data is not available, it is estimated that about half of them are expected to have experienced fetal-growth retardation. Is there any evidence to suggest that they could contribute to the stunting or underweight amongst under-five children, especially in the developing nations? In a prospective study from the slums of Dhaka [3], about 1600 newborns were followed till 12 months. The prevalence of

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Table 11.1 Interventions that could affect child undernutrition Sufficient evidence for universal implementation

Intervention with insufficient or variable effectiveness evidence

Implementation in specific contextual situations

Interventions with little or no effect

Breastfeeding promotion (Individual & group counseling)

Baby friendly hospital initiatives

Delayed cord clamping at birth

Mass media promotion of breastfeeding

Behavioral change communication for improved complimentary feeding

Dietary diversification strategies, home gardening

Conditional cash transfer programs (with nutritional education)

Growth monitoring

Vitamin A supplementation/ Cooking in iron pots fortification

Iron fortification and Vitamin D supplementation supplements programs

Zinc supplementation including in diarrhea

Deworming

Universal salt iodisation

Iodine supplements

Preschool feeding programs

Insecticide treated bednets

Hand washing/hygiene interventions Treatment of severe acute malnutrition

low birth weight in that population was about 46%, and 70% of LBW babies were growth retarded (<–2SD weight for age of NCHS reference standards). The follow-up revealed little or no catch-up in growth in weight with the mean Z-score being at –2.38 at birth and at –2.34 at 12 months. The mean length for age Z-scores also revealed no catch up and was lower at 12 months than at birth. Sayers et al [4] have reported the growth outcomes at 11 years of an aboriginal cohort of term growth retarded infants from Australia. The IUGR children were lighter by 4 kg and shorter by 2 cm than the non-IUGR children. Data from developed parts of the world suggest that a larger proportion of IUGR infants show catch up, compared to those from developing countries, yet about 44% are below the 5 percentile weight for age at 18 months and almost 13% are stunted at 12 months [5, 6]. Thus, the evidence suggests that a large proportion of IUGR remain underweight during early childhood and a smaller proportion remain stunted. The magnitude of persistent postnatal growth restriction amongst IUGR infants is probably larger amongst poorer communities, and could possibly contribute to the burden of underweight and stunted children being reported from these regions of the world. It appears logical to assume that the burden of malnutrition could potentially be reduced by reducing the burden of LBW, improving postnatal nutrition of LBW or both. LBW or fetal growth retardation causality has a complexity similar to that of postnatal malnutrition and there exists very little evidence supporting

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strategies that significantly contribute to its reduction. Some of the potential interventions include improving adolescent and maternal nutrition besides other socio-economic and medical interventions. The intrauterine reprogramming induced by fetal growth restriction doesn’t seem amenable to post-natal interventions for growth promotion. In fact, attempts to feed these children to improve their growth centiles are more likely to result in adult cardiovascular and metabolic disease without much increase in obesity amongst these children [7]. There is at present no evidence to support that improved nutrition of IUGR infants promotes significant growth and thus reduces postnatal growth failure amongst these sub-set of children. Breastfeeding promotion Breastfeeding has always been touted as an important strategy for child health and survival. Several publications also have underscored the unique nutritive values of breast milk and its potential long-term impact. What has not been very clear is its impact on nutritional status of children during the first 2 years of their life. A recent systematic review has observed that while breastfeeding promotion has an impact on reduction of child mortality, it has no significant impact on child nutrition especially stunting [8]. The exclusively breastfed children in the WHO Growth reference study were about 360 g and 100 g heavier at 4 and 6 months respectively, compared to the children in the NCHS reference growth curves derived from predominantly non-breastfed children [9]. After 6 months non-breastfed children gain more weight than breastfed children, although their median lengths are similar. Though breastfeeding doesn’t impact on undernutrition, it is an important strategy that must be promoted because of its large benefit on child survival. Complimentary feeding The transition from breastfeeding to family foods is a critical period for preventing child malnutrition. Complimentary feeding interventions are usually targeted in children of 6–24 months which is the peak age for growth faltering, micronutrient deficiencies and illness in most developing countries. After 2 years it is much more difficult to reverse the effects of malnutrition, especially stunting and some of these effects may be permanent. It is very difficult to assess the impact of complimentary feeding alone on growth since most trials have used fortified foods as the intervention. Improving the energy density of foods may have a benefit on growth in societies where traditional foods are low in energy density, and children are unable to compensate by increasing the quantum/volume of food intake. In most trials and programs, educational inputs are important cointerventions. The most common educational messages in most studies included continued breastfeeding during complimentary feeding, use of

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thick porridges for feeding, using animal food source, dietary diversity, responsive feeding and personal hygiene [8]. It has been observed that in food secure populations, educational intervention for complimentary feeding without provision of additional food resulted in a modest reduction in stunting (height for age Z-score (HAZ) was 0.25 (95% CI, 0.01–0.49) scores higher in the educational intervention group). On the other hand, in food insecure population, educational interventions alone had little impact on stunting; provision of complimentary foods reduced stunting (with or without education); the fed group had HAZ scores higher by 0.41 (95% CI 0.05–0.76) [10]. Thus, in situations with fragile food security, educational interventions alone have little impact on nutritional status, specially stunting. In such situations access to food must accompany educational interventions for any impact on nutritional status. Nutritional education Interventions composed of primarily nutritional education appear to have lesser impact on the nutritional behaviours of families and nutritional status of children, than interventions that incorporated child care, health and feeding components into it. A community-based cluster randomized trial in Bangladesh [11], demonstrated that nutritional educational interventions targeted to mothers of infants of 6–9-month old could prevent malnutrition amongst young children (Box 11.1). The study also suggested that the cost of preventing malnutrition in one child using the UNICEF’s “food-health-care” nutritional triangle model ranged from USD 21 to 37. It is also important to note that the targeted nutritional interventions are more effective in reduction of malnutrition when implemented early before onset of malnutrition, than after they become undernourished. In a cluster randomized trial in Haiti [12], the study compared two programs – a preventive model consisting of behavioral changes and communication component, which targeted all children of 6–23 months, and a recuperative model which provided, in addition, food assistance to all underweight children (WAZ score <–2) of 6–60 months. At follow-up, stunting, underweight and wasting were all 4–6 percentage points lower in the preventive arm. The weight for age, height for age and weight for height Z-scores were all higher in the preventive group compared to the recuperative group. The effect was more in children exposed to the full span of the intervention of 6–24 months than in those exposed for shorter duration. The effect on nutrition status was observed independent of the quality of the delivered intervention or the population’s utilization of health-care services. A key to the success of any health-care intervention is when communities participate in identifying their problems and its solutions, and participate in the implementation of the intervention. A good success story is the ‘Dular’ project in India, an initiative of the UNICEF to strengthen

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Box 11.1 Preventing malnutrition through nutrition and health education in rural Bangladesh Mothers of infants aged 6–9 months were provided messages on feeding, care of the child and health seeking. Focus group discussions with the mothers at baseline formed the basis for developing culturally appropriate messages used in the study. Along with these messages they were demonstrated the preparation of energy and protein rich local complimentary foods such as khichari (see Table 11.2). Both the quantitative and qualitative aspects of complimentary foods were explained to caregivers and separate feeding pots were identified in the household to provide estimates of the food intake of the infants. These interventions were provided by community health workers/counselors to small groups of women (6–8 per group). Nutrition education sessions were provided once a week for 3 months and then once every 2 weeks for another 3 months. The comparison group received standard nutritional counselling twice weekly under its integrated nutrition program. Table 11.2 Ingredients and preparation of Khichri [11]

K hi chri – ingredients and preparation I ngredi ents

Quanti ty

R ice Lenti l Oi l

2 fi stful (65 g) 1 fi stful (25 g) 5 teaspoonfuls ( 18.8 g) 1 medi um size ( 50 g) 1 medi um size ( 17.6 g) 1 piece (26 g)



Required amount of rice, lentil, oil boiled in water. After 10 min potato, vegetables and egg/meat/fish added. If green leafy vegetables are used, P otato they are added 5 min after boiling of rice. After that cooking pot is covered Onion and allowed to cook for 25 minutes. After cooking the expected weight of P umpkin/ khichri was about 650 g. Mothers instructed to cook in the morning and V egetabl es Garl ic/ gi nger ½ tespoonful ( 4 g) serve the amount in 5–6 servings to the child within 12 h. S alt ¾ teaspoonf ul ( 3 g) E gg/meat/fi sh* 1 piece (55 g) Water 4 glasses At the end of 1 year more mothers in the intervention group were giving 3 more times/day of complimentary feed (88.5%), khichari as the main complimentary food (15.4%), adding extra oil in food (61.3%) and using a separate pot for the child (91.8%) compared to the control group (24.5%, 4.4%, 21.5% and 76.8% respectively). At the end of the observation period, the children in the intervention arm had a higher weight gain (1.89 versus 1.31 kg, p<0.001). The proportion of normal and mildly malnourished children were higher in the intervention arm (88.9% versus 61.5%, p>0.001). The length for age Z-scores were also significantly higher in the intervention group compared to the control arm.

community participation and the ICDS. Community mobilization by local resource persons, inter-sectoral participation and networking resulted in improved maternal and child care. It was noted that in Dular project areas children received complimentary feeds earlier and there was a 45% lower prevalence of severe malnutrition [13]. Educational interventions for improving complimentary feeding are

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effective in populations which have sufficient means to procure appropriate foods. In populations with food insecurity, educational interventions would benefit only when provided along with food supplements. Food fortification including multiple micronutrient supplementations (MMN) Food fortification has been considered a complimentary strategy for improving the growth of children less than 2 years. A systematic review evaluated [10] six efficacy trials on the effect of fortification of complimentary foods on growth. Three trials involved home fortification of complimentary foods with micronutrient supplements (as sprinkles or crushed tablets). The other studies used cereal/legume mixes or a milk formulation. In all studies, the control group received unfortified foods. The only study that showed an effect on growth was a study from India which used a milk formulation. The children in the intervention group gained significantly more weight (0.21 kg, 95% CI 0.12, 0.31 kg) and had greater mean length (8.6 ± 1.14 versus 8.1 ± 1.37 cm). Review of 13 trials and 2 systematic reviews using multiple micronutrient supplementation on growth [8], noted that it increased the weight for age Z-score (WAZ) by 0.12 (95% CI 0.01, 0.23) compared to iron supplementation. Trials with three or more micronutrient supplementations resulted in 9.24 g/dl increase in haemoglobin (95% CI 5.13, 13.35) compared to trials using either placebo, one or two micronutrients. It thus appears that while food fortification improves weight gain, it appears to have inconsistent effect on linear growth and does not appear to impact on the prevalence of stunting. Using ready-to-use nutritional “multimix” supplements appears an attractive preposition for combating nutritional problems in pre-school children. In a randomized controlled trial amongst pre-school children in Brazil, the intervention arm received 10 g/day of a multimix (composed of rice bran, wheat flour, cassava, safflower seeds) added to the routine school meals each day for 6 months [14]. At the end of the observation period there was no significant difference in weight, height or haemoglobin levels between the two groups. It appears that these strategies do not improve nutritional status of pre-school children. There appears to be little benefit of micronutrient supplementation or fortification, except for iodine, on micronutrient status of young children. Micronutrient supplementation Amongst the several micro-nutrient deficiencies, iron, zinc and vitamin

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A appear most important in most developing countries. Review of randomized controlled trials (RCT) and systematic reviews on iron supplementation [8] indicate that iron-supplemented children had an average of 7.4 g/dl higher haemoglobin concentration compared to unsupplemented group (95% CI 6.1–8.7). Based on these observations, it has been estimated that reduction in the prevalence of anemia could range from 38% to 62% in non-malarial areas, while in malaria hyperendemic regions it could range from 6% to 32%. Fortification with iron alone in school children reduced prevalence of anemia by 70% (RR 0.30, 95% CI 0.17–0.51). Similarly, studies on use of sprinkles for home fortification in targeted children resulted in increase of haemoglobin (weighted mean difference 5.7 g/dl, 95% CI 1.78–9.57) and reduction in iron deficiency, anemia (RR 0.54, 95% CI 0.42–0.70) compared to placebo [8]. With regard to zinc it was observed while zinc reduced diarrheal morbidity and also child mortality, it had a significant beneficial impact on child nutrition. The average effect size for change in weight was 0.31 (95% CI 0.18–0.44). Similarly the mean effect size for change in height was 0.35 (95% CI 0.19–0.55) [8]. Vitamin A supplementation in the neonatal period has been used for mortality reduction and its effects have been equivocal. Its impact on undernutrition has not been demonstrated. Evidence suggests that untargeted iron supplementation should not be used in children as it may be detrimental in children. Zinc supplementation appears to have a positive effect on nutritional status of children, besides its benefit in reducing diarrheal episodes. Conditional cash transfers (CCT) Conditional cash transfers are becoming an increasingly popular program for poverty alleviation. The idea behind CCT is simple: to receive cash transfer, the families must undertake certain activities (such as regular health exams or regular attendance of children at school). In food insecure households in Central and South America, interventions of conditional cash transfer resulted in decline in prevalence of underweight from 15% to 10% and a 10% reduction in stunting from about 40% [8]. Deworming children An important issue is whether routine deworming as an adjunct intervention contributes to improved nutritional state in children. Review of published studies indicates that deworming children resulted in non-significantly higher haemoglobin compared to placebo. Single dose of a deworming

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agent resulted in a significant increase in weight by 0.24 kg (95% CI 0.15– 0.32 kg), while multiple dosing resulted in a weight increase of 0.10 Kg (95% CI 0.04–0.17). Mebendazole for deworming significantly reduced the risk of wasting by almost 47%. Deworming also improved increase in height. A single-dose strategy increased height by 0.14 cm (95% CI 0.04– 0.23), while multiple dose by 0.07 cm (95% CI 0.01–0.15) [8]. Routine deworming has no benefit on the nutritional status of children. In areas with heavy worm infestation, it could possibly impact by reducing anemia prevalence. Growth monitoring The need for growth monitoring of children to assess their nutritional and health status is undisputed. However, what is currently being debated is its impact in bringing about a change in childhood malnutrition status and utilization of health services. Studies (including projects from India such as the Tamil Nadu integrated nutrition project) have shown that children whose growth has been monitored, and whose mothers receive good nutritional counselling have better nutritional status. However, results from large scale programs have been equivocal. While interventions from Brazil have shown a benefit; those from the India (ICDS program) and Bangladesh (BINP) have not shown any benefit [15]. The reasons for this disparity in observations may lie in the effectiveness of nutritional counselling by the workers. For growth monitoring activities to be effective, counselling must be done well, but most often they are done badly. In spite of the equivocal evidence on its benefits, it provides several contact points for families to access health services. There is a need to strengthen growth promotional activities beyond just charting children’s weight on a monthly basis. In resource limited setting, growth charting may be limited to contacts at birth and during the immunization visits (6, 10, 14 weeks and 9 months) and sick child visits. Routine weight charting may be discontinued beyond 12 months in those children who show good growth; follow-up monitoring is required only in children showing growth faltering or those whose weight for age < –2SD. The capacity of health workers must be improved in terms of their knowledge and counselling skills so that effective nutritional education can be imparted to mothers. Growth monitoring should not be an end in itself, it should be the means of improving child health. Current evidence does not support growth monitoring as a strategy to reduce undernutrition in children.

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301

Managing malnutrition

Traditionally while mild-moderate forms of malnutrition have been treated on an outpatient basis and at home, severe acute malnutrition has been treated on an inpatient basis. This has historically been the textbook teaching, because most of the cases of severe acute malnutrition came late with physiological derangements and multiple complications. However, inpatient treatment is associated with huge opportunity and economic costs both to the families and health-care providers. These costs are often unaffordable and inpatient-treatment programs are associated with low coverage, low recovery, high mortality and high default rates. Review of global experience suggests that both delivery systems, namely inpatient (hospital or nutrition rehabilitation units) and outpatient (community) therapeutic care can be equally effective in treating children with malnutrition. It has become increasingly evident that children with severe acute malnutrition without complications can be treated as effectively as outpatients compared to the inpatient program at lower costs and default rates [16].

11.4.1 Inpatient (hospital) care Convention has been to admit all children with severe malnutrition – weight for height <70% of reference median or below 3 standard deviations of mean or those with symmetrical edema. However, admission criteria that use clinical signs along with mid-upper arm circumference measurement that can be used even by primary-care providers, especially in under-resourced scenario, are depicted in Table 11.3. The treatment during the first week consists of managing complications such as hypoglycaemia, hypothermia, dehydration, sepsis and other problems. Feeding the child as early as possible is an important component of initial treatment. Since these children are usually unable to tolerate large amounts of protein, they need a diet low in protein and high in carbohydrate. During initial treatment a formula F-75 (75 kcal per 100 ml) is used to feed the child (Table 11.4). The goal is to provide the child 130 ml/kg of this formula. If the child’s appetite is poor then the child is fed via a nasogastric tube. Once appetite improves, the child enters the rehabilitation phase which involves increase in feeding to achieve catch up growth, stimulate emotional and sensorial development. Catch up growth is facilitated by providing an F-100 (100 kacl/100 ml) (Table 11.4) dietary formula. This formula should be continued till the child reaches 90% of median weight for height. Once the child is eating well, becomes interested in its surroundings, has no edema, is free of illness, and is gaining at

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least 5 g/kg/day for 3 successive days, treatment can be shifted to nonresidential care in a nutritional rehabilitation centre or clinic. Table 11.3 Criteria for selecting children with severe acute malnutrition (age 6–59 months or 65–110 cm height as proxy for age) outpatient and inpatient care Outpatient therapeutic care

Inpatient care

(No complications)

(With complications)

MUAC < 115 mm

Bilateral pitting edema grade 3(a)

OR

OR

Bilateral pitting pedal edema grade 1 or 2* with MUAC > 115 mm

MUAC < 115 mm and bilateral pitting edema grade 1 or 2

AND all of the following: Good appetite Clinically well Alert

• • •

OR MUAC < 115 mm OR bilateral pitting edema grade 1 or 2 AND one of the following: • Anorexia • Lower respiratory tract infections • Severe palmar pallor • High fever • Severe dehydration • Not alert

Grade 1 – mild edema on both feet and ankles; Grade 2 – moderate edema on both feet and legs, hands or lower arms; Grade 3 – severe generalized edema, including both feet, legs, hands, arms and face (a)

Table 11.4 Composition of F-75 and F-100 dietary formula Ingredient

Fresh milk or equivalent Sugar Cereal flour (or powdered puffed rice) Vegetable oil Water to make

Amount F-75

F-100

30 ml 6g

75 ml 2.5 g

2.5 g 2.5 g 100 ml

7g 2.0 g 100 ml

Milk cereal diets do need cooking. Mix the flour, milk or milk powder, sugar, oil in a measuring jug. Slowly add cooled, boiled water up to 100 ml. Transfer to cooking pot and whisk the mixture vigorously. Boil gently for 4 minutes, stirring continuously. Some water will evaporate, so transfer the mixture to measuring jug and add enough water to make 100 ml. Cooking can be avoided if you use puffed rice powder or commercial precooked rice preparation as cereal flour. Give additional vitamins and

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minerals. Multi-vitamin supplement at twice RDA (should contain vitamin A, C, D, E and B 12 and not just vitamin B-complex), folic acid; 5 mg on day 1, then 1 mg/day, zinc; 2 mg/kg/day, copper; 0.3 mg/kg/day and iron 3 mg /kg/day.

11.4.2 Community management of severe acute malnutrition Community-based therapeutic care (CTC) is a community-based therapeutic intervention based on the principles of access, coverage and cost-effectiveness. The three basic premises of this model are that if malnourished subjects gain early access to a nutritional program before their condition deteriorates and stay in the program till recovery, the success rates are high. Second, to be sustainable and effective, community-based programs must involve the target populations. Third, for these programs to remain sustainable, investment must be made in social mobilization so that the key stakeholders can benefit from the positive feedback from individual success stories. CTC can be provided through day care nutrition centres, health clinics or domiciliary care. A recent review has analyzed the efficacy and effectiveness of these therapeutic models [17].

11.4.3 Health clinics Inpatient care of severely malnourished children has socio-economic dimensions that limit its acceptability. Ashraf et al [18] developed and prospectively evaluated a day-care clinic approach in Bangladesh. All children received protocolized management with antibiotics, micronutrients and milk-based diet from 8:00 am to 5:00 pm each day, while mothers were educated on continuation of care at home. They were transitioned to the day-care nutrition rehabilitation unit following resolution of acute illness. About 264 children were enrolled; 78%, 21% and 1% had marasmus, marasmus–kwashiorkor and kwashiorkor, respectively. One-third had pneumonia, 35% had diarrhea, and 17% had both pneumonia and diarrhea. Successful management was possible in 82% children, 12% discontinued treatment and 6% referred to hospitals.

11.4.4 Day-care nutritional centres These were envisaged as a simple building where upto 30 malnourished children could attend 6–8 hours for 5–6 days in a week, and receive three meals a day for about 3–4 months. Mothers would help to cook

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and clean, and learn good feeding and child care practices. Most studies did not document a benefit as default rates were high, sustainability difficult, and their popularity appears to have waned. However, only the program in Bangladesh appears to have been effective [18] (Box 11.2). Box 11.2 Managing malnutrition through Day care nutritional centres: Bangladesh experience The nutritional centres were set up in the poorest areas of Dhaka and facilities donated and were maintained by the local nutritional councils. The centres were open for 8 hours a day and manned by volunteers from the Urban Health Extension Program (UHEP). UHEP provided trained the volunteers, food and technical support. Each centre had 5 volunteers and 25 children, and the centres were supervised by weekly visits by physicians. At enrollment each child was given high dose of vitamin A and immunization and antibiotics if signs of infection were present. The children were provided 3 meals and 2 snacks/day. Locally available, low-cost and energy densed food, such as stuffed paranthas, lentils, halwa, khichuri, potato and high energy milk (1 kcal/ml). Mothers actively participated in meal preparation. Mothers were providing education on prevention of malnutrition, diarrhea, family planning, child care and hygiene. Children who completed the treatment had a weight gain of approximately 5 g/day over 4 weeks. No children died. The reasons for non-attendance included disruption of care of other children at home, loss of wages and girl child. Maintenance of these facilities without aid is a problem and therefore the sustainability of this model is questionable.

11.4.5 Domiciliary care The first step is identifying cases of severe acute malnutrition who qualify for community based or domiciliary care. Traditionally, the existing therapeutic programs have used either weight for age or weight for height of median reference (or Z scores), for identifying children needing inpatient care. Recognizing the difficulties of recording height by front line community health workers, the Integrated Management of Childhood Illness (IMCI) guidelines used weight for age and/or presence of severe visible wasting, severe pallor or bilateral pedal edema’ as criteria for screening children for inpatient care. However, often recording weights or objectifying severe pallor are problems in the community. The present recommendations using midupper arm circumference (MUAC), edema and complications for identifying children in need of outpatient therapeutic care or inpatient care are depicted in Table 11.3. It is important that all children are assessed by a trained health worker who can assess MUAC, respiratory rate, edema, pallor, temperature, hydration status, alertness and appetite. A vital step in the decision-making process is the child’s appetite. Appetite is assessed by giving the child some therapeutic diet or ready to use therapeutic food (RUTF) and see if the child eats it freely. It is vital that the child is provided sufficient time and a calm environment to eat the food.

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11.4.6 Nutritional treatment Energy dense therapeutic diets with low bulk are essential in the initial phase of management. However, these should be economical, available, and acceptable. These diets could be (i) home based (prepared/modified from the family pot); or (ii) ready-to-use therapeutic food (RUTF). Table 11.5 provides the typical ingredients of an RUTF. The first commercial RUTF was Plumpy’nut, which is a mixture of peanut butter, milk powder, oil, sugar, mineral/vitamin and protein mix (each packet of 92 g provides 500 kcal). This compares with the F-100 formula used in dietary rehabilitation of severe malnourished children in hospitals. Commercially available international RUTF may not be suitable, acceptable, costeffective and sustainable in most resource poor settings [19]. Local production of RUTF is however possible [20] (see Box 11.3). Each child needs about 200 kcal/kg/day of therapeutic diet. Feeding should be frequent (6 to 8 times per 24 hours), active, and hygienic. The mother must be counselled that the child consumes the therapeutic food before consuming other foods. If the mother is still breastfeeding, then she is asked to give the therapeutic diet after the breastfeed. The child is followed weekly at the centre (this could be a health centre, an anganwadi centre or even the clinic of a registered medical practitioner (RMP)). The child should receive mineral and multiple micronutrient supplements as per standard WHO protocol for inpatient management of such children. Box 11.3 Local production of RUTF For producing a few hundred kilos of RUTF needed each week, small scale production is possible. It requires a small room dedicated to food production and free of rodents and other pests, and a 40-L planetary bakery mixer. Such mixer can mix 25 kg of RUTF per batch. Oil and peanut butter should be directly added to the mixing bowl and combined at a mixing speed of 105 rpm till homogenous. A Z-shaped kneader blade rather than wire whisk device should be used to minimize the amount of air incorporated into the mixture. The sugar, milk powder and vitamin and mineral mixture are hand mixed as dry powder in a separate dedicated plastic container and then added into the electric mixing bowl. The RUTF are then mixed at 105 rpm for 6 minutes, 210 rpm for 6 minutes, and 323 rpm for 6 minutes. The RUTF can then be poured or hand packed into plastic bottles containing 250g; a typical daily dose for a malnourished child. Table 11.5 Recipe for typical RUTF Ingredients Full fat milk Sugar Vegetable oil Peanut butter Mineral–vitamin mixture

% weight 30 28 15 25 1.6

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11.4.7 Medical treatment At admission into the therapeutic program, each child should receive a single dose of vitamin A (it is not given if child has received it during the last 1 month or if edema is present). In children with edema it should be given before they leave the program, Amoxicillin (thrice a day) for 7 days, and in malarial areas appropriate anti-malarial medication. On the first follow-up visit, a single dose of Folic acid (5 mg) should be given, and Mebendazole/ albendazole (in children > 12 months) as single dose on the second follow-up visit. The child must be immunized as per the prevalent national guidelines.

11.4.8 Follow-up visits A recommended schedule for follow-up visits is weekly for 8–12 weeks at facility or at home. If home visits are possible, 2 contacts/week for the first 2 weeks is recommended. After 8–12 weeks the child should be followed once a month till 6 months. But experience in Africa suggests that children who have stayed in the program for 8–12 weeks and have recovered, remain nutritionally well for about 12 months even without follow-up visits.

11.4.9 Recovery and discharge from home-based program A child could be considered recovered if he/she has been on follow-up for a minimum of 2/3 months, has an MUAC>115mm, is edema free for at least 2 weeks, shows sustained weight gain (weight gain each week for at least 3 weeks), is clinically well and infection free. The guidelines for community management of severe malnutrition are summarized in Table 11.6 [21]. Table 11.6 Guidelines for community management of acute severe malnutrition ●

●

●

● ● ●

●

●

Children between 6 and 59 months only should be considered for community management of severe malnutrition Children eligible for enrollment are those with MUAC < 115 mm (or weight for height <70% of WHO reference median or < 3 SD of reference mean) with complications (see Table 11.3 for details) RUTF or locally available nutrient dense food can be used for rehabilitation. If RUTF is used, the children should receive 150–220 kcal/kg/day Children should receive appropriate mineral and vitamin supplements Medications could include antibiotics and/or anti-malarials at entry into program and deworming Criteria for effectiveness of treatment is a weight gain of at least 5 g/ kg/day Discharge from the therapeutic program can be considered when MUAC >115mm and the child is edema free.

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The success story with RUTF in domiciliary management of malnourished children is depicted in Box 11.4. Box 11.4 Home-based therapy of malnutrition with RUTFMalawi experience [22] Children of 10–60 months were randomly allocated to receive either standard therapy (F-100 formula during inpatient stay and at discharge a supplemented maize-soy blended flour) or RUTF (a locally produced RUTF which provided 175 kcal/kg/day and 5.3 g/kg/day). The children were followed up 2 weekly at clinic for assessment and receipt of food supplements. Children who received RUTF were more likely to achieve a weight for height Z-score >–2 compared to those on standard therapy (79% versus 46%); less likely to relapse or die (8.7% versus 16.7%). The home RUTF group also had fewer episodes of cough, fever or diarrhea on follow-up.

11.5

Guidelines for management of mild-moderate malnutrition

Non-severe forms of malnutrition are managed at home by counselling and educating care providers on feeding and care of the child. The IMCI feeding guidelines provide a good backbone for implementing nutrition management of children with milder forms of malnutrition (Table 11.7). Table 11.7 IMNCI feeding guidelines (6–59 months) 6–12 months

12 months up to 2 years

2 years or older

•

•

•

• •

• •

Breast feed as often as possible Give atleast 1 cup of complimentary foods per serving Give the child 3 servings/day if breast fed; if not atleast 5 servings/day Keep the child on your lap and feed with your own hands Wash your and child’s hands with soap and water before each feed

11.6

• • • •

Breast feed as often as possible Give atleast 1.5 cup of complimentary foods per serving Give the child 5 servings/day Sit by the child’s side and help finish the food Wash your child’s hands with soap and water before each feed

• • •

Give family foods in 3 meals each day Give the child also 2 snacks of nutritious food each day Ensure the child finishes the serving Teach the child to wash hands before each meal

Conclusion

Malnutrition in childhood is the result of multiple causes with a complex web of interactions. Its prevention requires a change in economic and sociocultural environment. Amongst the most effective interventions are those of nutritional and educational counselling of care providers. Sustainability of these impacts requires community mobilization and empowerment.

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Evidence suggests that uncomplicated severe acute malnutrition can be managed at home, and duration of stay of those needing hospital admissions can also be curtailed and dovetailed with the community management program, to reduce costs to families and the health system.

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(2008). Maternal and child undernutrition: global and regional exposures and health consequences. The Lancet 371, no. 9608, pp. 243–260. WHO (2006). WHO Multicentric Growth Reference Study Group. WHO Child Growth Standards: Length/height for age, weight for age, weight-for-length, weight-for-height and body mass index-for age: Methods and Development Geneva: World Health Organisation, 2006. ARIFEEN SE, BLACK RE, CAULFIELD LE , ANTELMAN G , BAQUI AH , NAHAR Q , ALAMGIR S, MAHMUD H (2000). Infant growth patterns in the slums of Dhaka in relation to birth weight, intrauterine growth retardation and prematurity. Am J Clin Nutr 72, no. 4, pp 1010–1017. SAYERS S, MACKERRAS D , HALPIN S, SINGH G (2007). Growth outcomes for Australian Aboriginal children aged 11 years who were born with intrauterine growth retardation at term gestation. Paediatr Perinat Epidemiol 21, no. 5, pp 411–417. Fitzhardinge PM and Inwood S (1989). Long-term growth in small-for-date children. Acta Paediatr Scand Suppl 349, pp 27–33, discussion 34. KARLBERG J and ALBERTSSON - WIKLAND K (1996). Growth in full-term small-forgestational-age infants: from birth to final height. Pediatr Res 38, no. 5, pp 733–739. Erratum in: Pediatr Res (January 1996), 39, no. 1, pp 175. BHARGAVA SK, SACHDEV HPS , FALL CHD , OSMOND C , LAKSHMY R , BARKER DJP , BISWAS SKD, RAMJI S, PRABHAKARAN D , REDDY KS (2004). Relationship of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood. N Engl J Med 350, no. 9, pp 865–875. BHUTTA ZA , AHMED T , BLACK RE , COUSENS S , DEWEY K , GIUGLIANI E , HAIDER BA , KIRKWOOD B , MORRIS SS , SACHDEV HP , SHEKAR M; Maternal and child undernutrition study group (2008). What works? Interventions for maternal and child undernutrition and survival. Lancet 371, no. 9610, pp 417–440. DEONIS M, ONYANGO AW , BORGHI E , GARZA C, YANG H ; WHO Multicentre Growth Reference Study Group (2006). Comparison of the World Health Organization (WHO) Child Growth Standards and the National Center for Health Statistics/ WHO international growth reference: implications for child health programmes. Public Health Nutrition 9, pp 942–947. DEWEY KG AND ADU -AFARWUAH S (2008). Systematic review of the efficacy and effectiveness of complimentary feeding interventions in developing countries. Matern Child Nutr 4, no. 1, pp 24–85. ROY SK , JOLLY SP , SHAFIQUE S , FUCHS GJ , MAHMUD Z , CHAKRABORTY B, ROY S (2007). Prevention of malnutrition among young children in rural Bangladesh by a foodhealth-care educational intervention: A randomized, controlled trial. Food Nutr Bull 28, no. 4, pp. 375–383. RUEL MT , MENON P, HABICHT JP, LOECHL C, BERGERON G , PELTO G , ARIMOND M, MALUCCIO J, MICHAUD L , HANKEBO B (2008). Age-based preventive targeting of food assistance RIVERA J

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and behaviour change and communication for reduction of childhood undernutrition in Haiti: a cluster randomised trial. Lancet, 371, no. 9612, pp 588–595. DUBOWITZ T , LEVINSON D , PETERMAN JN , VERMA G , JACOB S, SCHULTINK W (2007). Intensifying efforts to reduce child malnutrition in India: an evaluation of the Dular program in Jharkhand, India. Food Nutr Bull 28, no. 3, pp 266–273. GIGANTE FP , BUCHWEITZ M , HELBIG R, ALMEIDA AS , AROUJO CL , NEUMANN NA , VICTORA C (2007). Randomized clinical trial of the impact of a nutritional supplement “multimixture” on the nutritional status of children enrolled at preschools. J Pediatr (Rio J) 83, no. 4, pp 363–369. ASHWORTH A , SHRIMPTON R, JAMIL K (2008). Growth monitoring and promotion: review of evidence of impact. Matern Child Nutr 4, pp 86–117. COLLINS S , SADLER K , DENT N , KHARA T , GUERRERO S , MYATT M, SABOYA M , WALSH A (2006). Key issues in the success of community-based management of severe malnutrition. Food Nutr Bull 27, no. 3, pp. S49–S82. ASHWORTH , A (2006). Efficacy and effectiveness of community-based treatment of severe malnutrition. Food Nutr Bull 27, no. 3, pp. S24–S48. ASHRAF H , AHMED T , HOSSAIN MI , ALAM NH , MAHMUD R , KAMAL SM , SALAM MA , FUCHS GJ (2007). Day-care Management of Children with Severe Malnutrition in an Urban Health Clinic in Dhaka, Bangladesh. J Trop Pediatr 53, no. 3, pp 171–178. National workshop on Development of guidelines for effective home based care and treatment of children suffering from acute severe malnutrition (2006). Indian Pediatr 43, no. 2, pp 131–139. MANARY MJ (2006). Local production and provision of ready-to-use-therapeutic food (RUTF) spread for the treatment of severe childhood malnutrition. Food Nutr Bull 27, no. 3, pp S83–S89. WHO, UNICEF and SCN informal consultation on Community-Based Management of Severe Malnutrition in Children (2006). SCN Nutrition Policy Paper No. 21. Food Nutr Bull 27, no. 3. CILIBERTO MA , SANDIGE H , NDHEKA MJ , ASHORN P , BRIEND A , CILIBERTO HM , MANARY MJ (2005). Comparison of home based therapy with ready-to-use therapeutic food (RUTP) with standard therapy in the treatment of malnourished Malawian children: a controlled, clinical effectiveness trial. Am J Clin Nutr 81, no. 6, pp. 864–870.

Severe acute malnutrition in children

12 Severe acute malnutrition in children Kamal Raj

Kamal Raj, a public-health physician, graduated from Osmania University Hyderabad, India. He is post graduate in Community Nutrition in Low-Income Countries from the University of Sweden. Currently, Raj is Nutrition Specialist with UNICEF (India country office). Raj has a vast experience of working in treating war victims and displaced and refugee children in a number of countries. Raj’s specific interest is in the subject of management of severe acute malnutrition (SAM) and infant young child feeding (IYCF) practices of children who are infected and affected with HIV/AIDS.

12.1

An overview

Severe acute malnutrition (SAM) is defined by a very low weight for height (below -3 Z-scores of the median WHO growth standards), by visible severe wasting, or by the presence of nutritional edema (Table 12.1). Acute malnutrition is classified into severe acute malnutrition (SAM) and moderate acute malnutrition (MAM) according to the degree of wasting and the presence of edema. It is severe acute malnutrition if the wasting is severe with mid-upper-arm circumference (MUAC) <115 mm or W/H -3 SD WHO growth standards or there is edema. Acute malnutrition is defined as moderate acute malnutrition if the wasting is less severe (MUAC between 115–125 mm, W/H -2SD WHO growth standards); edematous cases are always classified as severe [1]. Table 12.1 Diagnostic criteria for SAM in children aged 6–60 months [2] Indicator

Measure (b)

Severe wasting Severe stunting(b) Bilateral edema(c) (a)

Weight for height MUAC Clinical sign

Based on WHO standards Independent indicators of SAM that require urgent action Cut-off increased from 110 to 115 mm to define SAM [2]

(b, c) (d)

Cut-off (a)

310

–3 SD < 115 mm(d)

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12.2

311

Clinical features

A path-physiological change that takes place in children with severe acute malnutrition (SAM) is very complex. Studies have shown that even experienced paediatricians have difficulties in understanding and diagnosing case of SAM correctly. Nutritional deficiencies are common in children with severe acute malnutrition. Angular stomatitis resulting from B vitamin deficiency is frequently observed. A smooth tongue in a SAM child can be due to B 12 or chronic foliate deficiency. Oral Candida is very common and affects the mouth, esophagus, stomach and colon. Disseminated Candida is a common infection that does not respond to routine antibiotics – most children need nystatin or ketoconazole. Gentian violet is not sufficient. Many children with SAM develop very thin skin with tissue fluid seeping through. Anemia is common among these children. Another common condition is photophobia, which is seen in more than half of the children, and in such cases eye ball can get injured during examination. All patients have gross osteoporosis, but fractures are rare. Affected hair becomes straight and discoloured; most malnourished children go bald. The ease with which the hair is pulled out is a measure of the reduction in protein synthesis and it is a useful sign in diagnosis of SAM. Blond hair has no prognostic significance. Scorbutic rosary is due to chronic Vitamin C or copper deficiency. Multiple small green mucoid stools are a common feature of malnutrition. Counting the stools can give a false impression of diarrhea. It is due to changes in the colonic metabolism and is not related to infections such as Entaemoeba. An orange stool when exposed to atmosphere turns green in malnourished children. Severely malnourished children have abnormal kidney and liver function; metabolizing and excreting drugs become difficult due to changed levels of the enzymes [3].

12.3

Severe acute malnutrition and mortality

Severe acute malnutrition (SAM) remains a major killer of children under five years of age. SAM contributes to one million child deaths every year [1]. Globally, it is estimated that there are nearly 26 million children who are severely acutely malnourished [1–4]. Most of these SAM children live in South Asia and in Sub-Saharan Africa (Box 12.1). In India currently 8.1 million children are severely wasted (severe acute malnutrition). India has 31.2% of the world’s severely wasted children and the largest pool of severely wasted children worldwide [5]. Details on SAM prevalence are presented below:

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Box 12.1 Wasting and stunting in children in Africa and India 70

6 0.9

Africa India 4 7.6

35

2 5.4 11 .3

0 W a sted

Stun te d

12.1 Percentage prevalence of wasting and stunting in Africa and India. In India, the rates of wasting and stunting is 25% and 61%, while severe form of wasting and stunting is reported to be 6.4 and 23.7 respectively [6]. The percentage prevalence is much higher than the sub-Saharan African countries (Figure 12.1), even though the latter is one of the most food insecure regions in the world. One of the most important contributing factors for the situation in Africa is that the prevention and out-reach programmes are very well-designed. In Africa, severe malnutrition is addressed through effective implementation of welldesigned strategies constituting community- and facility-care components with clear guidelines, treatment protocols in place with regular trainings, and capacity building of health workers and community workers. In India, no such guidelines are in place for care of SAM children [5].

Severe acute malnutrition (SAM) can be a direct cause of child death, or it can act as an indirect cause by dramatically increasing the case fatality rate in children suffering from such common childhood illnesses such as diarrhea and pneumonia. The risk of death is 5–20 times higher in severely malnourished children compared to well-nourished children. On an average, mortality rate in SAM children is estimated to be 9 times higher than those in well-nourished children [5]. Using existing studies of case fatality rates in several countries, WHO has extrapolated mortality rates of children suffering from severe acute malnutrition (Table 12.2). Table 12.2 Mortality rate in children with severe acute malnutrition [1] Country

Mortality rate

Congo, Democratic Republic of the Bangladesh Senegal Uganda Yemen

21% 20% 20% 12% 10%

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12.4

313

Management of severe acute malnutrition (SAM)

Along with efforts to prevent undernutrition, therapeutic programs are needed as “safety nets” in parallel with prevention programs (Box 12.2). Management of SAM calls for a specialized care considering the vulnerable health situation of children due to altered physiological state which involves multiple organ systems of the body. Until recently, the gold standard for management of SAM, as per the WHO recommendation, is to admit severely malnourished children to hospitals as inpatients for a period of at least a month. This requires many trained staff and substantial inpatient bed capacity. In places where such facilities are available, sufficient attention can be paid to the quality of care and there is adequate evidence that this approach can substantially decrease case fatality rates in both stable environment and emergency situations. However, the limitations of a hospital-based approach for addressing a large number of children, particularly when hospital capacity is poor, have been recognized for more than 30 years. Moreover hospital stays of several weeks for a child and mother are disruptive for families, especially when the mother has other children at home or when her labour is essential for the economic survival of the household. As a result, hospital-based management of severe malnutrition has been perceived as efficacious, but not effective, on a large scale, either as part of routine health services or in emergencies. Moreover, institution-based care reduces family or community involvement. Box 12.2 Prevention and management of SAM – a parallel effort Malnutrition, severe or otherwise, is estimated to be a contributing factor in over 50% of child deaths. Moderate malnutrition contributes more to the overall disease burden than severe malnutrition, since it affects many more children, even if the risk of death is lower. Preventing all forms of malnutrition therefore need to be accorded a high priority in developing countries. Reduction in child malnutrition depends on interventions during fetal development and early childhood. Preventive nutrition interventions need to focus on high priority population groups–women during pregnancy and lactation and young children. Children under 24 months of age require special attention since this is the period when the children are growing most rapidly and are most vulnerable to irreversible deficits in growth and development .However, existing prevention programs are inadequate, especially in the poorest countries or in countries undergoing an emergency crisis. Many children therefore go on to become severely malnourished, even when prevention programs are in place, and these children will require treatment. Therapeutic programs are required to be implemented in parallel with prevention programs [7].

In view of the above and also considering the fact that in many poor countries, majority of children who have severe acute malnutrition are never brought to health facilities; it has been felt that only an approach with a strong-community component can provide them with the appropriate

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care. In recent years, there has been a significant development in the treatment of SAM at community level. WHO and UNICEF recommend two major approaches for the treatment of SAM: facility- /hospital-based approach for clinical management (using the WHO protocol) and home- or community-based approach, an integrated response to acute malnutrition without medical complications. Facility-based management refers to treatment in a hospital or centre that provides skilled medical and nursing care on an inpatient basis. The term community-based management refers to treatments that are implemented with some external input, such as that provided by health worker for diagnosing the condition, instituting treatment, and monitoring the condition of child at home [7]. Severe malnutrition is both a medical and a social disorder. Addressing SAM therefore requires an integrated approach that combines facility and community-based quality feeding and care. Every child with SAM requires therapeutic food and care in a timely manner, for life saving and rapid weight gain and recovery. Care for children with SAM requires early case detection (before the development of medical complications), optimal therapeutic feeding and care protocols, and access to therapeutic foods. Successful management of the severely malnourished patients requires that both medical and social problems be recognized and corrected. If the illness is viewed as being only a medical disorder, the patient is likely to relapse when he/she returns home. The first step is to identify SAM children through a nutritional survey and the second step is to provide therapeutic feeding and other required treatment until the child regains its normal weight.

12.4.1 Identification of SAM Children Identification of SAM may be based on: (i) clinical criteria (presence of visible severe wasting or bipedal edema); or (ii) mid-upper-arm circumference (MUAC) of 11.5 cm in children 6–59 months of age. The cut-off recommended for screening using MUAC is as follows:

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(a) MUAC criteria Screening – Mid-upper-arm circumference (MUAC) ● Severe acute malnutrition (SAM): MUAC < 115 mm; ● Moderate acute malnutrition (MAM): MUAC = ≥115 and <125 mm; and ● Normal: MUAC ≥125 mm (b) Clinical criteria Bilateral pitting edema ● 0 = Absent ● + = Mild: both feet/ankles (Grade 1) ● ++ = Moderate: both feet, plus lower legs, hands, or lower arms (Grade II) ● +++ = Severe: generalized oedema including both feet, legs, hands, arms and face (Grade III)

(c) Weight for height criteria (using WHO 2006 standards—see Box 12.3) ● ●

SAM: –3SD WHO Growth Standards (2006) MAM: –2SD WHO Growth standards (2006)

MUAC tape is the most appropriate screening tool and has an advantage over all other methods, considering its simplicity, acceptability, precision, cost, accuracy, and the predictive value. In Bangladesh, Uganda and Malawi, MUAC has been successfully used for accelerating identification and for achieving a high coverage of SAM children for treatment in a short period [5]. The other anthropometric criterion of “weight for height” for diagnosis of SAM is complicated and operationally not feasible, as it requires use of many tools and complex calculation. This criterion may create confusion amongst the health workers or other grass-root workers.

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Box 12.3 Programmatic implications of using WHO child growth standards In 2006, the World Health Organization released new child growth standards. The introduction of the WHO new standards, with the Z-score criterion (weightfor-height –3 Z-score), for identifying children for admission into SAMtreatment programs has some important programmatic implications. Using < -3 Z-score implies the inclusion of children who are younger but have relatively higher weight-for-height on admission compared with the National Centre for Health Statistics (NCHS) reference that uses weight-for-height <70% of the median criterion for SAM case detection. Using the WHO standards in developing country situations results in 2–4 times increase in the number of infants and children falling below -3 SD compared to using the former NCHS reference. The introduction of the WHO child growth standards (and MUAC <115 mm) to identify SAM children will increase the caseload for therapeutic feeding programmes; however, at the same time, more children will be detected earlier and in a less-severe state; thereby resulting in faster recovery and lower case-fatality rates. Increasing number of children with SAM identified using the new WHO cut-offs has cost and human resource implications, especially in resource-poor settings [9].

Efforts to identify severely malnourished children need to be undertaken at community as well as at the outpatient department (OPD) and emergency ward within the hospital. In fact, every available opportunity for identification of SAM must be utilized so that maximum children are covered. All possible contact opportunities with children need to be exploited including home visits, immunization outreach sessions, community health centre, primary health centre (PHC) network and clinics. It is important that most peripheral child health workers or community workers are encouraged to identify severely malnourished children. Verification of identified SAM cases, if required and feasible, be undertaken by higher level of functionaries. Role of family members, including mothers, traditional birth attendants, link workers in the community (community volunteers, village adolescents, etc.), in identification of SAM children is therefore considered essential. In India, formal linkages between registered medical practitioners (RMPs) and government functionaries can be developed for identification and referral of SAM children in the community.

12.4.2 Therapeutic feeding programs – admission and discharge criteria Therapeutic feeding Details of therapeutic feeding such as F-75, F-100 are presented in Box 12.4 and on RUTF in Box 12.6.

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Box 12.4 Details of therapeutic feeding [10] Therapeutic milk F-100 F-100 should be used in accordance with the recommendations of doctors and nutritionists. This product contains all the nutrients necessary in the treatment of severe malnutrition; therefore it is recommended not to add anything else. Recommended use – Do not distribute to families. Use only in therapeutic feeding centres. Composition – Skimmed milk powder, vegetable fat, whey powder, malto-dextrin, sugar, mineral and vitamin complex. Preparation – Each sachet contains the quantity necessary to be added to 2 litres of boiled water in order to obtain 2.4 litres of therapeutic milk. Therapeutic milk F-75 F-75 therapeutic milk is to be used during the first phase of the dietetic treatment of severe malnutrition. F-75 therapeutic milk must be used in accordance with the recommendations of doctors and nutritionists. It is advisable to use this milk during phase 1 of the dietetic treatment of severe malnutrition (rehydration phase, treatment of medical complications and beginning of the nutritional rehabilitation). As this milk is not intended to gain weight to the child, its use should be restricted to phase 1 of the treatment. During the second phase, the standard therapeutic milk formula F-100 is used. F-75 therapeutic milk contains all the nutrients necessary for the treatment, therefore it is recommended not to add anything else. Recommended use – To be administered at the rate of 135 ml/kg/day in 8–12 meals per day. As the energy density is 75 kcal for 100 ml, this is equivalent to 100 kcal/bodyweight/day. Composition – Skimmed milk powder, vegetable fat, sugar, malto-dextrin, vitamin and mineral complex.

Admission criteria All children of 6–59 months who fulfil any of the following three criteria have SAM and should be treated and offered therapeutic feeding in one of the available settings: ●

● ●

(Weight/height or length) W/H or W/L < –3 Z-score (2006 WHO standards) or MUAC < 115 mm or Presence of bilateral oedema (+ and ++ admission to out-patient; +++ admission to in-patient care) [as explained above]

Admission and discharge from feeding programmes are based on MUAC or weight-for-height Z-score, using the WHO standards for children of 6– 59 months. Separate reference charts for boys and girls be used for admission and discharge until further evidence supports using a combined reference chart [6].

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MUAC continues to be used as an independent criterion for admission to therapeutic feeding program. The recommended current revised cutoff for identification of severe acute malnutrition of MUAC is <115 mm. Discharge criteria The recommended discharge criteria for therapeutic feeding programs are as follows: ●

●

Percentage weight gain of 15%. This criterion can be used for all children admitted to therapeutic feeding programs, either on weightfor-height or on MUAC. Weight-for-height > -1 Z-score WHO standards. This criterion can be used when children are admitted according to weight-for-height. ■ For children with edema, the same discharge criteria should be applied using the weight-after-edema has disappeared as the baseline. For children who have a weight-for-height above -3 SD or an MUAC above 115 mm after edema has disappeared, discharging after two weeks is usually sufficient to prevent relapse.

12.4.3 Community-based and facility-based care The care of SAM is presented under the following two sections: (a) Community-based care (b) Facility-based care Community-based management of SAM is based on early detection and assessment of children with SAM who have no medical complications. Those with complications, evidenced by loss of appetite assessed by conducting an appetite test (Box 12.5), require facilitybased treatment. Evidence suggests that about 80% of children with SAM who have been identified through active case findings, or through sensitization and mobilizing communities to access decentralized services themselves can be treated at home [1]. The community-based component of the treatment of severe malnutrition is recommended to be closely linked with the facility-based component so that children who are ill or who are not responding to treatment can be referred to the facility-based treatment. On the other hand, children admitted to facility-based care, which have regained their appetite, can be transferred for continued care in the community. Figure 12.2 presents a matrix of SAM management.

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319

Independent additional criteria

• No appetite • Medical complications

• Appetite • No medical complications

Type of therapeutic feeding

Facility based

Community based

Intervention

F-75 F-100/RUTF and 24hour medical care

RUTF, basic medical care

Discharge criteria (Transition criteria from facility to community-based care)

Reduced edema and good appetite (with acceptable1 intake of RUTF)

15–20% weight gain

12.2 SAM management [2]. 1

Child eats atleast 75% of their calculated RUTF ration for the day.

Box 12.5 Appetite test Poor appetite occurs with significant metabolic disturbance, intoxication, infection, and liver disease. Poor appetite is often the only sign of severe metabolic malnutrition and physiological de-compensation. Even a slight reduction of appetite can lead to malnutrition. Appetite test is recommended to be conducted in a separate quiet area. The first step is to explain to the mother how the test will be done. This is followed by the mother washing her hands and sitting comfortably with the child in her lap. A mother is then advised to offer calorie-dense food to the child. The ingredients of the recommended food comply closely with that of ready-to-use therapeutic food (RUTF) together with micronutrient and vitamin mix. The test usually takes a short time but may take up to one hour. The child must not be forced to consume the food and must be offered plenty of water to drink from a cup as he/she is taking the calorie-dense food. A child who finishes eating the minimum recommended amount of food is considered as having “passed” the test and is advised to be managed at the community-based care. On the other hand, if a child is able to continue the minimum recommended amount of food than this child is considered to have not passed the test and is referred for an in-patient/facility-based care.

When a child fails the appetite test than such a child directly gets admitted into the facility for further management. A child with a failed appetite test should not be treated at the community level. Children who pass the appetite test are examined by the community nurse or health worker or doctor for complications. Based on the assessment, it is determined whether a child is to be treated as an out-patient (community-based care) or in-patient. A child with serious medical complication is advised to be referred for in-patient treatment; these complications include the following: severe vomiting, hypothermia, pneumonia, extensive infection, very weak,

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apathetic, unconscious and fitting/convulsions. Severe dehydration based on history and changes in appearances are unreliable in a malnourished child and should not be used to diagnose dehydration. (a) Community-based Care In community-based therapeutic care, all children with SAM without complications are treated as outpatients. The community-based approach involves timely detection of severe acute malnutrition in the community and provision of treatment for those without medical complications with nutrient-dense foods such as ready-to-use therapeutic food (RUTF) at home. Box 12.6 presents details on RUTF. Programs of community-based care substantially reduce case-fatality rates and increase coverage rates substantially. SAM management programs recommend use of generic ready-to-use therapeutic foods (RUTF) with a defined composition and are designed to increase access to services, reduce opportunity costs, encourage early presentation and compliance, and thereby increase coverage and recovery rates. This approach promises to be a successful and cost-effective treatment strategy. However, communitybased management of severe wasting will only be effective if the affected children have timely and un-interrupted access to safe, palatable, and nutrient-rich ready-to-use therapeutic foods. Therefore, successful management of severe malnutrition does not require sophisticated facilities and equipment neither highly qualified personnel. It does, however require that each child be treated with appropriate feeding along with proper care and affection. Successful management of severe acute malnutrition in community settings, however, depends on three crucial factors. First, a provision for horizontal integration of programs for community management of acute malnutrition with existing health-system interventions, so that moderately and severely malnourished children with any complications are promptly recognized and referred for receiving essential lifesaving interventions in addition to food. There is little to gain from supply of therapeutic feeding such as RUTF alone if effective and timely treatment for malaria, pneumonia and diarrhea is not available. Second, in HIV-endemic populations, ensuring rapid and continued access to antiretroviral and ancillary support strategies for children with severe acute malnutrition is critical and the key to ensuring that children survive and benefit from nutrition interventions. Third, and perhaps the most important, is community mobilization and ensuring creation of demand and early detection which is extremely critical for community management of acute malnutrition, especially, large-scale programs that manage severe acute malnutrition.

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Success of community-based care of SAM children Experience in Ethiopia showed that in community-based therapeutic care, families became key participants in the rehabilitation of their children. Recovery rates were noted to be comparable with international standards, and coverage far exceeded that of traditional centre-based care. The success of community-based therapeutic care programs is evident from experiences of 21 implemented programs in Malawi, Ethiopia, and North and South Sudan between 2000 and 2005. A total of 23,511 cases of SAM were treated, and out of these coverage rate was 73% and recovery rate was 79.4%, and mortality rate was reported to be 4.1%. Of the SAM children, 76% were treated solely as out-patients [8]. A study in Malawi compared therapeutic feeding program coverage of severely malnourished children achieved by a community-based therapeutic care (CTC) program and a therapeutic feeding centre (TFC) program operating in neighbouring districts. Results revealed that CTC gave substantially higher program coverage than a TFC program [9]. Findings of a study from Niger suggest that satisfactory results for the treatment of severe malnutrition can be achieved using a combination of home- and hospitalbased strategies [5]. Community-based management of severe acute malnutrition could prevent the deaths of millions of children if properly combined with a facility-based approach for those malnourished children with medical complications and implemented on a large scale. Details regarding feeding, medicine and counselling are presented below. (i) Feeding Children identified for home-based management are treated at community level with the use of nutrient-dense foods such as ready-touse therapeutic foods (Plumpy Nut, BP100, or locally made RUTF) or other nutrient-dense foods at home. Children are required to eat a definite amount of RUTF as supplement (Box 12.6), along with breastfeeding or other home foods, until the discharge criteria from such special feeding are met. In some settings, production of locally appropriate therapeutic diet using locally available nutrient-dense foods with added micronutrients supplements may be possible but care needs to be taken to produce therapeutic food with adequate macro as well as micronutrient. Adequacy of nutrients is critical and appropriate feeding is essential not only for adequate weight gain but also for recovery to normality, i.e. children should return to physiological, immunological and anthropometric normality. In fact the rate of weight gain by itself is an inadequate measure of recovery of normality [3].

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Box 12.6 Ready-to-use therapeutic food (RUTF) RUTF are high-energy-fortified foods. WHO recommends RUTF for children 6– 59 months for home-based management of SAM children [1]. RUTF has a similar nutrient composition as F-100, which is the therapeutic diet used in hospital settings. But unlike F-100, RUTF are not water-based, meaning that bacteria cannot grow in them. RUTF contains iron while F-100 does not. RUTF has been remarkably useful in treatment of SAM and MAM, even normal children at times of hardship. RUTF should be given to children only after 6 months of age. WHO recommendation: exclusive breast feeding to children below 6 months. RUTF spread is an edible lipid-based paste that is energy dense, resists bacterial contamination, and requires no addition of water or cooking. RUTF are soft and can be consumed easily by children from the age of 6 months onwards. The primary production principles include grinding all ingredients to particle size <200 microns, producing the food without the introduction of water, and embedding the protein and carbohydrate components of the food into the lipid matrix. The most widely used RUTF spread is a mixture of milk powder, sugar, vegetable oil, peanut butter, vitamins and minerals. RUTF foods can be used safely at home without refrigeration and even where hygiene conditions are not optimal. Nutritional value 100 grams of RUTF (Nutriset’s Plumpy net) – Kcalories (545), of which 10% protein calories (at least half of the proteins contained in the foods should come from milk products) and 59 % lipidic calories. Vitamins – Vitamin A (910 μg), Vitamin D (16 μg), Vitamin E (20 mg), Vitamin C (53 mg), Vitamin B1 (0,6 mg), Vitamin B2 (1,8 mg), Vitamin B6 (0,6 mg), Vitamin 12 (0,53 μg), Vitamin K (21 μg), biotin (65 μg), folic acid (210 μg), pantothenic acid (3,1 mg), niacin (5,3 mg). Minerals – Calcium (320 mg), phosphorus (394 mg), potassium (1111 mg), magnesium (92 mg), zinc (14 mg), copper (1,78 mg), iron (11,53 mg), iodine (110 μg), sodium (189 mg), selenium (30 μg). RUTF spread can be produced in quantities sufficient to treat several hundred children using a plenary mixer in a clinic. RUTF cost about US$ 3 per kilogram when locally produced. A child with SAM will need 10–15 kg RUTF given over a period of 6–8 weeks. Production of larger quantities of RUTF spread can be achieved in partnership with local food companies. Production sufficient to meet the needs of several thousand children can be achieved with a dedicated production facility using technology appropriate for use in the developing world. Care must be taken to avoid aflatoxin contamination, and quality control testing of the product is essential.

The development of RUTF has allowed much of the management of SAM out of hospitals. RUTF is a paste-form spread which requires no adding of water. It can be safely and easily produced in small or large quantities in most settings worldwide. Several countries in Africa such as Niger, Congo, Malawi and Ethiopia are manufacturing RUTF following appropriate technology transfer. The development of RUTF has allowed much of the management of SAM out of the earlier traditional facility care. In Malawi, a large scale home-based therapy with RUTF-yielded acceptable results with respect

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to recovery and case fatality of 6–60-month old children without requiring formally medically trained personnel. In addition 1–5-year-old children with malnutrition and good appetite were successfully treated with homebased therapy with RUTF [10]. A controlled, comparative, clinical effectiveness trial in Southern Malawi compared the recovery rates (defined as reaching a weightfor-height Z-score > –2) among 10–60-month-old children with moderate and severe wasting, kwashiorkor or both receiving either home-based therapy with RUTF or standard in-patient therapy. It was found that home-based therapy with RUTF was associated with better outcomes for childhood malnutrition than standard therapy when compared for recovery rates, relapse, case fatality and prevalence of fever, cough and diarrhea [11]. During periods of food insecurity in developing nations, a recurrent challenge is to reach out to the affected populations in rural areas where malnutrition is widespread but distance or geographic location makes health services inaccessible. These areas may also be without trained health personnel or a health-care structure to treat malnutrition. In such situations, home-based therapy with RUTF is effective in treating malnutrition. For example in rural Malawi, home-based therapy and RUTF were used to successfully treat children with severe malnutrition by village-health aides with nearly 94% of the children recovering from SAM. The results demonstrate that home-based therapy with RUTF administered by trained village-health aids is an effective approach to treating malnutrition in areas lacking health services. In Malawi, home-based treatment of 1–5-year olds with RUTF, both locally produced and imported RUTF, were similar in efficacy in treatment of severe childhood malnutrition. Results of a study from Senegal indicate that home-based rehabilitation of severely malnourished children with locally produced RUTF was successful in promoting catch-up growth. The locally produced RUTF was as well accepted as the imported version and led to similar weight gain [12]. The efficacy of RUTF and F-100 in promoting weight gain in malnourished children was compared in 70 severely malnourished Senegalese children (6–36 months) who were randomly allocated to receive 3 meals of either F-100 (n=35) or RUTF (n=35) in addition to the local diet. It was found that the energy intake and the rate of weight gain were significantly greater in those receiving RUTF than in those receiving F-100, whereas time to recovery was significantly shorter in the RUTF group. In India the acceptability and energy intake of imported RUTF was compared with cereal-legume-based khichri among malnourished children 6–36 months. RUTF and khichri were both well-

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accepted. However, the energy intake from RUTF was higher due to its better energy density [13]. Lessons learnt [14] from experiences in Africa indicate the following: 1. A community-based approach using RUTF makes effective SAM management possible in settings where in patient treatment is just not possible. 2. Large numbers of children can be treated with community-based approach. 3. Outcome of community-based management of SAM with RUTF is atleast as good as inpatient management in terms of survival. 4. Outcome of management with RUTF is superior to management with blended flours in terms of weight and height gain and presumably of survival. (ii) Routine medicine Children with SAM suffer from infections; they need appropriate medicines to treat any existing infections, along with essential micronutrient deficiencies. The following chart presents the medicines and nutrients recommended to be given to children admitted directly to the out-patient or for community-based care (Table 12.3). 12.3 Routine medicines for systemic treatment of SAM children – community-based care [3] Vitamin A

1 dose at admission (recommended dose as presented below age wise) For children with bilateral pitting oedema (additional one single dose on discharge) 6 months to 1 year: 100,000 IU 1–5 years: 200,000 IU

Folic acid

1 dose at admission

Amoxicillin Malaria Measles vaccine Iron Albendazole

1 dose at admission + 7-day treatment at home According to national protocol 1 dose on the 4th week (4th visit) No (RUTF contains required amounts of Iron) 1 dose on the 2nd week (2nd visit) only for children ≥12 months 1–2 years: 200 mg; 2–5 years: 400 mg

(iii) Nutrition and health counseling Nutrition health counseling is an important component in the community-based care of SAM and is a critical factor contributing to success of SAM management. Community worker should be assigned

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the task of providing nutritional counseling to mother of a SAM child. Health workers therefore need to be well-trained in technical issues as well as in counseling skills. Field-level functionaries play an extremely crucial role in ensuring regular home visits are made and mothers counseled in order to ensure compliance to the treatment advised as well as for ensuring long-term sustainability of the nutritional status of children. Conducive environment needs to be fostered for counseling. Besides the primary care giver, counseling of other decision-makers in the family is important. Uniformity and accuracy in the messages is essential. Content of the message needs to be simple, appealing, logical, short, technically correct, culturally acceptable, and practical. These messages need to be backed up by appropriate services. Capacity building of counselors is essential. (iv) Surveillance Following the enrolment in the community-care component, each child is assessed weekly on the following criteria: ■ ■ ■ ■ ■ ■

MUAC Edema Weight Body temperature Appetite Standard clinical signs (stool, vomiting, etc.)

Anthropometry (MUAC and weight) are recommended to be used only by the health workers or trained child care frontline workers. Recommended frequency of follow-up visits by the health worker is as follows: (i) first 2 weeks: 2 contacts/week separated by at least 48 hours; (ii) 3rd to 8th week: once a week; (iii) from the 8th week onwards till 6 months: every 4 weeks (shift back to weekly follow up if any danger signs occur again); and (iv) end point: 6 months or MUAC of 115 mm and more, whichever is later. The recommended anthropometric norms for satisfactory improvement are as follows: ●

No further weight loss from the baseline in a non-edematous child: at first follow-up visit; and weight gain of at least 5g/day/kg body weight, irrespective of age, at any weekly follow-up visit. These are as per the Sphere minimum standards. (Minimum standards: Reference values have been developed by the Sphere project, which are applicable to both normal as well as emergency situations. These standards give an indication of what might be considered “acceptable”

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and “bad” functioning under average conditions where the other programs are also functioning). Based on findings of the surveillance, following assessment, analysis, classification and actions are recommended: (a) Recovered. The child on a follow-up for a minimum period of 12 weeks is free of edema for at least 2 weeks, achieves mid-upperarm circumference of 115 mm or more, is gaining weight regularly, is free of infection, and immunized for age. (b) Non-responder (within first 4 weeks). Child does not lose edema in 4 weeks or does not start gaining weight in 2 weeks. If the child develops a danger sign at any time during first 4 weeks, the child should be referred to a hospital. If no danger sign develops, it is advisable to discuss with local health provider and decide on future management; (c) Relapse (after 4 weeks). Edema reappears or there is no weight gain in two consecutive visits or the child develops danger signs. The child should be referred to hospital; A child being treated at home that deteriorates (non-responders or relapse cases described above) or develops a complication should be transferred to in-patient care for a few days before continuing their treatment at home. It is only appropriate to refer SAM patients to facilities where the proper training in the care of the severely malnourished has been accomplished; in particular, the staff in emergency wards need to understand that the standard treatment of complications given to children can lead to the death of a child if the child is severely malnourished. For e.g., the management of a severely malnourished child if it includes IV infusions and multi-drug regimens can lead to fluid overload and can die from heart failure and other organ failures. Children with severe acute malnutrition is not an easy condition to diagnose correctly, it is commonly misdiagnosed as it is viewed very clinically and not with a public health point of view. The two arms of the program should be integrated so that there is smooth transfer of SAM children from one to the other mode of treatment. (d) Defaulter. These are children who are not traceable for at least two recommended visits. It is important to track such cases.

(b) In-patient facility-based care The treatment of SAM occupies a unique position between clinical medicine and public health. Hospitals treating SAM are commonly

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challenged with extremely ill patients who need intensive medical and nursing care. Most of these medical-care facilities are in the poorest parts of developing countries with severe capacity constraints, in particular, very few skilled staff. Additionally, the caregivers of children come from economically disadvantaged families whose existence depends on daily labour. Admitting their children into a medical-care facility puts great demands on their time. Such constraints need to be taken into account to achieve an impact at a population level. It is well-documented that high case fatality rates in children with SAM can be substantially reduced by methodically following standardized treatment protocols such as the WHO protocol for in-patient management [15]. Experiences of over the past decade indicate that the survival of malnourished children improves substantially if the WHO guidelines are followed systematically. A halving of deaths, from 40% to 20% has been regularly reported when the guidelines are followed to a large extent including special feeds, antibiotics, electrolytes avoiding intravenous fluids except in shock and not giving diuretics for edema are followed [16]. A meticulous follow-up of guidelines has been reported to reduce the mortality to below 10%. This involves appropriate training, supervision and monitoring of treatment and attentiveness to danger signs, and a high level of diligence in performing all tasks. Successful implementation of WHO protocol in hospital settings has been reported from Bangladesh and South Africa [17, 18]. In India and Bangladesh, WHO-modified guidelines for the treatment of SAM have been used for a small number of children [19, 20]. In such modified protocols, nutrient adequacy, as attained in milk-based therapeutic diets such as F-75 and F-100, is observed to be difficult to achieve with low-cost local foods combined with micronutrient supplements. (i) Phases of management Phase I – Patients without an adequate appetite and/or an acute major medical complication are initially admitted to an in-patient facility (in hospitals or at health centres) for Phase-1 treatment. The children are given milk-based formula like F-75 (refer to Box 12.4) to promote recovery of normal metabolic function and nutrition–electrolytic balance. This is a period of stabilization of SAM children. Transition phase – Once the child in Phase 1 stabilizes and is ready to continue further in the out-patient, a transition phase is introduced because a sudden change to large amounts of diet, before physiological function is restored, can be dangerous and lead to electrolyte

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disequilibrium. During this phase the patients start to gain weight with the milk-based formula F-100 (see Box 12.4) and increased energy is introduced. Criteria to progress from Phase 1 to transition phase: ● ●

Return of appetite Beginning of loss of edema

Phase II – For all in-patients, as soon as they regain their appetites and are ready for Phase II, they should be treated as out-patients, and an outpatient program should be in place to take care of these patients who have come out of the transition phase (Figure 12.2). (ii) Surveillance Following the enrolment in the facility-care component, each child is recommended to be assessed daily on the following criteria: ● ● ● ●

●

Weight Degree of edema (0 to +++) Body temperature (twice) Standard clinical signs (stool, vomiting, dehydration, cough, respiration and liver size) A record is taken (on the intake chart) if the patient is absent, vomits or refuses a feed, and whether the patient is fed by naso-gastric tube or is given IV infusion or transfusion.

It is important that the MUAC is checked weekly, and height once in three weeks. It needs to be appreciated that many children have psycho-social deprivation and in emergency situations, many have seen parents or relatives suffer or die. Such children require a caring environment and love. There is no place for strict staff, oppressive rules, or blame of the parents. The mother is the primary carer and her wishes need to be always considered. (iii) Diagnosis and treatment of complications When a patient develops a complication, always transfer him/her to Phase 1 for treatment (in-patients are transferred back to Phase 1 and out-patients to facility-based treatment). WHO-management protocol recommends the following 10 steps to be followed in 2 phases – stabilization and rehabilitation [15]. 1. Treat/prevent hypoglycemia 2. Treat/prevent hypothermia

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Treat/prevent dehydration Correct electrolyte balance Treat/prevent infection Correct micronutrient deficiency Start cautious feeding with F-75 Achieve catch up growth by feeding F-100 after appetite returns Provide sensory stimulation and emotional support Prepare for follow-up after recovery

Details of hospital-based care, presented in WHO-management protocol, are essential to be followed. Details with reference to item 3 on rehydration is presented below as an example of the complex details of management that need to be taken into consideration. (a) Treat/prevent dehydration Since SAM children are sensitive to excess sodium intake. Treating a malnourished child who is not really dehydrated with IV fluids is very dangerous. Misdiagnosis of dehydration and giving inappropriate treatment is the commonest cause of death in severe malnutrition. The treatment of dehydration is different in the severely malnourished child from the normally nourished child. Infusions are almost never used and are particularly dangerous. ReSoMal (ORS with low sodium content) must not be freely available in the unit – but only taken when prescribed. The management is based mainly on accurately monitoring changes in weight of the child. Severely wasted patients cannot excrete excess sodium and retain it in their body. This leads to volume overload and compromise of the cardiovascular system. The resulting heart failure can be very acute (sudden death) or be misdiagnosed as pneumonia. (i) Diagnosis History of recent change in appearance of eyes History of recent fluid loss. No oedema – Oedematous patients are over-hydrated and not dehydrated (although they are often hypovolaemic from septic shock) ● Check the eyes lids to see if there is lid-retraction – a sign of sympathetic over-activity ● Check if the patient is unconscious or not ● Oedema comes from salt and water excess – over hydration. A conscious oedematous patient must never be given intravenous fluids. ● ●

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(ii) Monitoring rehydration Fluid balance is measured at intervals by weighing the child – the change in weight gives a very accurate estimate of fluid balance. It is recommended not to attempt to measure the volume of fluid lost since this is much less accurate and very time-consuming – it is quick and accurate to weigh the child. It is recommended to monitor the following every hour: the respiration and pulse rate, the heart sounds, in order to monitor the size of the liver, it is recommended to mark the liver edge on the skin with a pen before any rehydration treatment starts. It is advised to only rehydrate until the weight deficit (measured or estimated) is corrected and then Stop – Do not give extra fluid to “prevent recurrence”. If child is conscious, give ReSoMal and if un-conscious give IV fluids – Darrow’s solution or half saline and 5% glucose or Ringer lactate and 5% dextrose at 15 ml/kg in the first hour and reassess the patient. If the patient is improving, give 15 ml/kg in every 2nd hour and if not improving strongly suspect that the patient has developed Septic shock and treat accordingly. (iii) Reassess status of hydration Formally reassess in one hour, if there is no weight gain, and then increase the rate of administration of ReSoMal by 5 ml/kg/h. Later reassessing every hour becomes important if there is clinical improvement but there are still signs of dehydration; continue with the treatment until the appropriate weight gain has been achieved. If there is no weight gain and there is deterioration in a child’s condition with the re-hydration therapy, then the diagnosis of dehydration was definitely wrong. Stop and start the child on F-75 or equivalent diet. For diagnosis and treatment of other dehydration, heart failure, anemia, hypoglycaemia and fever, it is essential to follow the WHO protocol. Box 12.7 presents the WHO “Emergency Treatment Wall Chart”. Box 12.7 WHO emergency treatment wall chart [21] Emergency treatment of severely malnourished children Severely malnourished children are different from other children. So they need different treatment.

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Condition

Immediate action

Treat shock Shock is if the child is lethargic or unconscious and cold hands

If child is in shock, 1. Give oxygen 2. Give sterile 10% glucose (5 ml/kg) by IV 3. Give IV fluid at 15 ml/kg over 1 hour, using one of the following solutions in order of preference: • half-strength Darrow’s solution with 5% glucose (or dextrose) • Ringers’ lactate with 5% glucose* or • half-normal saline with 5% glucose* or *if either of these is used, add sterile potassium chloride (20 mmol/l) if possible. 4. Keep the child warm. 5. Measure and record pulse and respirations every 10 minutes.

Plus either: Slow capillary refill (longer than 3 seconds) or Weak fast pulse

Monitor closely: use the Critical Care Pathway Initial Management Chart

If there are signs of improvement (pulse and respiration rates fall), repeat IV 15ml/kg for one more hour If there are no signs of improvement after the 1st hour of IV fluid, assume child has septic shock. In this case: 1. Give maintenance fluids (4 ml/kg/h) while waiting for blood. 2. Order 10 ml/kg fresh whole blood and when blood is available, stop oral intake and IV fluids. 3. Give a diuretic 4. Transfuse whole fresh blood (10 ml/kg slowly over 3 hours). If signs of heart failure, give packed cells instead of whole blood.

Treat severe dehydration Assume severe dehydration if there is history of watery diarrhea, thirst, hypothermia, sunken eyes, weakness or absent radial pulse, cold hands and feet, reduced urine output.

Do not give IV (intravenous) fluids except in shock 1. Give ReSoMal 5 ml/kg in every 30 min for 2 hours (orally or by NG). Do not give standard ORS to severely malnourished children. 2. Measure and record pulse and respirations every 30 minutes. 3. Give ReSoMal 5–10 ml/kg/hour for next 4– 10 hours in alternate hours with F-75. STOP rehydration if 3 or more signs of rehydration or any signs of over hydration (increased respiratory rate and pulse rate, increase oedema and puffy eyelids). Only give ReSoMal for up to 10 hours. Monitor during rehydration for signs of overhydration: • increasing pulse and respiratory rate • increasing oedema and puffy eyelids Check for signs at least hourly. Stop if pulse increases by 25 beats/minute and respiratory rate by 5 breaths/minute.

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Treat very severe anemia Very severe anemia is Hb less than 4 g/dl

1. 2. 3. 4.

Treat hypoglycaemia Hypoglycaemia is a blood glucose <3 mmol/L Assume hypoglycaemia if no dextrostix available

Treat hypothermia Hypothermia is a rectal temperature <35.5°C (95.9°F) or an underarm temperature <35°C (95°F).

Emergency eye care Corneal ulceration

If very severe anemia (or Hb 4–6 g/dl and respiratory distress): Stop all oral intake and IV fluids during the transfusion. Look for signs of congestive failure. Give furosemide 1 ml/kg IV at the start of the transfusion. If no signs of congestive failure, give whole fresh blood 10 ml/kg body weight slowly over 3 hours. If signs of heart failure, give 5–7 ml/kg packed cells rather than whole blood.

Perform Dextrostix test on admission, before giving glucose or feeding. If hypoglycaemia is suspected and no dextrostix are available or if it is not possible to get enough blood for test, assume that the child has hypogly caemia and give treatment immediately without laboratory confirmation. If conscious: 1. Give a bolus of 10% glucose (50 ml) or sugar solution (1 rounded teaspoon sugar in 3 tablespoons of water). Bolus of 10% glucose is best, but give sugar solution or F-75 formula rather than wait for glucose. 2. Start feeding straightaway: feed after every 2 hours (12 feeds in 24 hours). Use feed chart to find amount to give and feed every 2–3 hours day and night. If unconscious, give glucose IV (5 ml/kg of sterile 10% glucose), followed by 50 ml of 10% glucose or sucrose by NG tube. If hypothermia For all children: 1. Feed straightaway and then every 2–3 hours, day and night. 2. Keep warm. 3. Use the kangaroo technique, cover with a blanket. Let mother sleep with child to keep child warm. 3. Keep room warm, no draughts. 4. Keep bedding/clothes dry. Dry carefully after bathing (do not bathe if very ill). 5. Avoid exposure during examinations, bathing. 6. Use a heater or incandescent lamp with caution, do not use hot bottle water or fluorescent lamp. If corneal ulceration, 1. Give Vitamin A immediately (<6 months 50,000 IU, 6–12 months 100,000 IU, >12 months 200,000 IU) 2. Instill one drop atropine (1%) into affected eye to relax the eye and prevent the lens from pushing out.

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Condition

Immediate action

Treat hypothermia

If hypothermia For all children: 1. Feed straightaway and then every 2–3 hours, day and night. 2. Keep warm. 3. Use the kangaroo technique, cover with a blanket. Let mother sleep with child to keep child warm. 3. Keep room warm, no draughts. 4. Keep bedding/clothes dry. Dry carefully after bathing (do not bathe if very ill). 5. Avoid exposure during examinations, bathing. 6. Use a heater or incandescent lamp with caution, do not use hot bottle water or fluorescent lamp.

Hypothermia is a rectal temperature <35.5°C (95.9°F) or an underarm temperature <35°C (95°F).

Emergency eye care Corneal ulceration

If corneal ulceration, 1. Give Vitamin A immediately (<6 50,000 IU, 6–12 months 100,000 months 200,000 IU) 2. Instill one drop atropine (1%) into eye to relax the eye and prevent from pushing out.

months IU, >12 affected the lens

In case a child does not respond to treatment, steps to be followed are presented in Figure 12.3.

12.3 Steps to follow when children fail to respond to treatment [22].

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(b) Special problems observed with individual children – in-patients and out-patients Apart from problems encountered with children who have failed responding to the treatment, there are other following issues, observed in both in-patients as well as out-patients, which need to be taken care of: (i) In-patients ●

●

●

Insufficient food provided. Reasons could be food taken by siblings or caretaker, sharing of caretaker ’s food, vitamin or mineral deficiency, mal-absorption, psychological trauma (particularly in refugee situations and families living with HIV/AIDS). Rumination may occur. Rumination is a condition which occurs in up to 10% of severely malnourished, emotionally impaired children. This condition is suspected when a child eats well, but fails to gain weight. Children with this condition regurgitate food from the stomach into the mouth, and then vomit part of it and swallow the rest. This usually happens when they are ignored. It is important that children are observed for such signs by the care taker. Such children are usually thought to have vomiting without diarrhea because they often smell of vomit, and may have vomit-stained clothes or bedding. They are often unusually alert and suspicious, may make stereotyped chewing movements, and do not appear distressed by vomiting. Rumination is best treated by staff members who have experience with this problem and give special attention to the child. Infections like diarrhea, dysentery, pneumonia, tuberculosis, urinary infection/ Otitis media, malaria, HIV/AIDS, schistosomiasis/ leishmaniasis, hepatitis/cirrhosis are common. Congenital abnormalities (e.g., Down’s syndrome), neurological damage (e.g., cerebral palsy), inborn errors of metabolism are other serious underlying diseases.

(ii) Out-patients In addition to the details presented under (i), specific problems observed with SAM out-patient cases are sharing of foods within the family, sibling rivalry, unwilling caretaker, caretaker overwhelmed with other work and responsibilities. (c) Innovative models for care of severely malnourished (i) Nutrition Rehabilitation Centre (NRC) is an approach tried in many countries, including a few states in India. The approach is new and

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requires in-depth review before it is considered to be scaled up to other parts of the country. In NRCs, children receive treatment for the complications associated with severe wasting and are fed formula F-75 or F-100 in quantities adapted to their metabolic needs. Children and their mothers stay in the NRC for 2–4 weeks, with the associated opportunity cost to the child’s mother and siblings. The NRC treatment has two phases – stabilization phase and rehabilitation phase. The stabilization phase at NRCs usually lasts for 2–5 days. During this period, metabolism of children gets stabilized, infections are under control, and appetite returns. The following 21–30 days is the rehabilitation phase that aims at rebuilding the child’s wasted tissues. The limitation of NRC is evident from the efforts undertaken in large state of India, Bihar. There are eight NRCs that provide care to about 120 children per month. For effective management of SAM, the state government would need to establish over 5,500 NRCs and recruit over 8,300 staff to provide care for estimated 1,000,000 children annually with severe wasting. The NRC model is costly. Moreover, it is estimated that, 80–90% of children who are admitted to NRCs do not have medical complications and can therefore be considered for community therapeutic care program described under A. (ii) Community Therapeutic Care (CTC) model The CTC delivery model was conceived, developed, and implemented in complex emergency contexts. CTC model is a community-based model and seeks to provide fast, effective and cost-efficient assistance in a manner that empowers the affected communities. CTC equips communities to deal more effectively with future periods of vulnerability and therefore is a model which creates a platform for long-term solutions to the problems of food security and public health. Experience of implementing CTC in transitional and developmental contexts is currently being acquired in Bangladesh, Ethiopia, Malawi and Zambia. CTC is complementary to traditional Therapeutic Feeding Centres (TFCs) and Supplementary Feeding Programs (SFP), integrating them into a broader framework that better takes into accounts the social, economic and political realities of food insecurity and malnutrition. Through decentralizing distributions, engagement with communities, working with local health care providers and outreach, CTC improves access to services, case finding and follow up. An international humanitarian nongovernmental organization “Concern Worldwide” has piloted this model and is now implementing and researching CTC approaches to manage acute malnutrition [23].

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12.5

Monitoring and evaluation of SAM management program

Effectiveness of each intervention must be reviewed at regular intervals. International standards put forward by Sphere have provided benchmarks to monitor and evaluate emergency nutrition programming (Sphere represents a unique voluntary initiative comprising a broad array of humanitarian actors with aim to improve the quality of assistance to people affected by disasters.) [24]. Reference values have been developed by the Sphere project, which are applicable to both normal as well as emergency situations. They give an indication of what might be considered “acceptable” and “bad” functioning under average conditions where the other programs are also functioning. These standards are as follows: Recovery rate = No. of patients discharged for recovery / Total no. of exits Death rate = No. of patients died in the programme / Total no. of exits Defaulter is a patient who is absent from the programme for 2 consecutive weighing. Defaulter rate = No. of true defaulters / Total no. of exits Length of stay – This indicator should be calculated only for the recovered patients1 for each category. Mean length of stay = sum of (No. of days for each recovered patient) / No. of recovered patients Rate of weight gain – The average weight gain is calculated for all recovered patients for each patient category. The rate of weight gain for an individual is calculated as the discharge weight minus the minimum weight multiplied by 1000 to convert the weight gain to grams. This is then divided by the minimum weight. Lastly, this total weight gain is divided by the number of days from the day of minimum weight to the day of discharge, to give g/kg/d. Average weight gain (g/kg/day) = Total individual weight gains/Total no. of individuals Box 12.8 Management of SAM in India The development of the community-based approach for the management of severe acute malnutrition provides a new impetus for putting the preventive measure into practice and re-visit guidelines of management of SAM in developing countries. It is urgent that SAM management, along with preventive action, is added to the list of cost-effective interventions to reduce child mortality. A consultation meeting was held in India in 2009 to review the global lessons learned and reach a consensus on medical nutrition therapy (MNT). Consensus Statement of the National Consensus Workshop on Management of SAM Children through Medical Nutrition Therapy held on 26th and 27th November

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2009 [25] is as follows: “In India 8.1 million children are estimated to suffer from severe acute malnutrition (SAM). In a nation marching ahead on the economic front, the magnitude and serious consequences of SAM among children makes it unethical not to urgently initiate measures to prevent and treat SAM. Protecting lives and promoting optimum development of SAM children is also a human rights issue. Up to 15% under-5 children with SAM require in-patient management because of medical complications. The remaining 85% (without medical complications) can be managed through a community- and/or home-based care approach. There is an urgent need to update both facility- and home-based care recommendations for the management of SAM among children in India, on the basis of latest evidence. Medical Nutrition Therapy (MNT) is only a component of the entire process of managing SAM children and being a time-limited therapeutic intervention it should not be viewed as being in conflict with the objective and accepted process of attaining food and nutrition security or promoting appropriate Infant and Young Child Feeding (IYCF) practices for children with or without SAM. However, adequate caution should be exercised to ensure that MNT for SAM does not interfere with measures for the holistic prevention of childhood undernutrition. Ready-to-use therapeutic food (RUTF) as per WHO and UNICEF specifications is a medical nutrition therapy based on sound scientific principles with a balanced composition of type I and type II nutrients. Apart from anthropometric recovery, RUTF results in physiological and functional (including immunological) recovery. It has a specific composition which has been tested and proved effective in functional recovery of SAM children. RUTF should not be confused with ready-touse food (RTUF) or any other products or preparations. Global evidence, primarily from Africa, indicates that RUTF-based nutrition therapy is effective for facility- and home-based management of SAM children who do not have medical complications, and can be scaled up for community or home-based management for children over six months of age. Pilot experience from India (Bihar and Madhya Pradesh) suggests that RUTF is effective for nutritional therapy of SAM children and can also be scaled up. Similar experience from Maharashtra has been reported with other locally formulated products. Other models from West Bengal and Gujarat, on a smaller scale, have also showed similar weight gains with locally formulated products. There is a suggestion from observational data in Madhya Pradesh that RUTF may be superior to standard treatment with F-100 and IAP formulations. However, there is no head-to-head comparison of effectiveness of RUTF with locally formulated products. Further, all of these experiences from India relate to weight gain and not to height gain or physiological or functional recovery. A qualitative study undertaken in mid 2009 from six states of India suggests that against the backdrop of fragile food security and faulty feeding practices, mothers who are time-constrained tend to reach out to market foods to feed their children, which may be of sub-optimal nutrition quality. Further, the families do not recognize the signs of undernutrition until children develop severe malnutrition and medical complications. Considerable sensitivities exist regarding the possibility of commercial exploitation of undernutrition through aggressive marketing and supply of international productbased nutrition therapy and erosion of (i) exclusive breastfeeding during the first six months of life; and (ii) continued breastfeeding between 6 and 24 months of life. Further, any action has to be in consonance with the Infant Milk Substitutes Feeding Bottles, and Infant Foods (Regulation of Production, Supply and Distribution) Act 1992 as amended in 2003 (IMS Act) (http://www.bpni.org/docments/IMS-act.pdf) and the Supreme Court orders on the Right to Food Act (http:// www.righttofoodindia.org and http://www.sccommissioners.org). Indian manufacture of RUTF is feasible, can be scaled up and even industrial production for export has been started by at least a couple of units. The fear of commercialization can be obviated by following principles of (i) non-proprietary product; (ii) partially decentralized manufacture with public-sector involvement; (iii) public health system being the sole procurement agency with a specific strategy that ensures purchase from multiple producers; and (iv) prescribed product, which is not freely available. Product-based

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nutrition therapy including RUTF can be introduced on a pilot basis at scale (district or state level) utilizing existing systems for sustainability. The pilot project should be introduced when a delivery design and plan of action is developed and is in place as a part of the larger system to deal with childhood undernutrition. RUTF should be used only: ● As therapeutic and not supplementary feeding ●

Above six months of age

●

For a limited time period (4–8 weeks) until the child recovers from SAM, which should be defined in explicit treatment protocols

MNT could be operationalised by the health ministry through the Integrated Management of Newborn and Childhood Illnesses (IMNCI) module, which also has a component for the management of SAM. The Integrated Child Development Services (ICDS) system could converge for the identification and referral of children with SAM and the follow-up of these children after their discharge from therapeutic feeding. To aid the evaluation process in an observational manner, outcome measures should be recorded after some time of operationalisation of intervention program and include follow-up of rehabilitated children. Regulatory issues would need to be resolved between the two nodal authorities (Drug Controller General of India and Food Safety and Standards Authority of India) before MNT can be operationalised. The feasibility of manufacturing, regulation and registration as a food, and use and distribution as a drug should be explored. Food and nutrition security and preventive aspects should be ensured during treatment for and after recovery from SAM to prevent relapses. Urgent research issues include: ●

Comparison of RUTF with home-based and locally formulated products

●

Physiological recovery and longer benefits of the above treatments

●

Effect of introduction of RUTF on breast feeding

●

Operationalisation and economic analysis in different settings

References 1. 2.

3.

4. 5.

6.

WHO/ WFP /UNSCN / UNICEF (2007). Community-based management of severe acute malnutrition. A joint statement. WHO / UNICEF . WHO child growth standards and the identification of severe acute malnutrition in infants and children (2009). A joint statement by WHO and UNICEF. GOLDEN M AND GRELLETY I . State of the Art Training on Integrated Management of Severe Acute Malnutrition, hosted by NRHM, ICDS, Maharashtra State Nutrition Mission, Organised by UNICEF Delhi, 24–27th November, 2008, Pune. LINKAGES PROJECT . Complementary feeding. http://www.linkagesproject. org/ technical/compfeeding.php (accessed on May 2010). AIIMS (2009). National Consensus Workshop on Management of SAM Children through Medical Nutrition Therapy. Compendium of Scientific Publications, A Summary, 26–27th November, 2009. NATIONAL FAMILY HEALTH SURVEY (NFHS – III ), 2005–2006. International Institute for Population Sciences, Mumbai, and ORC Macro, Calverton; September 2007, 274–284.

Severe acute malnutrition in children 7.

8.

9.

10.

11.

12.

13.

14.

15.

16. 17.

18.

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21.

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(2006). Proceedings of the WHO, UNICEF and SCN information consultation on community-based management of severe malnutrition in children, Food and Nutrition Bulletin 27, no. 3, pp S99–S104. THE LANCET EDITORIAL (2007). Ready-to-use therapeutic foods for malnutrition. The Lancet 369, no. 9557, p 164; and COLLINS, S , DENT, N, BINNS, P , BAHWERE, P , SADLER , K , HALLMAN , A (2006). Management of severe acute malnutrition in children. Lancet 369, no. 9563, pp 1992–2000. SANDIGE H , NDEKHA MJ , BRIEND A , ASHORN P and MANARY M (2004). Home-based treatment of malnourished Malawian children with locally produced or imported ready-to-use food. J Pediatr Gastroenterology and Nutrition 39, no. 2, pp 141–146. LINNEMAN Z , MLTILSKY D , NDEKHA M , MANARY MJ, MALETA K , MANARY MJ (2007). A large-scale operational study of home-based therapy with ready-to-use therapeutic food in childhood malnutrition on Malawi. Matern Child Nutr 3, no. 3, pp 206–215. CILIBERTO MA , SANDIGE H , NDEKHA MJ , ASHORN P, BRIEND A , CILIBERTO HM , MANARAY MJ (2005). Comparison of home-based therapy with ready-to-use therapeutic food with standard therapy in the treatment of malnourished children: a controlled clinical effectiveness trial. Am J Clin Nutr 81, no. 4, pp 864–870. SADLER K , MYATT M, FELEKE T , COLLINS S (2007). A comparison of the program coverage of two therapeutic feeding interventions implemented in neighbouring districts of Malawi. Public Health Nutr vol 10, no. 9, pp 907–913. DUBE B , RONGSEN T , MAZUMDAR S, TANEJJA S, RAFIQUI F, BHANDARI N , BHAN MK (2009). Comparison of ready-to-use therapeutic food with cereal legume-based Khichri among malnourished children. Indian Pediatr vol 46, no. 5, pp 383–388. BRIEND A . Therapeutic nutrition for SAM children: Summary of African experience. National Consensus Workshop on Management of SAM children through Medical Nutrition Therapy, AIIMS Delhi, November 26–27, 2009. WHO (1999). Management of Severe Malnutrition: A manual for Physicians and other senior health workers WHO, Geneva 1999. http://whqlibdoc.who.int/hq/ 1999/a57361.pdf (accessed in January 2007). ASHWORTH A , JACKSON A UAUY R (2007). Focusing on malnutrition management to improve child survival in India. Indian Pediatr 44, no. 6, pp 413–416. HOSSAIN MI , DODD NS, AHMED T , MIAH GM , JAMIL KM , NAHAR B , MAHMOOD CB (2009). Experience in managing severe malnutrition in a government tertiary treatment facility in Bangladesh. J Health Popul Nutr 27, no. 91, pp 72–80. ASHWORTH A , CHOPRA M, MCCOY D , SANDERS D , JACKSON D , KARAOLIS N , SOGAULA N , SCHOFIELD C (2004). WHO guidelines for management of severe malnutrition in rural South African hospitals: effect on case fatality and the influence of operational factors. Lancet 363, no. 9415, pp 1110–1115. PARAKH A , DUBEY AP , GAHLOT N , RAJESHWARI K (2008). Efficacy of modified WHO feeding protocol for management of severe malnutrition in children: a pilot study from a teaching hospital in New Delhi, India. Asia Pac J Clin Nutr 17, no. 4, pp. 608–611. HOSSAIN MM , HASSAN MQ , RAHMAN MH , KABIR A , HANNAN AH , RAHMAN AKMF (2009). Hospital management of severely malnourished children: comparison of locally adapted protocol with WHO protocol. Ind Pediatr 46, no. 3, pp 213–218. WHO (2003). Guidelines for inpatient treatment of severely malnourished children. WHO, Geneva.

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22. State of the art training on integrated management of SAM by Professor Michael Golden and Dr. Yvonne Grellety, Pune, India 2008. 23. The sustainability of community-based therapeutic care (CTC) in non-emergency contexts. http://www.fantaproject.org/downloads/.../CTC_a_Manual_v1_ Oct06.pdf. 24. Humanitarian charter and minimum standards in disasters. http:// www.sphereproject.org/. 25. SACHDEV HPS, KAPIL U and VIR S (2010). Consensus Statement: National Consensus Workshop on Management of SAM children through Medical Nutrition Therapy. Indian Paediatrics, 47 (August 17), p. 661.

13 Prevention and management of overweight and obesity in children Anura Kurpad and Sumathi Swaminathan

Anura Kurpad, MD, PhD, FAMS, a physiologist and nutritionist, is the Dean of St John’s Research Institute, and Head of the Nutrition Division. His primary interests are in energy and protein metabolism and requirements, body composition, adaptation to undernutrition, and in fetal development. Sumathi Swaminathan, PhD, is a nutritionist. She is an honorary lecturer at St John’s Research Institute, with interest in childhood obesity. Dr Swaminathan is currently conducting epidemiological studies in overweight and obesity in urban and rural regions.

13.1

Introduction

Over the past decade, there is an increased focus on childhood overweight and obesity that has developed into a world-wide phenomenon both in the developed and the developing nations. The World Health Organization [1] reports that world-wide 22 million children under the age of 5 are obese. Obesity is defined as a condition in which excess body fat has accumulated to an extent that health may be adversely affected. It is debatable whether obesity is merely a condition or a disease [2]. It seems reasonable to call it a disease, and to make a public policy for the prevention of obesity more definitive in terms of disease prevention and management. In 2004, Bray [3] suggested that obesity meets the criteria needed to call it a disease. It has an etiology – an imbalance between energy intake and expenditure. It has a pathogenesis in the feedback systems involving neurochemicals in the brain, and the neural and endocrine messages that respond to the intake of food. The pathology of obesity lies in its enlarged fat cells, including cytokines, procoagulants, inflammatory peptides, and angiotensinogen. These secretory products of fat cells and the increased mass of fat are responsible for the associated metabolic diseases, such as diabetes, hypertension, heart disease, sleep apnea, and some sorts of cancer. Treatment consists of techniques to alter the balance between energy intake and energy expenditure. Obesity and overweight are major risk factors for many diseases.

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Since overweight and obesity result from an imbalance between energy intake and expenditure, it makes sense that preventive strategies are also dependent on modulating these variables successfully. In normal healthy children, a homeostatic regulation ensures a balance between energy intake and expenditure, and energy storage for growth (approximately 84 kJ/day), thereby resulting in the maintenance of body weight and body stores [4, 5].

13.2

Maintenance of energy balance

Energy intake, energy expenditure and energy storage in the body result in the energy balance in children. This homeostatic regulation is governed by the first law of thermodynamics, that is, energy cannot be created or destroyed. Energy intake is defined as the caloric or energy content of food as provided by the major sources of dietary energy: carbohydrate (16.8 kJ/g), protein (16.8 kJ/g), fat (37.8 kJ/g) and alcohol (29.4 kJ/g). Most of the energy expended is for the basal metabolic rate (BMR) which is for the maintenance of basic physiologic functions for sustenance of life such as heart beat and respiration. Since under most measurement situations, the resting metabolic rate or resting energy expenditure (REE) is more practical with the rate being approximately 3% more, BMR and REE are used interchangeably. The REE in an average child is roughly 2.94 kJ/ minute. The other components of energy expenditure are the thermic effect of a meal (TEM), which is the energy expended to digest, metabolize and store ingested macro-nutrients, and physical activity or activity energy expenditure (AEE). TEM comprises about 10% of the caloric content of a meal while AEE is the most variable component of energy expenditure dependent on an individual (Figure 13.1). Apart from these, children require additional energy for growth. However energy cost of growth relative to total energy needs is small, except in the first few months of life. P h ysica l a ctivity (PA )

Th erm ic effe cts o f fo o d/m e al (TE F/T E M )

B a sa l M e tab olic R a te (B M R )

13.1 Components of energy expenditure.

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When energy intake exceeds energy expenditure, a state of positive energy balance occurs. Normally, ingested carbohydrate is used up immediately for energy, and through adaptive processes any excess is stored as glycogen for urgent needs (e.g. exercise). However no such adaptive mechanism exists for fat and therefore fat with low metabolic costs for storage, is the preferred energy store in the body [4]. Regulation of energy intake occurs through short-term signals that control hunger, food intake and satiety, and through long-term signals that relate to the conservation of energy stores, lean tissue or both. In the short term regulation, gastro-intestinal signals provide important inputs to the brain and the hormones released from the stomach and intestines are inhibitory. For example, the YY3-36, the major circulating form of peptide YY (PYY), a gut hormone produced by the L cells of the small intestine produced in this manner, when infused into lean or obese subjects led to a decrease in food intake by approximately 30%. However, ghrelin, a peptide produced by the stomach and proximal small intestine, stimulates food intake, and has been observed to decline after a meal and to rise before the next meal. In Prader-Willi syndrome, ghrelin levels are elevated and marked by hyperphagia. In longterm regulation, the adipose tissue is involved in the feedback regulation of energy balance by production of a number of peptide hormones. Leptin and adiponectin are two of the most important ones. The absence of leptin produces massive obesity, and treatment of leptin-deficient individuals reduces food intake and body weight. However, in obese people leptin has little or no effect on both food intake and body weight, as they are leptin resistant leading to already high levels of leptin in the circulation [6, 7, 8].

13.3

The epidemic of obesity in children

The current epidemic which is largely a result of rapid urbanization with consequent rapid changes in demographic, nutritional and socio-economic transition has resulted in increased energy intake due to modern food processing and marketing techniques, coupled with the decline in energy expenditure because of automation, mechanized transport and increases in sedentary occupation and leisure pursuits, for example, use of computers and television [9, 10, 11, 12]. Overweight and obesity in children are most common in the North America, United Kingdom and South-Western Europe [1]. In the latest report by Centers for Disease Control, in the United States, 13% were obese, (more males than females), while 15.8% were overweight, with linear increases from 25.1% in 1999 to 28.8% of overweight/obese children from high schools [13]. In the United Kingdom, prevalence of overweight in children aged 2–10 years increased from 23% to 28% from 1995 to 2003 [1]. Overweight data from 79 out of 147 developing countries on

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pre-school children, using the criteria of weight-for-height above 2 standard deviations (SD) from the National Center for Health Statistics/World Health Organization international reference (1978), indicated that 3.3% children below 5 years of age were overweight in 1995, with the percentage highest in Latin America and Caribbean (4.4%), followed by Africa (3.9%) and then Asia (2.9%). However, in absolute numbers Asia had the highest numbers of overweight children [14]. In the most recent analysis of prevalence in 60 out of 191 regions of the World Health Organization, the most dramatic increase is in the industrialized countries. From the 1970s to the 1990s, prevalence doubled or tripled in large countries of Canada and United States in North America, Brazil and Chile in South America, Australia and Japan in the Western Pacific, Finland, Germany, Greece, Spain and United Kingdom in Europe, with prevalence ranging from 20% to 30%. Estimated figures of overweight and obesity for school-aged children in the year 2010, is 1 in 5 in urban China (which was 1 in 8 in 1997), 46% in the Americas, 41% in the Eastern Mediterranean region, 38 % in the European region, 27% in Western Pacific region and 22% in South East Asia [15]. An increasing gradient in immigrant populations from the first generation of immigrants to the third has been demonstrated, in Hispanic and AsianAmerican adolescents, indicating an important role of acculturation or assimilation into lifestyles in industrialized countries being a risk factor for obesity [16]. A matter of concern, especially in the lower and middle income countries, is the transition from undernutrition to overnutrition problems, causing a double burden of both under- and overnutrition. For example, in Brazil between 1975 and 1997, prevalence of overweight in children between 6 and 18 years of age increased from 4.1% to 13.9%, while prevalence of underweight decreased from 14.8% to 8.6% [15, 17]. Prevalence rates of overweight and obesity in school children in India reported from studies from various regions vary from 4% to 30% [18–24]. Box 13.1 Trends of childhood obesity in India In urban school children in Delhi [24], prevalence increased from 16 % in 2002 to 24 % in 2006–2007. In Ernakulam district in Kerala, prevalence increased from 4.94% in 2003 to 6.57% in 2005. Probable causes of childhood obesity in India 1. Rapid urbanization and globalization with marked changes in food availability and consumption, as well as changes in physical activity patterns. 2. High prevalence of low birth weight. 3. High prevalence of stunting. Nutritional stunting causes changes such as lower energy expenditure, higher susceptibility to the effects of a high fat diet, lower fat oxidation and impairment in regulation of food intake which could result in later obesity [25, 26, 27].

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345

Developmental aspects of growth, weight gain and later obesity (Figure 13.2)

Adipose tissue is found in the fetus after the 14 th week of gestation. At birth, about 13% of the body mass consists of adipose tissue doubling to about 28% at the end of the first year for a normal weight infant. The percentage of fat in the body mass of children again increases during puberty. During the first year of life, fat accumulation is characterized by increase in the volume of adipocytes. However, during the pubertal period fat accumulates largely through an increase in the number of adipocytes, without further change in the fat cell volume. Two mechanisms play a role in this process; one regulates the breakdown or storage of fat within the cell through lipolytic and lipogenic mechanisms, and another which regulates the number of cells through proliferation from pre-adipocytes or removal through apoptosis or merger of fat cells. Age-dependent differences are seen in the formation of adipose cells from pre-adipocytes, with maximum proliferation and capacity for differentiation during the first year of life and just before puberty. Unlike adults, adipose tissue in children has a higher proportion of smaller fat cells, indicating a higher rate of formation of new cells in childhood. Epigen etic susc eptibility to chronic diseases if later diets ina ppropriate

C urren t nu tritiona l transition

Low B irth W t & nu tritiona l program m ing

Inadeq uate growth

R apid Inadeq uate foetal nutrition

G row th

Adult v is cera l obesity, H /T, diabe tes

C hild Stunted

W om an M alno uris hed Pregnancy Low W eig ht G ain

Adoles cent Stunted

13.2 Developmental aspects weight gain and obesity [12].

The pubertal growth spurt is associated with significant changes in body composition, with girls tending to accumulate more fat than boys.

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Fat gain occurs in both boys and girls in early adolescence, but then ceases and even reverses temporarily in boys, but continues through adolescence in girls. Body Mass Index (BMI) as a measure of body fatness in adolescents is influenced by maturation status, race and distribution of body fat [28]. A number of factors are related to obesity during childhood as well as in adolescence and adulthood.

13.4.1 Intra-uterine period and birth weight The earliest evidence pertaining to undernutrition of the mother during the period of pregnancy and later obesity came from the Dutch famine study [29]. This report in 1976 consisted of several natural cohorts based on their intra-uterine exposure to the Dutch famine. During World War II, the Germans restricted food for the population of Northern Holland and consequently food intake declined from approximately 1500 kcal to approximately 1000 kcal for about a 6-month period. The cohort, exposed to famine in the last trimester, was found to have a reduced prevalence of obesity at the age of 18 years. However, individuals exposed to famine in the first 2 trimesters of pregnancy had an increased prevalence of obesity at age 18. These observations were attributed firstly, to a period of adipocyte replication in the third trimester and secondly, to the nascent organization of the hypothalamus in earlier pregnancy. Hence, the responsiveness to caloric intake might be set by the responsiveness of the hypothalamus and sympathetic nervous system to intra-uterine substrate availability. Evidence is also available linking higher birth weights (>3500 g) with overweight and obesity in late adolescence [30]. However, this has been attributed to increase in lean body mass rather than fat mass. Programming of lean body mass rather than that of fat mass, could explain associations between birth weight and later BMI. The association of low birth weight with a smaller proportion of lean mass, and hence lower metabolic activity, could with environmental influences associated with energydense diets have the propensity to lead to later obesity [31]. A recent study of obese children (mean age 10.4 years) indicates that those with high birth weights had a higher adiponectin level, higher whole-body insulin sensitivity index, lower hepatic insulin resistance index, lower plasma insulin and free fatty acid concentrations during oral glucose tolerance test (OGTT), and lower trunk fat percent than normal or low birth weight children [32]. There is a great deal of recent literature on this issue, which is out of the scope of this chapter; interested readers are referred to recent reviews on the subject [28, 33].

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13.4.2 Weight gain in infancy, childhood and adolescence Rapid weight gain, especially during infancy, has been shown to be associated with obesity in later life. A rapid weight gain pattern from birth to 4 months [34] and during the period of infancy [35] has been associated with obesity in childhood and young adulthood. A recent study [32] has shown that increased fetal growth and infant weight gain between 0 and 2 years were associated with relative protection from the development of central obesity and insulin resistance among obese children and adolescents, possibly an indicator of healthy obesity. However, rapid weight gain after 4 years led to insulin resistance. Body mass index increases through infancy and then drops from the second to the fifth year. There is then, a gradual rise from the sixth year of life through adolescence. This sudden increase around 5–7 years of age is termed “adiposity rebound”. Early adiposity rebound is probably a reflection of rapid weight gain during infancy and possibly early maturation [29]. An early adiposity rebound is associated with increased risk of adult obesity. The likelihood of children with very early adiposity rebound (by 43 months) being obese at the age of 7 years was found to be high (OR 15.00, 95 % CI: 5.32 to 42.30) in the Avon Longitudinal Study of Parents and Children (ALSPAC). Early adiposity rebound (44–61 months) too, showed an association (OR 2.01, 95 % CI: 0.81 to 5.2) [35]. A study of 1400 adults in Delhi [36], India, indicated that children with early adiposity rebound of 5 years or younger had the highest body mass index in later childhood, and this persisted into adulthood. These children had the lowest ponderal index (body weight in kg3/height (cm) × 100) at birth, the lowest body mass index from birth to 2 years of age. Catch-up growth is a property in human growth wherein children return to their genetic trajectory after a period of growth arrest or delay, for example because of illness. This is most commonly observed in the first 2 years of life, especially after severe intra-uterine growth restraint. These children have been shown to have greater BMI, percentage body fat and total fat mass and central fat distribution [35, 37]. Concentrations of cord blood leptin are positively related to ponderal index at birth but inversely related to weight gain in infancy, and thus low concentrations of this hormone at birth may provide a signal for catch-up growth through reduced inhibition of satiety [37]. Cord leptin concentrations (a surrogate measure of fat mass) of newborn children in the Pune Maternal Nutrition Study, were similar to that of newborns from a white Caucasian population recruited in the study although mean birth weights were lower, suggesting higher adiposity in Indian babies [38]. During adolescence the location of body fat changes and is a period of increased risk of development of obesity, especially in girls. In men, ~10 % of adult obesity begins in early adolescence, while in women this proportion is ~ 30% [29]. A link between early age of onset of menarche to obesity has

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been observed. However, findings in the Bogalusa Heart Study [39] and the study conducted at National Institute of Child Health and Human Development Study of Early Child Care and Youth Development [40] indicate that much of the apparent influence of menarcheal age on adult obesity, is inversely, due to the influence of childhood obesity on both menarcheal age and adult obesity.

13.4.3 Stunting Stunted children (height-for-age below 2 SD of standard growth reference charts) constitute one-third of the children globally, mainly in the developing countries [28]. Although stunting indicates the level of longterm undernutrition in the population, it has also been linked to the overweight observed in Russia, Brazil, Republic of South Africa and China due to the nutrition transition [41]. Childhood nutritional stunting was associated with impaired fat oxidation, a factor predicting obesity since dietary fat that is not oxidized has to be stored [42]. This is a matter of concern as it adds to the burden of obesity in developing economies.

13.5

Assessment of overweight and obesity in children

There are several commonly used tools to assess overweight and obesity in children. The most common is the body mass index, followed by the waist circumference, skinfolds and bio-electrical impedance analysis.

13.5.1 Body mass index (BMI) As the primary purpose for assessing overweight and obesity is to estimate the risk to health at the individual level and to compare populations and to facilitate monitoring of obesity, these assessments are primarily based on anthropometry, with body mass index being most widely used both clinically and epidemiologically followed by waist circumference. BMI is used as it is closely correlated with body fatness. The adult BMI cut-offs are not appropriate for children as they are still growing [28, 43, 44]. Age and sex specific BMI cut-offs are needed for proper classification of overweight and obesity in children for the primary reason that BMI increases with normal growth and maturation after the period of adiposity rebound. At present, the World Health Organization’s sex-specific body mass index (the weight in kilograms divided by the square of the height in meters) for age charts is used extensively to assess overweight and obesity in children from birth to 19 years of age [45, 46]. The present standards for age and sex specific BMI charts, have evolved from the Multi-centre growth reference study of the World Health Organization

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for children from birth to the age of 5 years from Brazil, Ghana, India, Norway, Oman and the USA. Recently, the WHO 2007 charts for the 5–19 year age group has been released by reconstructing the 1977 NCHS/WHO growth reference from 5 to 19 years, using the original sample (a non-obese sample with expected heights), supplemented with data from the WHO Child Growth Standards (to facilitate a smooth transition at 5 years) [46]. The 2007 BMI values for both sexes at +1 SD (25.4 kg/m2 for boys and 25.0 kg/m2 for girls) are equivalent to the overweight cut-off used for adults (>25.0 kg/m2), while the +2 SD value (29.7 kg/m2 for both sexes) compares closely with the cut-off for obesity (>30.0 kg/m2). These growth charts are given in the Appendix. Prior to this, different measures and definitions were used to identify overweight and obese children. Therefore, comparisons across populations from different countries and within regions were a major problem, as different criteria were used. Table 13.1 indicates the criteria used for the past few decades to define overweight and obesity. Apart from these, several countries had developed reference charts using local data (for example France, UK, Singapore). Table 13.1 Criteria used to evaluate overweight and obesity in children prior to 2006 and 2007 growth charts [99]

Data and reference population

Classification

Overweight

Obesity

WHO Reference

Child (6–9 years): WHZ> 2(a)

US NHANES 1 Child (6–9 years): no reference Adoles-cent data (1971–74) (10–18 years): BMI > 85th perce-ntile and subsca-pular and triceps skinfolds > 90th percentile

Adolescent (10–18 years): BMI 85th percentile (called as “at risk” overweight) IOTF reference > BMI-for-age cutoffs derived from BMI-age curves passed BMI of 25 at age 18 “Old” US BMI > BMI 85th perce-ntile (called as “at risk” percentiles overweight) “New” US BMI > BMI 85th percentile percentiles (2000 (called as “at risk” CDC Growth Chart) overweight) European – French > BMI 90th percentile BMI reference

Source [93]

> BMI-for-age cut-offs derived from BMI-age curves passed BMI of 30 at age 18

Data from USA, [94] Brazil, Britain, Hong Kong, the Netherlands and Singapore US NHANES 1 [95] > BMI 95th percentile (called as “overweight”) data (1971–74) > BMI 95th perce-ntile (called as “overweight”) > BMI 97th percentile

US NHANES [96] data (1971– 1994) Data from the [97, French population 98]

WHO – World Health Organization; WHZ – weight-for-height z score; NHANES – National Health and Nutrition Examination Survey; IOTF – International Obesity Task Force; BMI – Body Mass Index; CDC – Centers for Disease Control and Prevention. (a) A z-score of 2 corresponds to the 97.7th percentile.

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13.5.2 Waist circumference The waist circumference is a good indicator of fatness and health risks in children. However, although waist circumference is a very useful measure of fat distribution in children, appropriate cut-off points for high or low health risks have not yet been developed [28, 47, 48]. Abdominal visceral fat as measured by the DEXA instrument correlates highly with waist circumference [47]. Evidence exists linking accumulated visceral adipose tissue to increased health risks and metabolic disorders in children. In research studies, childhood waist circumference is more efficient than BMI in predicting insulin resistance, blood pressure, serum cholesterol and triglyceride levels [48].

13.5.3 Skin-fold thickness Skin-folds are predictive of total body fat. The skin-folds at the triceps, biceps, supra-iliac and sub- scapular regions are normally taken using skinfold calipers. However, there is little evidence to indicate that it performs better than BMI as an indicator of body fat. Hence it is not recommended for routine clinical use to assess overweight in children, although it is used extensively for research. Moreover, there is a lack of reference data in children [48].

13.5.4 Bio-electrical Impedance analysis (BIA) McCarthy et al [49] have developed centile curves from 1985 children aged 5–18 years using the total fat body fat results from a bio-impedance segmental body composition analyzer. The shape of the fat curves obtained matched the changes in fat patterning with human growth especially during puberty when there is an increase in lean mass in boys, while there is an increase in fat mass in girls. These changes are not reflected in BMI curves. These curves have been proposed as an alternative or as an addition to using the body mass index curves.

13.6

Risk factors for overweight and obesity

13.6.1 Genetic and gene–environment interactions Studies on twins, siblings, and family, both nuclear and extended, have indicated that an individual’s chances of being obese are increased when relatives are obese. The results of a study based on Danish Adoption Register indicate that there is a strong influence of genetic factors in obesity. Twin studies on heritability show that for body mass, body mass index and fat mass, quantitative sex differences were observed and genetic variance of 84%, 85% and 81% of total variation in men and 74%, 75% and 70% in

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women for each of these respective three parameters were observed. [50] Other studies also indicate a heritability factor of 40–70%. The Human Obesity Genome Map results [51] up to the year 2005 have identified 253 quantitative trait locis (QTL) from 61 genome-wide scans. One may erroneously conclude that since genes account for so much of variation in BMI, environment may have no impact. However genes are expressed in appropriate environments. The present rapid increase in overweight and obesity is an indication that environmental conditions for obesity expression are being created [28]. The study of how phenotype affects gene expression is called epigenetics. It has been shown that fetal programming occurs during the intra-uterine period wherein the fetus adapts to reduced nutrients and these physiological adaptations lead to life-long changes in structure and function of the body [52]. Parental obesity could mediate obesity in children through both genetic and shared environmental factors leading to familial clustering. Among low income children, maternal obesity in early pregnancy doubled the risk of obesity between 2 and 4 years of age [53]. Large babies tend to become overweight when there is a parental history of overweight. The risk of becoming overweight adolescents was approximately 5 to 7 times higher when the mother was overweight [54]. Offspring of women who had diabetes during pregnancy are more likely to become obese later in childhood and to have a higher prevalence of impaired glucose tolerance than the off-spring of women who are non-diabetic [28]. In a multi-ethnic sample in the U.S., it was found that increasing hyperglycemic values lead to an increased risk of offspring obesity at 5 to 7 years of age [55]. The odds ratio of adolescent overweight was 1.4 (CI: 1.1–2.0) among children born to mothers with gestational diabetes mellitus (GDM) [56]. Ethnicity also plays a role, although one may take ethnicity to really represent a gene-environment interaction. Insulin resistance has been observed in British South Asians. The same trend was also observed in British Asian children compared to British children, reflecting an increased sensitivity to adiposity [57]. In the US, non-white teens (Hispanic, African Americans) were also shown to be more likely to have metabolic syndrome compared to white children [58].

13.6.2 Environmental factors A drastic change has occurred in the environment both at home and in the community. This environment has had an effect on the way children eat. Socio-economic status seems to have an effect on overweight in children in the developed countries. The odds of developing overweight were higher in children from the lower socio-economic status in the European Youth Heart Study [59]. Low socio-economic status was related to high BMI in children 6–18 years of age which was mediated by the poor quality of

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breakfast [60]. In India, prevalence of overweight and obesity in children seems to be higher in the higher socio-economic groups [18, 24]. With the advent of globalization and its focus on freer movement of capital, technology, goods and services, major changes in lifestyles linked to diet, physical activity have occurred leading to the problem of overweight and obesity [10]. In the past decade, major developments in food manufacturing, processing and retail sectors have occurred. The agricultural policies and the multifarious industries contributing to all aspects of the food chain are responsible for the progressive cheapening of meat, butter, oils, fats and sugars, whilst the relative price of fruits and vegetables increased [12]. The changing nature of food supply globally, with fresh food sales and marketing decreasing and supermarkets, hypermarkets emerging with increased consumer demand for processed foods, food marketing and promotion through mass media, food advertising and food prices, have contributed in various ways to the “obesigenic” environment. Liberalization of direct foreign investment and trade liberalization has also resulted in increased availability of processed foods of greater variety. Global agricultural policies also have a bearing on the types of foods being marketed. Both food intake and physical activity have been affected through these changes [10, 61]. Tobacco usage has also had an impact, with maternal smoking being associated with subsequent adiposity in children [35, 62].

13.6.3 Dietary factors Breast-feeding In a study by Von Kries [62] on over 9357 German children, aged 5–6 years, breastfeeding was reported to be a significant protector against overweight and obesity – with 35 % reduction in adulthood if children are breast fed up till 3–5 months. This association was however not observed with obesity at the age of 5 years [63]. Breastfeeding could have a programming effect in preventing obesity as it is found that breastfed children have higher insulin levels. Energy-dense foods Energy Density (ED) refers to the amount of energy per gram of food and depends on the content of fat, carbohydrate, protein and water. Water has the greatest impact on energy density, as it contributes to weight without energy. Fibre also decreases the energy density of foods. The high energy of fat influences energy density. Energy dense foods have been implicated in the increase in overweight and obesity in children. These foods can reduce satiety and increase appetite, leading to over-eating in adolescents [48]. Data from the ALSPAC study revealed that a higher dietary pattern consisting of a high dietary energy density, low fiber intake and a high fat intake at ages 5 to 7

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years was associated with higher odds of excess adiposity at 9 years of age [64]. Preference for energy-dense foods (e.g. sweet, fatty) is likely to be an evolutionary trait conferring survival advantage in periods of scarcity [11]. The World Health Organization (2003) [65] has cautioned the use of sugarsweetened beverages by children as evidence that each glass of sugarsweetened beverage consumed increases the risk of obesity in children by 60%. Energy dense foods are also micro-nutrient poor. Dietary carbohydrates are not directly responsible for weight gain, but indirectly they may play a role by inducing a reduction in fat oxidation, especially in children who drink large quantities of soft drinks with high sugar content [66]. Frequency of eating away from home Worldwide eating foods away from home have been implicated as a cause for increased energy intakes [61, 67–69]. Outside the home the type of foods consumed as snacks are often high in fat, sugar and/or starch. Portion sizes, especially in fast food joints have increased to promote their food products. Large portion sizes also have the propensity to increase energy intake even from the pre-school period [70, 71]. Research has indicated that very young children have an innate control of appetite and are able to match intake to energy needs. But this biological mechanism can be overridden by environmental and social factors in older children [28].

13.6.4 Physical inactivity Globally, more people are driven by technology based, comfort oriented lifestyles, resulting in changes in the activity patterns of children towards more sedentary living. Physical activity is an important determinant of body weight and physical activity and physical fitness are important modifiers of morbidity and mortality in adults. Children who regularly participate in at least 3 hours per week of sports activities are protected against total and regional fat accumulation, with increase in lean and bone mass and physical fitness compared to children who do not participate in sports activities [72]. Television viewing, video games and computer games have been associated with childhood obesity in a few studies. Time spent viewing television is considered to be a major contributor to obesity [73, 74]. Studies on obese and non-obese children have also shown that decreased physical activity could either be a cause or a consequence of obesity. A study conducted on obese and non-obese children in Hong Kong [75] showed a significant difference between the 2 groups in the amount of time spent on sedentary activities, with the obese group spending 51% more time than non-obese children. The ratio of active-to-sedentary waking time was 0.6 for obese children and 1.9 for non-obese children. In a school study of 4700 school children aged between 13 to 18 years the percentage

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of children overweight was higher in those with lower physical activity [18]. This behavior could then track to adulthood and these children will continue to be obese adults as well as be prone to other non-communicable diseases. Evidence regarding the dietary and physical activity factors which promote or protect against overweight and obesity are presented in Table 13.2. Table 13.2 Evidence table for factors that might promote or protect against overweight and weight gain [100] Convincing Probable

Regular physical activity High dietary NSP/fibre intake Home and school environments that support healthy food choices for children Breastfeeding

Possible

Low glycemic index foods

Insufficient

Increased eating frequency

Sedentary lifestyles High intake of energy dense foods(a) Heavy marketing of energy dense foods(a) and fast food outlets Adverse social and economic conditions (developed countries especially for women) High sugar drinks Protein content Large portion sizes of the diet High proportion of food prepared outside the home (western countries) “Rigid restraint/periodic disinhibition” eating patterns Alcohol

Energy dense foods are high in fat and/or sugar; energy dilute foods are high in NSP/ fibre and water such as fruit, legumes, vegetables and whole grain cereals. (a)

13.6.5 Other plausible factors A few plausible causes for which evidence exists and which are relevant to children are sleep debt, endocrine disruptors, reduction in variability in ambient temperature, pharmaceutical preparations, increasing gravida age of the mother and intergenerational effects [76]. Several cross-sectional studies have indicated that the number of hours of sleep in children is inversely related to BMI [74, 77]. Although sleep and weight gain could be related through hormonal factors causing decreased levels of leptin and increased levels of ghrelin, it could also be associated with an increased sympatho-adrenal secretion of cortisol and catecholamines. Additionally, too little sleep and impaired quality of sleep may affect the chronobiology and adipocyte function adversely [78].

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Environmental endocrine disruptors are lipophilic, environmentally stable, industrially produced substances that can affect endocrine function and include dichlorodiphenyltrichloroethane, some polychlorinated biphenols, alkyl phenols, organophosphates, phthalates, carbamates, heavy metals, solvents, etc [76, 79]. These industrial chemical toxins could cause weight gain by interfering with weight homeostasis possibly by causing alterations in weight controlling hormones, altered sensitivity to neuro-transmittors, or altered activity of the sympathetic nervous system. Chemicals with estrogenic activity like diethylstilbesterol, a synthetic estrogen also causes weight gain [79]. Being in the thermo-neutral zone (TNZ), that is, the range of ambient temperature in which energy expenditure is not required for homeothermy increases energy stores. With increase in air-conditions, the time spent in TNZ has increased. Some pharmaceutical preparations induce weight gain. Some examples are medications like anti-depressants, anticonvulsants, anti-diabetics, steroid hormones, antihistamines and protease inhibitors. The usage of most of these pharmaceuticals has increased in the past three decades [76]. Increase in gravida age has also been implicated in some studies for increasing odds (~7%) of obesity in the offspring. Intergenerational effects could also lead to obesity, and this influence could date to two generations back when oocytes form in the grandmother and this could occur partly through epigenetic (e.g. methylation) events. Maternal obesity and resulting diabetes during gestation and lactation could possibly promote the same conditions in subsequent generations [76].

13.7

Consequences of overweight or obesity

Pediatric overweight and obesity has resulted in several co-morbidities which were considered rare in children earlier. There is a rising prevalence of, for instance, Type 2 diabetes, which was unheard of even about a decade ago. Obesity driven insulin resistance, impaired glucose metabolism and cardiovascular risk factors are also evident in overweight and obese children.

13.7.1 Long-term consequences in adulthood Whether childhood obesity tracks into adulthood is an important question that has to be answered so that measures to prevent obesity in childhood are of more relevance. Meta-analysis of several studies indicates that the more extreme the obesity of the child, the more the risk of obesity in adulthood. About 26–41% of obese pre-school children and about 42– 63% of obese school-age children were obese as adults. The risk of adult obesity was at least twice as high for obese compared to non-obese children [80].Other health consequences of overweight and obesity have been listed in Table 13.3.

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13.8

Children at special risk of obesity

At an individual level, children with physical disabilities like cerebral palsy, those treated for epilepsy, adolescents with Type 1 diabetes, children on centrally acting drugs like anti-depressants, those treated with glucocorticoids, and those with psychological problems are prone to obesity. Likewise children with specific genetic disorders such as Downs’s syndrome, Table 13.3 Health consequences of childhood overweight and obesity [25, 44, 78] Metabolic/Endocrine Type 2 diabetes mellitus Insulin resistance/impaired glucose tolerance Metabolic syndrome Menstrual abnormalities in girls Hypercorticism Polycystic ovary syndrome Cardio-vascular Atherosclerosis High blood pressure Dyslipidemia Abnormalities in left ventricular mass Abnormalities in endothelial function Raised triglycerides Pulmonary Asthma Obstructive sleep apnea Gastroenterological Non alcoholic fatty liver disease Non-alcoholic steatohepatitis Cholelithiasis Gastro-esophageal reflux Renal Proteinuria Orthopaedic Increased risk of fracture Flat feet Blounts disease Slipped capital femoral epiphysis Ankle sprains Neurological Idiopathic intra-cranial hypertension Psychological Low self-esteem Depression Other Raised C reactive protein/ systemic inflammation Long-term consequences Tracking of obesity to adulthood Cardiovascular risk factors in adulthood Impact on adult morbidity and pre-mature mortality

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Prader-Willi Syndrome, Duchenne muscular dystrophy (DMD), Albright hereditary osteodystrophy (AHO), Fragile X syndrome, Bardet-Biedl syndrome and some single gene disorders are prone to obesity. Some endocrine disorders, for e.g. Cushing’s syndrome, hypothyroidism, hyperadrenocorticism also cause obesity [28, 47, 81].

13.9

Prevention

With the massive increases in the epidemic of overweight and obesity, and with treatment being a more difficult option, the major strategy will be to focus on prevention of overweight and obesity which target environmental factors. The main aim of prevention is to decrease the prevalence of obesity during the period of childhood as well as to prevent modifiable risk behaviors tracking into adulthood. Prevention strategies include encouragement of an active lifestyle as well as healthy eating. At the population level, the World Health Organization [2, 43] recommends 3 modes of preventive measures: universal prevention, selective prevention and targeted prevention. 1. Universal prevention – Targeted at the population as a whole. The aim of this is to stabilize the level of obesity and eventually lower the incidence and hence prevalence of obesity. This is achieved through lifestyle modifications of improvement in diet and increase in physical activity levels and reduction in smoking and alcohol consumption. 2. Selective prevention – Educate sub-groups of populations with a high risk of obesity so that they can deal effectively with risk factors which may be genetic and which pre-dispose them to obesity. 3. Targeted prevention – Aims to prevent weight gain and reduce the number of people with weight related disorders in those individuals who are already overweight or in those who are not yet obese but with biological markers associated with excess adiposity. WHO 2003 [65] recommends some preventive strategies in infants, children and adolescents: Infants and young children ● ● ●

●

The promotion of exclusive breast-feeding during the first 6 months. Avoiding the use of added sugars and starches when feeding formula. Instructing mothers to accept their child’s ability to regulate energy intake rather than to force-feed them. Assuring the appropriate micro-nutrient intake needed to promote linear growth.

Children and adolescents ● ●

Promote an active lifestyle Limit television viewing

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Promote intake of fruits and vegetables Restrict intake of energy-dense and micro-nutrient-poor foods (e.g. packaged snacks) Restrict intake of sugar-sweetened soft drinks

Additional measures include modifying the environment to enhance physical activity in schools and communities, creating more family interactions (e.g. family meals), limiting exposure of young children to heavy marketing practices of energy-dense, micro-nutrient poor foods and providing necessary information and skills to make healthy food choices. Promotion of age appropriate serving sizes, consuming adequate amounts of dietary fiber, fruits and vegetables, avoiding use of sugar-sweetened drinks and limiting the intake of salt is required [82]. Recent dietary reference intakes recommend [83] a fat intake of 30–40 percent of energy in children 1–3 years old and 25–35% in children 4–18 years old, a carbohydrate intake of 45–65% of energy in all children and protein intakes of 5–20% energy in children 1–3 years old and 10–30% of energy in children 4–18 years old. Monitoring the growth of children, is important such that there is an improvement of linear growth in the first 2 years of life (the period when length recovery takes place) while rapid excessive weight gain is prevented relative to height thereafter. Weight should be monitored to prevent a rapid weight gain of ≥1 SD in weight-for age z score during the first year of infancy, the period of adiposity rebound as well as during the pre-pubertal phase. In fact, preventive steps should begin before conception, starting a healthy weight before pregnancy and avoiding either excessive or low weight gain during pregnancy. Since a link between maternal and child malnutrition and later chronic disease exists, concerted effort to achieve a marked reduction in LBW is a priority. If young girls and women have sufficient intakes of animal protein, folic acid and vitamin B12, prevalence of LBW can decrease [84, 85, 86, 87]. In developing countries, avoidance of overfeeding to stunted population groups should be ensured. Nutrition programs designed to control or prevent undernutrition need to assess stature in combination with weight to prevent providing excess energy to children of low weightfor-age but normal weight-for height [66]. It is important to monitor obesity prevention programmes so that they do not lead to the development of clinical eating disorders or risky behavior such as smoking to control weight [16]. With evidence pointing towards the increase in overweight and noncommunicable diseases, probably tracking through to adulthood all over the world, promotion of physical activity during the childhood years should be a public health priority.

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The WHO (2003) [65] recommends ●

●

At least 30 minutes of cumulative moderate physical activity everyday (walking/ brisk walking as well as other appropriate, healthy and enjoyable physical activities and sport for all actions), with children of all ages requiring an additional 20 minutes of vigorous physical activity three times a week. Moderate intensity exercise of a nonstructured nature facilitates most of the disease prevention goals and health promoting benefits. Restrict TV viewing, video games and use of computers to a total of ≤2 hours per day.

At the present date, the WHO website [88] indicates that 60 minutes of moderate- to vigorous-intensity physical activity each day that is developmentally appropriate and involves a variety of activities is the minimum required for children between 5 and 18 years of age, although the official recommendations are not yet released. Further recommendations [89] to promote physical activity especially in Indian children are as following: At the parent–child level – This includes encouragement of parents to promote physical activity from the period of infancy, by stimulating and encouraging the child to walk and play once he/she learns to do so, support for children’s participation in appropriate, enjoyable physical activities, familial participation in games and sports activities and household chores (for example, walking, swimming and other recreational activities), restricting TV viewing to less than 2 hours a day. At the school–student level – Physical education must be compulsorily integrated into the school and college curriculum. Emphasis on competition should not be the sole objective. Emphasis should be placed on play and activities rather than “exercise”. In sporting events, participation should be stressed and competition deemphasized. Lack of space in the school for play activities should be compensated for by obtaining permission to use public playgrounds for the children so that all students in the school avail of the physical education classes. Suitable games should be conceived for children with mild and major disabilities and this should be incorporated in the physical education program. Elementary school students should develop basic motor skills that allow participation in a variety of physical activities, and older students should become competent in a select number of lifetime physical activities they enjoy and succeed in. Discourage the use or withholding of physical activity as punishment. At a government–community level – Playground facilities and safe play areas for children should be increased and adequate infrastructure provided, especially in urban areas. Safe and level pedestrian paths for the public to walk should be provided. Mass media should be used to promote physical activity.

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13.9.1 Effectiveness of intervention programmes to prevent obesity in children The goal of intervention programmes is to promote healthy eating, active living and positive self-esteem rather than to achieve ideal body weight. An effective intervention programme should use a multi-strategic approach involving multi-levels of the society which is aimed at both population and the individual [16]. Modifications in diet include increasing the intake of fruits and vegetables, reducing the use of snacks and soft drinks and fats, while modifications in physical activity are targeted at reducing sedentary behavior, by watching less television or playing video games and increasing activity to moderate intensity. Systematic reviews of these programmes have shown that most of these programs have been conducted as randomized control trials in school-based settings or in clinics. Intervention effects were stronger in adolescent age group than pre-adolescents, females than males, in programmes with parental involvement, those in which focused short and simple messages were relayed over a short period of time than long term periods. Very few long-term follow-ups have been done and hence sustainability of prevention programmes, which is most important, is not known [16, 90, 91]. The “Trim and Fit” (TAF) programme initiated by the Singapore government in 1992 [92] as a concerted effort to prevent childhood obesity by initiating changes in school catering, nutrition education, and increased physical activity, was effective in reducing obesity rates, although it was highly criticized for focusing on children with weight or fitness problems leading to stigmatization and eating disorders. TAF was also seen to be a reverse acronym for FAT. This programme was scrapped due to these problems, and the Ministry of Education initiated another programme targeting all school children called the Holistic Health Framework (HHF). In India, a comprehensive programme for prevention of childhood obesity [24] called MARG has been initiated. This programme aims to promote nutrition and physical activity by education through lectures and leaflets, and through staging drama, skits and debates. The aim is to target 5 lakh children in 15 cities of North India.

13.10 Management and treatment The basis of management of overweight and obesity in children differs from that of adults, in that prevention of weight gain is more important rather than weight loss as lean body mass increases as children get older and growth cannot be curbed. This eventually ensures that fat mass stays constant and leads to normal body weight. Essentially both the family

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and child are involved in the process of management and an increase in daily activity and healthy eating habits is recommended. Higher energy expenditure can be achieved more effectively through increased general activity in schools and play rather than through competitive and structured sports. Encouragement is given to curb TV viewing, videogames and computer which is a source of major physical inactivity. In diets of obese children, only small reductions in energy intake should be made so that sufficient energy and nutrients are available to ensure normal growth and development [16, 43]. Care must be taken to provide adequate nutrition as it has been observed that energy restriction in obese children on well-controlled weight reduction diets have led to reduction in height velocity [16]. Pharmacotherapy is used only in extreme cases. The guiding principles [6] for treatment of overweight should be: ●

● ● ●

●

Establish individual treatment goals and approaches based on the child’s age, degree of overweight, and presence of co-morbidities. Involve the family or major caregivers in the treatment. Provide assessment and monitoring frequently. Consider behavioral, psychological and social correlates of weight gain in the treatment plan. Provide recommendations for dietary changes and increases in physical activity that can be implemented within the family environment and that foster optimal health, growth and development.

Box 13.2 International Obesity Task Force (IOTF) The IOTF is part of the International Association for the Study of Obesity (IASO) The task force is a “global network of expertise, a research led think tank and advocacy arm of International Society for the Study of Obesity”. IOTF works in collaboration with the World Health Organization, other NGOs and stakeholders to address the challenge of alerting the world to the growing health crisis of obesity and to persuade governments to act immediately on this rising problem It has key experts looking at obesity in relation to: Prevention Childhood obesity Management Economic costs (Source: http://www.iotf.org/)

Overweight and obesity in childhood is a major public health problem in the present world and unless preventive action is taken using all collaborative resources of the community and governments, the problem will escalate to such proportions that lead to major economic losses.

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APPENDIX [Source: WHO website] B M I-fo r-ag e B oys B irth to 5 yea rs(z-score s) 22

22

21

21 3

20

20 19

BM I (kg /m 1)

10

2 18

18 17

1 16 15

0

17 16 15

14

1- 14

13 12

2- 13 3- 12

11

11

10

10

M on ths

2 4 6 8 10 2 4 6 8 10 2 4 6 8 10 2 4 6 8 10 2 4 6 8 10 1 ye a r 5 ye a rs 3 ye a rs B irth 2 ye a rs 4 ye a rs A g e (co m pleted m on th s an d ye ars

BM I-fo r-ag e Girls B irth to 5 ye a rs (z-sc ore s )

22

22

1

BM I (k g /m )

21

3

21

20

20

19

2 19

18

18

17

1 17

16

16 0

15 14

15

1- 14

13

2-

12

3-

13 12

11

11

10

10

M o n th s

2 4 6 8 B irth

2 4 6 8 10 2 4 10 1 ye a r 2 ye a rs

6 8 10 2 4 3 ye a rs

A g e (co m p le te d m on ths a n d ye ars

2 4 6 8 10 6 8 10 5 ye a rs 4 ye a rs

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B M I-for-ag e B oys

2

B M I (kg /m )

B irth to 5 year s (pe rcen tiles ) 22

21

20

20

19

19

18

9 7th 1 8

17

8 5th

17

16

16

15

5 0th 1 5

14

1 5th 1 4

13

3 rd 1 3

12

12

11

11 10

10 M on th s 2 4 6 8 10 2 4 6 8 10 2 4 2 4 6 8 10 1 yea r 3 yea rs B irth 2 yea rs

2 4 6 8 10 6 8 10 5 yea rs 4 yea rs

A g e (co m plete d m on ths a n d ye ars

BM I-for-age Girls B irth to 5 ye a rs (pe rcen tiles) 21

21

20

20

BM I (kg/m 2 )

19

9 7th

19

18

18

17

8 5th 1 7

16 15

16 5 0th 1 5

14

1 5th 1 4

13

3 rd

13

12

12

11

11

10 10 M onth s 2 4 6 8 1 0 2 4 6 8 1 0 2 4 6 8 1 0 2 4 6 8 1 0 2 4 6 8 1 0 1 yea r 5 yea rs 3 yea rs 4 yea rs 2 yea rs B irth A g e (co m pleted m on th s an d ye ars

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BM I-for-age Boys 5 to 19 ye ars (z-sco re s) 36 34

3 36 34

32

32

30

2 30 28

B M I (kg/m 2)

28

M on th s yea rs

26 24

1 26 24

22

0 22

20

-1 2 0

18 16

-2 1 8 -3 1 6

14

14 12

12 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 69 3 6 9 3 6 9 3 6 9 3 69 3 6 9 1 0 11 1 2 1 3 1 4 1 5 1 6 1 7 1 8 1 9 7 6 5 8 9 Ag e (co m pleted m on ths an d ye ars)

BM I-for-age G irls 5 to 19 ye ars (z-sco re s)

B M I (kg /m 2)

36 34

3 36 34

32

32

30

2 30 28

28

26 1 24

26 24 22

0

14

20 -1 1 8 -2 1 6 -3 1 4

12

12

20 18 16

M on th s yea rs

22

5

3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 69 3 6 9 1 0 11 1 2 1 3 1 4 1 5 1 6 1 7 1 8 1 9 6 7 8 9 A g e (co m pleted m on th s an d ye ars)

Prevention and management of overweight and obesity...

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B M I-fo r-ag e B oys 5 to 1 9 y ea rs (p erc en tile s) 30

30 9 7th

28

28

25

8 5th

24

2

B M I (k g /m )

24

M on th s Ye ars

26

5 0th

22

22

20

1 5th 2 0

18

3 rd 1 8

16

16

14

14

12 5

12

3 69 36 9 369 369 369 369 3 69 3 69 3 69 3 69 369 369 3 69 369 6 8 9 1 0 11 12 13 14 15 16 17 18 19 7 A g e (co m plete d m on ths a nd y e a rs )

BMI-fo r-ag e Girls 5 to 19 yea rs (p ercentiles) 9 7 th 28

28

26 8 5 th 24

26

B M I (kg /m 2)

24 22

5 0th

20

20 1 5th

18

3 rd

M on ths Years

22

18

16

16

14

14

12

12 3 6 9 36 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 3 6 9 36 9 3 6 9 3 6 9 3 6 9 3 6 9 36 9 5 6 7 8 9 1 0 11 1 2 1 3 1 4 1 5 1 6 1 7 1 8 1 9 A ge (co m plete d m on th s a nd years)

14 Human immunodeficiency virus (HIV) and nutrition Minnie Mathew

Minnie Mathew, PhD, was the senior Programme Adviser with the United Nations World Food Programme till 31 October 2009. During her tenure with the World Food Programme, Dr Mathew contributed significantly in influencing policy regarding positioning nutrition high in the agenda in the care and treatment of HIV. She has developed nutrition-counseling materials in collaboration with the National AIDS Control Society (NACO), which are being used all over the country.

14.1

Introduction

Human immunodeficiency virus (HIV) is a retrovirus that can lead to acquired immunodeficiency syndrome (AIDS), a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections. HIV infection in humans is a pandemic. As of January 2006, the Joint United Nations Programme on HIV and AIDS (UNAIDS) and the World Health Organization (WHO) estimated that AIDS has killed more than 25 million people since 1981, making it one of the most destructive pandemics in history. In 2007, 33.3 million (30.6–36.1 million) people were estimated to be living with HIV, 2.5 million (1.8–4.1 million) people became newly infected and 2.1 million (1.9–2.4 million) people died of AIDS [1]. India is a low-prevalence country with 2.47 million people living with HIV with a national prevalence of 0.36% as reported by the National Aids Control Organisation (NACO) in 2006 [2]. It may be pointed out that this (National Family Health Survey (NFHS-3)) data is based on a household survey among the general population, and excludes high-risk groups such as sex workers, men having sex with men (MSM), injecting drug users (IDUs), truckers and so on. NFHS-3 [3] suggests a prevalence figure of 0.28 %. If the high-risk groups are also taken into account – as they have been by NACO – then the prevalence estimate rises.

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Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, or breast milk. Within these bodily fluids, HIV is present as both free-virus particles and virus within infected immune cells. The four major routes of transmission are unprotected sexual intercourse, contaminated needles, and transmission from an infected mother to her baby at birth, or through breast milk. Transmission through blood transfusions or infected blood products can be eliminated by appropriate screening of blood products for HIV. Of significance to nutritionists is the mother-to-child transmission since it entails feeding options for the infant. The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. A number of studies suggest that about 50–80% vertical transmission of HIV takes place at around the time of birth. In the year 2003 upto 30th November, out of 57,781 AIDS cases reported to NACO, 1,551 (2.68%) cases are due to mother-to-child transmission (MTCT) [4]. In the absence of treatment, the transmission rate between the mother and child is 25%. However, with drug treatment, this can be reduced to 1%. Breastfeeding also presents a risk of infection for the baby and therefore guidelines on infant feeding for infants born to mothers with HIV have been developed (described later in the chapter). HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages and dendric cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of infected cells; and thirdly, killing of infected CD4+ T cells by CD8 Cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections. If untreated, eventually most HIV-infected individuals develop AIDS (Acquired Immuno Deficiency Syndrome) and die. About one in ten remains healthy for many years, with no noticeable symptoms. A strong immune defense reduces the number of viral particles in the blood stream, marking the start of the infection’s clinical latency stage. Clinical latency can vary between 2 weeks and 20 years. Good nutrition is a key for living longer with HIV. This chapter focuses on the key principles of good nutrition which is important for people living with HIV. While good nutrition can help in building the immune system, it does not over time preclude treatment.

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14.2

The clinical course of infection, immune system and infection

Infection with HIV is associated with a progressive decrease of the CD4+ T cell count and an increase in viral load. The stage of infection can be determined by measuring the patient’s CD4+ T cell count, and the level of HIV in the blood. The initial infection with HIV generally occurs after transfer of body fluids from an infected person to an uninfected one. The first stage of infection, the primary, or acute infection, is a period of rapid viral replication that immediately follows the individual’s exposure to HIV leading to an abundance of virus in the peripheral blood with levels of HIV commonly approaching several million viruses per millilitre. This response is accompanied by a marked drop in the numbers of circulating CD4+ T cells (T cells belong to a group of white blood cells known as Lymphocytes, and play a central role in cell mediated immunity). This acute viremia is associated virtually in all patients with the activation of CD8+ T cells [5], which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8+ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4+ T cell counts rebound to around 800 cells per ml (the normal value is 1200 cells per ml). A good CD8+ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus. During this period (usually 2–4 weeks post-exposure) most individuals (80–90%) develop an influenza or mononucleosis-like illness called acute HIV infection, the most common symptoms of which may include fever, pharyngitis, rash, mouth and esophagal sores, and may also include, but less commonly, headache, nausea and vomiting, enlarged liver/spleen, weight loss, thrush, and neurological symptoms. Infected individuals may experience all, some, or none of these symptoms. Symptoms have an average duration of 28 days and usually last at least a week although duration of symptoms may vary. Because of the non-specific nature of these illnesses, it is often not recognized as a sign of HIV infection. Even if patients go to their doctors or a hospital, they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. Consequently, these primary symptoms are not used to diagnose HIV infection as they do not develop in all cases and because many are caused by other more common diseases. However, recognizing the syndrome is important because the patient is much more infectious during this period. HIV directly attacks and destroys the cells of the immune system. Nutritional deficiencies affect the functioning of the immune system that may influence viral expression and replication, further affecting HIVdisease progression and mortality.

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People with HIV and AIDS, whose immune systems are compromised, have difficulty in resisting a variety of serious infections and conditions. Infections affect the nutritional status by reducing the dietary intake and nutrient absorption, and by increasing the utilization and excretion of protein and micronutrients as the body mounts its ‘acute phase response’ to invading pathogens. This leads to increased utilization of antioxidant vitamins (e.g. vitamins E and C, and betacarotene) as well as several minerals (e.g. iron, zinc, selenium, manganese and copper), which are used to form antioxidant enzymes. ‘Oxidative stress’ occurs when there is an imbalance between the prooxidants and antioxidants, causing further damage to cells, proteins and enzymes. Our immune system is an efficient, complex defence system which protects us against bacteria, viruses, and other diseasecausing organisms. Immune-system maintenance requires a steady intake of all the necessary vitamins and minerals. This can be accomplished by eating a well-balanced diet including plenty of fruits and vegetables and yoghurt products on a regular basis. Regular consumption of fermented dairy products such as yoghurt may enhance the immune defences in the gut. Energy intake has an important influence on immune activity. Undernourished people are at greater risk from infections. Weightreduction schemes using diets with less than 1200 kcal per day can also reduce immune function. Excessive energy intake may also compromise the immune system’s ability to fight infection. Obesity is linked to an increased rate of infectious disease. Diets that are high in fat seem to depress the immune response and thus increase the risk of infections. Reducing fat content in the diet can increase immune activity. This might not just affect infections but could also strengthen the type of immune cells, which can fight tumour cells. It is important to include oily fish, nuts, soy or linseed oil in the diet since a right balance of different fatty acids is important. Multivitamin and mineral fortification and supplements can boost immunity.

14.3

Treatment for HIV infection

There is currently no vaccine or cure for HIV or AIDS. The only known method of prevention is avoiding exposure to the virus. There is an antiretroviral treatment, known as post-exposure prophylaxis which is believed to reduce the risk of infection if begun directly after exposure. Current treatment for HIV infection consists of antiretroviral therapy/ ART. Box 14.1 presents details on ART.

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Box 14.1 Antiretroviral therapy (ART) Antiretroviral (ARV) drugs inhibit the replication of HIV. When ARV drugs are given in combination, HIV replication and immune deterioration can be delayed, and survival and quality of life improved. WHO recommends that in resource-limited settings, a single first-line regimen should be identified for the treatment of the majority of new patients. This regimen consists of 2 nucleoside analogs and either a non-nucleoside or abacavir, or a protease inhibitor. Zidovudine (ZDV)/3TC is the initial recommendation for a dual nucleoside analog with d4T/3TC, ZDV/ddI and ddI/3TC as possible alternatives. Efavirenz and nevirapine are recommended non-nucleosides, while recommended protease inhibitors include ritonavir-boosted PIs (indinavir, lopinavir, saquinavir) or nelfinavir. A second line regimen needs to be chosen to substitute first line regimens when needed (for toxicity or treatment failure). Effective HIV and AIDS care requires antiretroviral therapy (ART) as a treatment option. Without access to ART, people living with HIV and AIDS cannot attain the fullest possible physical and mental health and cannot play their fullest role as actors in the fight against the epidemic, because their life expectancy will be too short.

ART has been highly beneficial to many HIV-infected individuals. ART allows the stabilisation of the patient’s symptoms and viremia, but it neither cures the patient, nor alleviates the symptoms and high levels of HIV, often ART resistant, return once treatment is stopped. Moreover, it would take more than a lifetime for HIV infection to be cleared using ART. Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to a large reduction in HIV-associated symptoms. Non-adherence and nonpersistence with ART is the major reason for most individuals failing to benefit from it. The reasons for non-adherence and non-persistence with ART may include poor access to medical care, fear of side effects, stigma in the absence of inadequate social support and drug abuse. The timing for starting HIV treatment is still debated. There is no question that treatment should be started before the patient’s CD4 count falls below 200, and most national guidelines say to start treatment once the CD4 count falls below 350; but there is some evidence from cohort studies that treatment should be started before the CD4 count falls below 350. Delaying treatment in patients with CD4 counts >200 does not appear to increase risk of progression. Viral load, while highly predictive of progression in untreated HIV disease, does not predict clinical response to antiretroviral therapy. Patients started on antiretroviral therapy with CD4 counts >350 are likely to experience considerable toxicity as well as emergence of drug-resistant virus in the absence of a compelling clinical benefit. Initiation of therapy should be based on CD4 count and the patient’s ability to comply with complex and potentially toxic regimens [6]. Many ARV drugs are inconvenient to take and are associated with unpleasant effects including nausea, diarrhea, headache, and central

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nervous system toxicity. They may also cause occasional life-threatening adverse effects such as hypersensitivity reactions, acute hepatitis, lactic acidosis, and pancreatitis. Furthermore, long-term use of ARV has been linked with increased risk of myocardial infarction. If therapy can safely be delayed most patients would prefer to wait. Secondly, the absolute risk of AIDS-related diseases has been felt to be sufficiently low at CD4 counts above 250 that delay can be considered, given the disadvantages of treatment [7]. In India the National AIDS Control Organization (NACO) [8] recommends ART when the CD4 count is below 200 if the patient is asymptomatic or has mild symptoms. With advanced symptoms, it suggests treatment if CD4 is <350 and initiating ART before CD4 drops below 200. For People Living with HIV (PLHIV) with severe and advanced symptoms, treatment is recommended irrespective of CD4 count. In India, free ART is provided through ART centres managed by the State AIDS Control Societies (SACS). ART is not without side effects. Some of these related to nutritional intake and nutritional status include nausea and vomiting, abdominal pain, diarrhea, vomiting, lack of appetite, dry mouth and anaemia. These will be considerably reduced over a period of time and therefore should not influence adherence to ART. Metabolic alterations occur resulting in fat-redistribution syndrome, with central obesity and loss of subcutaneous fat. Development of hyperglycemia and lipid abnormalities may increase the risk of diabetes, heart disease, and stroke. Insulin resistance, a common side-effect of medications used to treat HIV, increases the risk of diabetes, especially in patients who are older or have a family history of the disease. Food and drug interactions are an important issue for effectiveness and tolerability of ART regimens. All these conditions warrant dietary modifications.

14.4

HIV and implications on nutrition status

Nutrition is a life-sustaining treatment and the role of nutrition in the treatment of HIV is critical. HIV affects each person differently. Anorexia and oral/gastrointestinal symptoms such as pain, nausea, vomiting, malabsorption and diarrhea may arise from HIV infection, secondary infections, encephalopathy or drug therapies. Inability to eat food, which is associated with complicated medical regimens or fatigue adds to the nutritional risk. Opportunistic infections are associated with increased resting energy expenditure, and ART may be associated with increased or decreased resting energy expenditure. Clinically, these symptoms may prevent adequate nutritional intake resulting in continued weight and lean

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tissue loss, vitamin or mineral deficiencies and poor nutritional status. Chemical dependency and socioeconomic factors can limit access to proper food and nutrition. The malnutrition that results can itself contribute to an increased immuno-compromised state. Poor nutritional status may result from multiple causes: depressed appetite, poor nutrient intake and limited food availability; chronic infection, malabsorption, metabolic disturbances, and muscle and tissue catabolism; fever, nausea, vomiting and diarrhea; depression; and the side effects of drugs used to treat HIV-related infections. HIV-infected patients may be at nutritional risk at any point in their illness. Severe malnutrition and weight loss, particularly loss of lean tissue, and delayed weight gain and height velocity in children, can affect morbidity and mortality.

14.4.1 Weight loss and wasting in HIV and AIDS The wasting syndrome typically found in adult AIDS patients is a severe nutritional manifestation of the disease. Wasting is usually preceded by a change in appetite, repeated infections, weight fluctuations, and subtler changes in body composition such as changes in the lean body mass (LBM) and body cell mass, which are more difficult to measure than changes in weight alone [9]. Due to illness, appetite is usually lost while there is an increase in nutritional requirements. In such situations, weight loss can be dangerous with a reduction in body’s ability to fight off infections and recover. Weight loss in PLHIV typically follows two patterns: slow and progressive weight loss from anorexia and gastrointestinal disturbances; and rapid, episodic weight loss from secondary infections. Even relatively small losses in weight (5%) have been associated with decreased survival in PLHIV and are therefore important to monitor [10]. Weight loss and wasting in PLHIV develop as a result of three overlapping processes: (i) reduction in food intake, (ii) metabolic alterations, (iii) nutrient malabsorption and effect of drugs. (1) Reduction in food intake may be due to painful sores in the mouth, pharynx, and/or oesophagus. Fatigue, depression, changes in mental state and other psychological factors may affect the appetite and interest in food. Economic factors affect food availability and the nutritional quality of the diet. Drugs or opportunistic illnesses may cause symptoms that make eating unappealing. Some drugs also alter your sense of taste or smell, and this may, in turn, affect your diet.

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(2) Side effects from medications, including nausea, vomiting, metallic taste in the mouth, diarrhea, abdominal cramps and anorexia also result in lower dietary intake that can cause the weight loss associated with HIV and AIDS. Reduction in food intake is believed to be the most important cause of the slow and progressive weight loss experienced by PLHIV. (3) Metabolic alterations due to the impact of infection on protein, fat and carbohydrate metabolism result in increased energy and protein requirements as well as in inefficient utilization and loss of nutrients. Changes in metabolism occur during HIV infection due to severe reduction in food intake as well as from the immune system’s response to the infection. When the intake of food is restricted, the body responds by altering the production of insulin and glucagon, which regulate the flow of sugar and other nutrients in the intestine, blood, liver and other body tissues. Over a period of time, the body uses up its carbohydrate stores from muscle and liver tissue and begins to break down body protein to produce glucose. This process causes protein loss and muscle wasting. (4) Nutrient malabsorption accompanies frequent bouts of diarrhea due to a compromised immune system. Some HIV-infected individuals have increased permeability and other intestinal defects even when asymptomatic [11]. It is possible that HIV infection itself, particularly of the intestinal cells, may cause epithelial damage and nutrient malabsorption [12]. Malabsorption of fats and carbohydrates is common at all stages of HIV infection in both adults and children [13]. Fat malabsorption, in turn, affects the absorption and utilization of fat-soluble vitamins (vitamins A and E), further compromising the nutritional and immune status. Weight normally fluctuates by a few kilograms but a loss of 3–5 % of normal body weight is not normal and it is important to understand the cause of the weight loss, and what might be done to prevent it. Equally important are the signs of muscle wasting – thinning in the arms, legs, buttocks, and face. This implies examining the diet to ensure adequate intake of calories to prevent the body from using its stored resources. It may mean increasing the amount of calories or protein in the diet and exercise. Although weight loss is a common symptom of HIV, there are actions that can be taken to prevent it. Because HIV-related weight loss has many causes, different solutions may be appropriate at different times. It is important to identify the underlying problems. There could be intestinal infections, which prevent proper food absorption. Drugs taken for opportunistic infections can cause nausea. Or there could be a loss

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of appetite. It is easier to address the problem by identifying the underlying cause. Omega-3 fatty acids have been proposed for the treatment of HIV-related problems in more than one ways. Box 14.2 presents details on omega-3 fatty acids and mechanism reported in small trails. Large scale trials have not been studied. Box 14.2 Omega-3 fatty acids – role in HIV Fish oil contains omega-3 fatty acids, “good fats” that have many potential healthpromoting properties. HIV-induced weight loss involves inflammation and responds to treatment with anti-inflammatory drugs. Fish oil also has antiinflammatory effects. HIV lipodystrophy (HIVL) is associated with increased in vitro release of pro-inflammatory cytokines from subcutaneous adipose tissue, implying a heightened systemic inflammatory state, independent from ART. Omega-3 fatty acids, being anti-inflammatory, play a vital role in HIV. Studies suggest that poor absorption of fats and carbohydrates occurs at all stages of HIV infection in both adults and children and results in excess nutrient loss. Poor absorption of fat, specifically, reduces the absorption and use of fatsoluble vitamins (such as vitamins A and E). This can further compromise nutrition and immune status. Fish oil ingestion can boost the activity of enzymes related to metabolism. Specifically, enzymes related to fatty acid beta-oxidation, omega-oxidation, and malic were 1.2-, 1.6-, and 1.7-fold higher in the fish oil-supplemented diet, compared to those only receiving the high fat diet. Oxidative stress occurs when there is an imbalance between the pro-oxidants and antioxidants – in other words, when there are not enough antioxidants to meet the demands of the pro-oxidant cytokines. This stress is believed to increase HIV replication and transcription, leading to higher viral loads and disease progression. For this reason, many studies have examined the impact of antioxidant vitamin supplementation on HIV transmission and disease progression. Omega-3 fatty acids can serve as an antioxidant and relieve the ‘Oxidative stress’.

14.4.2 Metabolic changes in HIV One of the earliest, often undetected, signs of HIV infection is deterioration of the small intestine where absorption of nutrients occurs. Moreover, it appears that there is an increase in requirements for certain nutrients. These are the two primary reasons. For many HIV cases, there is a decrease in many of the body’s vitamins and minerals. A number of metabolic disorders have been reported among patients on ART, such as high serum lipids and elevated liver enzymes. However, results are still limited and controversial [14]. Persons on ART can develop lipodystrophy. Typical symptoms of the syndrome may include a loss of subcutaneous fat in the face, arms, and legs; increased fat deposits in the abdomen and upper back; changes in cholesterol and other blood lipids; and insulin resistance. The metabolic complications of this condition become more significant as patients spend

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more time on ART. Persons on this therapy may develop type-2 diabetes, which is four times the usual risk; and concerns are also increasing about the related risk of heart disease. Preliminary results from a study conducted by Bernasconi et al. [15] point to protease inhibitors as a cause of elevated uric acid, triglyceride and total cholesterol values. Metabolic and body composition changes associated with ART have been well documented in HIV-infected adults, but there have been few reports in children. A study conducted by Meneilly et al. [16] showed that a significant number (62%) of children on ART develop changes in metabolic parameters or body composition, although the relationship to use and duration of ART is unclear. The long-term clinical implications of these changes have yet to be determined. Puberty seems to be the time when HIV-infected children taking potent ARV are more likely to develop lipodystrophy and metabolic complications, especially in children with a severe underlying HIV infection. Once developed, lipodystrophy and metabolic changes seem to be extremely stable with time [17]. Puberty seems to be the time when HIV-infected children taking potent ARV are more likely to develop lipodystrophy and metabolic complications, especially in children with a severe underlying HIV infection.

14.4.3 Nutrition in common HIV-related conditions (a) Diarrhea is common amongst people with HIV. It can be caused by HIV itself, or by infections in the intestine. Intestinal infections are often caused by the same bacteria and parasites that cause food poisoning. They can be serious for people with HIV and need to be treated. Diarrhea has been reported as a side effect of some antibiotics. With some drugs, diarrhea goes away after the first few weeks of treatment – but some people find that it becomes a permanent feature of living with the drug. The severity of diarrhea can also differ between people. Diarrhea can cause loss of valuable nutrients. Diet needs to be modified or changed if there is diarrhea. Fatty food can worsen diarrhea. Dairy products in the diet may also contribute to diarrhea because of lactose intolerance. Eating bananas, chicken and fish can help restore levels of potassium, which are commonly depleted in people with bad diarrhea. Coffee, carbonated beverages, raw vegetables and spicy food should be avoided as these can make diarrhea worse. High-fibre foods such as brown rice and whole grain bread contain lots of nutrients, but they can also contribute to diarrhea. These may be replaced with white bread and rice during bouts of diarrhea. Some fruits and

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vegetables are also high in fibre (like corn for example) and may contribute to diarrhea. Other fruits and vegetables are easily tolerated and some may even help stop diarrhea. Since there is a loss of water and minerals in diarrhea, drinking extra water can help in rehydration. (b) Nausea has many causes and is a common side effect of many HIV drugs. It is important to determine what is making you nauseous. Nausea can be a sign of gastrointestinal infections or other intestinal problems. Changes in the diet will help. In extreme conditions, it may not be possible to eat anything. Small frequent sips of ginger drinks or soup will help. Even if not eating, body fluids need to be replaced. In addition, it is not advisable to go without solid foods for more than two days. Generally, cold foods without much of an odour are easier to take in conditions of nausea. Several small meals will be easier to take than one large one. Food should be eaten slowly. Lying down immediately after a meal can also cause nausea. (c) Oral conditions may have an impact on food intake. Mouth or throat infections like thrush, dental problems, or mouth ulcers can all be painful barriers to eating. The best way to resolve this problem is to treat the infection or have the necessary dental work. When these problems cannot be quickly resolved, there are strategies to help in consuming appropriate nutrients over the short term. Milk is good if there is no lactose intolerance. This will provide nutrients. Soft moist foods can be consumed. Fats will not only soften foods but are also a good source of energy. Straw can be used for liquids if most of the problems are located in the mouth. Heating food too much can be avoided as hot foods can cause pain, especially for those with dental problems. Changes in the tissues of the mouth are associated with deficiencies in some vitamins, particular B complex vitamins and vitamin C. Since these deficiencies have been observed in people with HIV, B complex supplement or a vitamin C supplement might help ward off oral problems. The role of B complex vitamins and vitamin C in preventing oral conditions has not been well studied. (d) Lack of appetite. Rather than eating a whole dinner at frequent intervals, small snack-like meals can be eaten. Protein and nutrient intake can be increased with high protein snacks like nuts, seeds, puddings, cheese or peanut butter and crackers. Taking walks before meals or other exercises can stimulate appetite. It is good to keep favourite foods on hand as there is greater likelihood of eating more. Doctor can prescribe drugs, which are appetite stimulants. These drugs can help in eating more.

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(e) Lactose intolerance. A large percentage of people with HIV seem to become lactose intolerant. One study found that 70% of HIV+ participants were lactose intolerant. This means that dairy products like milk, cheese and ice cream may cause diarrhea, gas, and bloating. Lactose is also added into a lot of processed foods. Lactose is sometimes added to prepare foods/meals, so if one can tolerate only very small amounts of lactose, it’s important to check food labels and lists of ingredients. One should look not only for milk and lactose among the contents, but also for such words as ‘whey’, ‘curds’, ‘milk by-products’, ‘dry milk solids’, and ‘non-fat dry milk powder’. These words denote that the food contains lactose. Several products with lactose content are available in India as well as other developing countries. Examples include: ● Bread and other bakery foods ● Candies ● Pancake, biscuit, or cookie mixes ● Breakfast cereals ● Soups ● Non-dairy powdered coffee creamers ● Margarine ● Salad dressings There are products especially designed for lactose-intolerant people, including lactase capsules that can be taken before eating. Many people find these capsules helpful, particularly if taken on occasional basis, so they don’t have to worry when they go out to dinner. There are also lactosereduced dairy products. For many people, being lactose intolerant may mean avoiding dairy products altogether. Since dairy products are good sources of protein it is important to get additional protein from sources other than dairy products along with calcium and vitamin D supplements to avoid deficiencies of those vitamins. Whey protein, an expensive product, is used by some people to supplement protein intake; whey protein is derived from dairy products. However, whey protein formulas or products are often lactose reduced, it is important to check the lactose content.

14.5

Nutritional requirements for People Living with HIV (PLHIV)

14.5.1 Energy requirements Studies point to low-energy intake combined with increased energy demand due to HIV and related infections as the major driving forces behind HIVrelated weight loss and wasting. Based on the increased resting energy

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expenditure (REE) observed in studies on HIV-infected adults, it is recommended that energy needs be increased by 10% over accepted levels for otherwise healthy people. The goal is to maintain body weight in asymptomatic HIV-infected adults. Although studies on energy expenditure have not shown an increase in the overall total energy expenditure (TEE), this may have been the result of individuals compensating by reducing activity-related energy expenditure (AEE). Since maintaining physical activity is highly desirable for preserving the quality of life and for maintaining muscle tissue, it is undesirable that energy intake should only match a reduced level of AEE. The estimated energy requirement therefore allows for normal AEE levels in addition to an increased level of REE. Energy requirements of adults Increased energy intake of about 20–30% is recommended for adults during periods of symptomatic disease or opportunistic infections (OI) to maintain body weight. HIV doesn’t kill anybody directly. Instead, it weakens the body’s ability to fight disease. Infections, which are rarely seen in those with normal immune systems, are deadly to those with HIV. People with HIV can get many infections (OIs). Many of these illnesses are very serious, and they need to be treated. Some can be prevented too. This takes into account the increase in REE due to HIV-related infections. However, such intakes may not be achievable during periods of acute infection or illness, and it has not been proven that such high intake levels can be safely achieved during such periods. Moreover, it is recognized that physical activity may be reduced during HIV-related infections and the recommended increased intake is based on the energy needed to support weight recovery during and after HIV-related illnesses. Intake should therefore be increased to the extent possible during the recovery phase, aiming for the maximum achievable up to 30% above normal intake during the acute phase. Energy requirements of children Few studies exist on the energy expenditure in HIV-infected children. The energy requirements of children can vary according to the type and duration of HIV-related infections, and whether there is weight loss along with acute infection. Although the finding of increased REE in asymptomatic disease has not been replicated in children, similar to asymptomatic HIVinfected adults, an average increase of 10% of energy intake is recommended to maintain growth. Based on clinical experience and existing guidelines to achieve catch-up growth in children irrespective of

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the HIV status, energy intakes for HIV-infected children experiencing weight loss need to be increased by 50 to 100% over established requirements for otherwise healthy uninfected children. In the absence of specific data to support specific recommendations for managing severe malnutrition in HIV-infected children, existing WHO guidelines [18] are advised to be followed. Research is needed on the specific energy requirements of HIV-infected children. WHO guidelines are the basis of the following requirements for various nutrients. Energy requirements of pregnant and lactating women Pregnancy is a particularly vulnerable time for women because their nutritional requirements of energy, vitamins and minerals increase by up to 30%, yet their usual daily intakes are frequently below the recommended dietary allowance (RDA) for healthy pregnant women. Malnutrition during pregnancy, therefore, may further erode the immune status of HIV-infected women and make them more vulnerable to disease progression, although this hypothesis has not yet been proven. Specific data are absent regarding the impact of HIV and AIDS and related conditions on the energy needs during pregnancy and lactation, over and above those requirements already identified for non-infected women. Thus, for now, the recommended energy intake for HIV-infected adults should also apply to pregnant and lactating HIV-infected women.

14.5.2 Protein requirements Protein is important to PLHIV because it is the primary component of muscle, and plays a crucial part in many of our metabolic processes. When PLHIV lose weight, they often lose muscle. This is called muscle wasting. It is important to eat enough food to prevent the body from using the energy stored in the body as muscle. Research also suggests that a high-protein diet and regular exercise may help PLHIV to avoid muscle wasting. Eating more protein may also help to regain lost muscle mass. An approximate rule of thumb is 100–150 g/day for HIV-positive men and 80–100 g/day for HIVpositive women. The protein intake should not be greater than 15–20% of the total calories; a diet extremely rich in protein can stress the kidneys.

14.5.3 Fat requirements PLHIV may experience medication-related high cholesterol and triglyceride levels, requiring caution with regard to cardiovascular disease (CVD). Omega-3 fatty acids, a type of polyunsaturated fat found in fish and other foods such as flaxseeds, beans, peas, are protective against

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CVD. The amount of saturated, monosaturated and polyunsaturated fat in the diet should be 7:10:10 percent, respectively of the total caloric intake.

14.5.4 Requirement of micronutrients The role of micronutrients in HIV and AIDS has special importance in individuals and populations with marginal or low micronutrient intakes. Studies from both industrialized and developing countries report that PLHIV have decreased absorption, excessive urinary losses, and low blood concentrations of vitamins A, B1, B 2, B 6, B10, C, E, as well as of folate, beta-carotene, selenium, zinc and magnesium [19, 20]. Currently, it is not known whether these deficiencies are independent markers of disease progression resulting from a compromised immune system, or whether they are causally related to the development or exacerbation of the symptoms of HIV and AIDS. This distinction is important to determine whether the nutritional deficiencies can be reversed, and whether nutritional therapy and management can slow or alter the course of the disease. Antioxidants The process of breaking down food into energy involves a chemical reaction called oxidation. Food break down is one of many oxidative processes in our bodies. During this process, molecules called free radicals are produced. Although free radicals are a normal part of the oxidation process, they can damage the membranes of the body’s cells in much the same way that rust damages the body of a car. To control this process the body produces an antioxidant, called glutathione, in the walls of the cells. External sources of antioxidants present in food are beta-carotene, selenium and vitamins A, C and E. During HIV infection, many researchers have observed an increase in free radicals. The cause of this increase is not completely understood. A decrease in antioxidants in general and glutathione in particular has also been observed. Having low levels of glutathione in the body is associated with a lower survival time for PLHIV. Vitamin A requirements of adults Of all the micronutrients, the role of vitamin A in HIV has received the greatest attention. This is because of its well-known role in affecting child morbidity and mortality, as well as early observations that vitamin A status was associated with increased risk of mother-to-child transmission (MTCT)

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of HIV; HIV viral load in breast milk, vaginal secretions [21, 22]; progression to AIDS; adult survival; and infant morbidity and mortality. The potential for vitamin A supplementation to positively impact the course of HIV and AIDS was promising to pursue, since vitamin A is beneficial in HIV-negative populations, is inexpensive, and relatively easy to administer with minimal side effects. Several studies in Africa have measured the impact of vitamin-A supplementation on various HIV-related outcomes in children. In South Africa, supplementation of vitamin A in HIV-infected children reduced morbidity due to diarrhea by about 50% in one study and improved immune status in another study. In Tanzania, vitamin-A supplementation reduced all-cause mortality by 63% among HIV-infected children in the age group of 6 months to 5 years, and was associated with a 68% reduction in AIDSrelated deaths and a 92% reduction in diarrhea-related deaths. Periodic vitamin A supplementation has been shown to reduce all-cause mortality and diarrhea-related morbidity in vitamin-A-deficient children, including HIV-infected children. In keeping with WHO recommendations, 6 to 59 month old children born to HIV-infected mothers living in resourcelimited settings should receive periodic (every 4 to 6 months) vitamin A supplements (100,000 IU for infants 6–12 months of age and 200,000 IU for children >12 months of age). Currently, there is insufficient evidence to recommend an increased dose or frequency of vitamin A supplementation in HIV-infected children. According to published reports, daily antenatal and postnatal vitaminA supplementation for HIV-infected women in well-designed, randomized controlled trials was not able to reduce the MTCT of HIV; on the contrary, in some settings, it actually increased the risk. Thus, daily intake of vitamin A by HIV-infected women during pregnancy and lactation should not exceed one RDA. In areas of endemic vitamin A deficiency, WHO recommends that a single high dose of vitamin A (200,000 IU) be given to women as soon as possible after delivery, but no later than six weeks after delivery. Research is under way to assess further the effect of single-dose, postpartum vitamin A supplementation among HIV-infected women. Micronutrients and anemia Anaemia is a common problem among PLHIV, affecting asymptomatic HIV-infected adults and children as well as people with AIDS. The causes of anemia associated with HIV and AIDS are not well understood. Anemia may result from cytokine-induced suppression of red blood cell (RBC) production; chronic inflammation; opportunistic infections (OIs) and/or reduction in dietary intake (including iron), absorption and retention.

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Anemia may also be caused by certain antiretroviral (ARV) drugs (e.g. zidovudine, which suppresses bone marrow function and synthesis of RBCs), as well as by nutritional deficiencies of iron, folate, riboflavin, and vitamins A and B12. Studies have found that anaemia is associated with HIV-disease progression and a two-to-four-fold increased risk of death in HIV-infected individuals. The risk increases with the severity of the anaemia. One longitudinal study in Europe found that the risk of death increased by 57% for every 1 g/dl decrease in the haemoglobin level in HIV-infected subjects, after controlling for CD4 cell counts, viral load, and use of ARVs. This risk was greater than the risks observed with a 50% reduction in the CD4 cell count and a ‘log’ increase in the HIV viral load. On the other hand, studies also suggest that reversing anaemia can slow down the progression of HIV disease and prolong survival [23]. It is worthwhile to mention that although anaemia is common among PLHIV, advanced HIV disease may also be characterized by an increase in iron stores in the bone marrow, muscle, liver and other cells. This accumulation of iron is probably a result of the body’s attempts to withhold iron from plasma, although other factors (e.g. use of zidovudine, cigarette smoking and blood transfusions) may also play a role. Increased iron stores can predispose to microbial infection and also cause oxidative stress, with implications for HIV-disease progression. Additional research is required to identify approaches for managing anaemia in PLHIV. (i) Iron–folate supplementation for pregnant and lactating women Iron–folate supplementation is a standard component of antenatal care for preventing anaemia in pregnant women and improving foetal iron stores. WHO recommends daily iron–folate supplementation (400 μg of folate and 60 mg of iron) during the first six months of pregnancy to prevent anaemia, and twice-daily supplements to treat severe anaemia. As with other chronic infections, HIV causes disturbances of iron metabolism and anaemia. In view of iron’s potential adverse effects, for example, its pro-oxidant activity, which might accelerate disease progression, research on the safety of iron supplementation in adults and children with HIV infection is recommended. Based on available evidence, however, the approach to caring for HIV-infected women is the same as that for uninfected women. (ii) Multiple micronutrient supplements Observational studies indicate that low blood levels and decreased dietary intake of some micronutrients are associated with faster HIV-disease

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progression and mortality, and increased risk of HIV transmission. However, the methodological limitations of these studies preclude definitive conclusions about the relationship between micronutrient intake and blood levels, and HIV infection. Studies have shown that even people who eat good food are likely to have vitamin and mineral deficiencies when they have HIV. Zinc, selenium, magnesium, carotenoids and vitamins A, B2, B 6, B12, and E intakes have all been shown to be often low. This can happen before visible sicknesses occur, and before the stage that we call AIDS. Supplementation has been shown to be associated with significant slowing of disease progression. Some studies show that supplements of, for example, B-complex vitamins, and vitamins C and E can improve immune status, prevent childhood diarrhea and enhance pregnancy outcomes, including better maternal weight gain during pregnancy, and a reduction in foetal death, preterm birth and low birth weight. The effect of these micronutrients on HIV disease progression and mortality is under study. Several neurological problems in HIV disease have been attributed to nutritional deficiencies, especially that of vitamin B12. Low intake of Bcomplex vitamins is associated with faster progression of HIV disease. PLHIV should be able to get enough of most of these vitamins from supplements that are taken as pills. Vitamin E is necessary for proper functioning of the immune system. It increases humoral and cell-mediated immune responses, including antibody production, phagocytic and lymphocytic responses, and resistance to viral and infectious diseases [24]. Vitamin E is one of the few nutrients (another is vitamin A) for which supplementation at higher than daily recommended levels have been shown to increase immune response and resistance to disease. The oxidative stress created by HIV and related opportunistic infections (OIs) increases the utilization of the antioxidant vitamin E. Deficiency, in turn, further debilitates the immune system because of its role in immune stimulation and functioning, leaving PLHIV more susceptible to OIs. A study in Zambia among AIDS patients suffering from persistent diarrhea found that oral supplementation with vitamin E and other nutrients did not affect either mortality or diarrhea-related morbidity, possibly because of severe fat malabsorption accompanying late-stage disease. Selenium deficiency impairs the immune system and has been associated with faster HIV disease progression and reduced survival in adults [25] and children [26]. Selenium is believed to play an important role in metabolizing reactive oxygen species (‘free radicals’) and reducing oxidative stress because it is an essential cofactor for glutathione perodixase, an antioxidant enzyme.

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Findings of a study conducted in France suggest that selenium (and beta-carotene) supplementation may reduce the impact of oxidative stress on HIV disease. Zinc plays a role in HIV infection because HIV requires zinc for gene expression, replication and integration. Thus, persons with HIV infection may have low plasma zinc levels yet higher zinc intakes may be associated with faster HIV replication and disease progression. Zinc supplementation among AIDS patients, however, has shown substantial benefits. In a study in Italy, daily zinc supplementation (200 mg/day) for one month reduced the incidence of OIs (particularly Pneumocystis carinii and Candida), stabilized weight, and improved CD4 cell counts among adults with AIDS who were also receiving ART a s c o m p a r e d w i t h c o n t r o l s w h o r e c e i v e d A RT b u t n o z i n c supplementation. These findings suggest that zinc supplementation should be approached cautiously and must take into account dietary intake of the mineral. Zinc supplementation, in short courses and carefully monitored, may be useful for strengthening resistance to OIs in persons with AIDS [27]. Studies have shown that even people who eat well and adequately are likely to have vitamin and mineral deficiencies when they have HIV infection. Normal recommended dietary levels for vitamins and minerals are often not adequate for PLHIV. Food alone is not enough. Supplementation has been shown to be associated with significant slowing of disease progression. Multiple micronutrient supplements may be needed during pregnancy and lactation. Pending additional information, micronutrient intakes at the RDA level are recommended for HIV-infected women during pregnancy and lactation. The optimal micronutrient supplement composition that will be safe, ensure nutritional adequacy, and potentially produce the greatest benefits in HIV-infected pregnant and lactating women in different settings has not yet been defined. Additional research is required to determine the safety of nutrient supplements such as zinc, iron and vitamin A, and to determine whether different multiple micronutrient supplements are needed for HIV-infected women compared with uninfected women. HIV-infected adults and children should consume diets that ensure micronutrient intakes at RDA levels. However, this may not be sufficient to correct nutritional deficiencies in HIV-infected individuals. Several studies raise concerns that some micronutrient supplements, e.g. vitamin A, zinc and iron, can produce adverse outcomes in HIV-infected populations. Safe upper limits for daily micronutrient intakes for PLHIV still need to be established. Some efforts being undertaken in this context are presented in Box 14.3.

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HIV and appropriate support

(a) Nutrition guidelines Appropriate nutrition is important for PLHIV. Many studies have shown that people living with HIV who are malnourished are likely to get sick more often, and have shorter survival times than other HIV+ people. Poor nutrition has also been observed to weaken the immune system. There is a need to balance the amount of energy consumed as food with the amount of energy the body needs to maintain itself, and to conduct daily activities. The body may also be less capable of taking in nutrients and therefore energy. This is called malabsorption. Malabsorption may be caused by bacterial or parasitic infections in the intestines. It may be caused by changes in the intestines due to HIV. Malabsorption may occur in conditions of diarrhea caused by drugs taken. PLHIV need to pay attention to their diet to get the best possible nutrient balance. They may also need to supplement certain specific nutrients. If a person with HIV does not take in enough nutrients, their energy intake is decreased and they may begin to lose weight. Following guidelines will help to stay healthy and get the nutrients needed. ● ●

● ● ●

● ● ● ● ●

Healthy dietary principles Maintenance of lean body mass and normal growth in children and the treatment of wasting Management of metabolic complications due to drug therapies Management of drug and food or nutrient interactions Management of gastrointestinal symptoms that may influence the types and amount of food ingested Appropriate use of nutritional supplements Role of exercise Food safety Nutrition during pregnancy Access to infant formula and food as an alternative to breastfeeding

(b) Some dietary guidelines for PLHIV Nutritional management is integral to the care of all patients with HIV. HIV results in complicated nutritional issues for patients, and there is growing evidence that nutritional interventions influence health outcomes in PLHIV. This means eating well, which is important since the immune system requires protein to fight infection. But in order for the body to properly use the protein, fat and carbohydrate in food, it needs adequate levels of vitamins and minerals.

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Because many of the weight-loss problems seen in HIV are related to low food intake, many small meals throughout the day, rather than 2 or 3 large ones, is suggested. Having HIV is unlikely to mean drastic changes to the diet – a good diet will consist of a balance of the following items: (i) Carbohydrates Carbohydrates make up most of the Indian’s diet. Carbohydrates can be simple sugars. They can also be complex carbohydrates, which are long strings of sugar molecules linked together. Complex carbohydrates are found in breads, cereals, and pastas, as well as in fruits and vegetables. They provide energy as well as vitamins and minerals. They are usually the most desirable sources of carbohydrates. Simple sugars are fine in moderation, especially if they help increase intake of other nutrients by making the meals more appealing. Carbohydrates are important because they provide the body with quick, easily used energy. Carbohydrates help you maintain the energy balance, so that the body does not have to draw on stored energy sources like fat and muscle. Fruits and vegetables provide vitamins, minerals, fibre and energy. One should eat five portions a day. A portion is equal to a whole piece of fruit, a heaped serving spoon of vegetables, a small glass of fruit juice, or a handful of dried fruit. Meat, poultry, fish, eggs, beans nuts provide protein, minerals and vitamins. One should eat two or three portions per day. A portion is equal to two medium-sized eggs, a 100 g piece of meat, a 150 g piece of fish, or a small can of baked beans. Dairy products such as milk, cheese, and yoghurt provide vitamins, minerals and calcium. Three portions can be eaten per day. A portion is equal to a third of a pint of milk, a small pot of yoghurt, or a matchbox-sized piece of cheese. (ii) Fats Fats such as cooking oils, butter, margarine, meat and other proteinbased foods provide energy, essential fatty acids and the fat-soluble vitamins A, D, E and K. They also provide calcium and phosphate. It is recommended that about one-third of the daily calorie intake should come from fats. Eating too much fat can lead to weight gain and increased levels of blood fats. This can increase chances of developing cardiovascular disease and some cancers. There is no increased need for fats for PLHIV. Some PLHIV have difficulty in absorbing fats. It may be due to intestinal damage caused by opportunistic infections, or by HIV itself.

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Steatorrhea can cause diarrhea, bloating, or changes in the colour of the stool. If one has steatorrhea, very little of the fat eaten is absorbed. Since it is still important to have some fat in the diet, it is important to drink liquid supplements or other products that contain a type of fat called MCT (medium-chain triglycerides). This type of fat is easy to absorb. Excessive amounts of saturated fats can raise the body’s cholesterol levels. Saturated fats are animal fats like those found in butter, or as part of red meat. High triglyceride and cholesterol levels are associated with a higher risk of heart attacks and stroke. Recently, both high triglyceride and cholesterol levels have been observed in some PLHIV on ART. In some studies, polyunsaturated fats (found in some vegetable oils such as corn and peanut oil, and in most margarines) been shown to reduce Tcells, and with them the functioning of the immune system. While these studies were not HIV-specific, it may still be wise for PLHIV to avoid eating a lot of polyunsaturated fat. Polyunsaturated fats are much less likely to increase cholesterol than saturated fats. Monounsaturated fats are also found in vegetable oils like olive oil and canola oil. These are not suspected of being immune suppressive. Monounsaturated fats do not normally increase cholesterol levels like saturated fats, but they are sometimes modified when heated during processing. For this reason, many people look for olive oil that is “cold pressed”. Omega-3 fatty acids are called essential fatty acids because they must be present in the diet. The body can’t manufacture them. They are found in the oils of most fish and seafood, as well as in flaxseed and some beans and peas. Eating foods rich in omega-3 fatty acids has been shown to reduce the risk of heart attack, and to have a positive influence on cellmediated immunity (the part of the immune system most damaged by HIV infection). Studies on PLHIV have shown that by using omega-3 fatty acids reduced triglyceride levels and, if they had no new opportunistic illnesses, it helped them gain weight.

(c) Fluids Fluid helps replace water lost in sweat and urine. Water also transports nutrients throughout the body and keeps the kidneys functioning in a healthy way. By sweating, and losing lot of fluid in other ways, like vomiting or diarrhea, one can lose important minerals. As in normal condition, PLHIV should drink at least 8 glasses of water a day. Box 14.3 highlights the positive impact of nutrition supplement and counselling for PLHIV

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Box 14.3 People living with HIV (PLHIV) – Impact of Nutrition Supplements and Counselling– A field trial on integrating nutrition support as a part of care and treatment of PLHIV World Food Programme in collaboration with Tuberculosis Research Institute in a non-randomized interventional study of PLHIV in Tamil Nadu, India found that PLHIV were more malnourished, anaemic and hypoproteinemic than socio economically matched controls. It was noted that in resource poor setting, with a high background level of malnutrition, HIV infection resulted in adverse nutritional status of individuals. Decrease in the body weight, BMI, mid-arm and hip circumferences with a reduction in the FFM (fat free mass that is, total mass minus fat mass) and BCM (body cell mass) (in males) and triceps skinfold thickness and percent body fat (in females) may be the earliest indication of decline in the nutritional status of HIV-infected patients. The intervention group received nutritional supplement in the form of 3 kg pack of a blended micronutrient fortified food every month to be consumed 100 g/day (100 g of the supplement provides 400 calories, 15% protein, 6% fat fortified with vitamins A, B1 , B2 , B12 , C, Niacin and folic acid). The control group did not receive supplement for the first 6 months. Both groups received nutritional counselling, prophylaxis and psychosocial support. Anthropometric, laboratory and dietary assessments were done at baseline and at 6 months for all patients. Body composition by BIA (bioimpedance analysis) measured in a sub-group of patients, repeated at 6 months. Quality of life using WHO–Quality of life index protocol was assessed every 6 months. Data was entered in Excel/EpiInfo and analyzed using SPSS statistical package. Both the intervention and Control Groups were compared at baseline. Paired t-test used to compare values at 0 and 6 months. After 6 months of nutritional supplementation there was a significant increase in weight, BMI and mid-arm circumference (MAC). CD4 cell count remained unchanged in the intervention group but decreased significantly in controls without nutritional supplementation. Though all sub-groups showed improvement, weight gain was maximum in the lowest CD4 count strata. Men and women with CD4<200 showed increase in body fat content.

Based on the findings of the above study (Box 14.3), integration of nutritional support (counselling and nutrition supplementation) for PLHIV was recommended to be included into National AIDS Control Programme of India (see Box 14.4). Box 14.4 National AIDS Control Programme, India National Aids Control Organization (NACO) was established in 1992, under Ministry of Health and Family Welfare [23]. NACO formulates policy and implements programs for prevention and control of HIV and AIDS in India. NACO coordinates and manages the National AIDS Control programme (NACP). At the state level, the state governments have established State AIDS Control societies for effective management and implementation of National AIDS Control Programme at the state level. First two phases of NACP have been completed and the third Phase of the NACP III (2007–2012) has placed the highest priority on preventive efforts, while at the same time seeking to integrate prevention with care, support and treatment. According to NACP III, there will be investment in community care centres to provide psychosocial support, outreach services, referrals and palliative care to PLHIV.

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In March 2007, NACO approved a programme to provide nutritional supplement to children enrolled under their ART programme in the country. Under this programme, fortified powdered supplement made of wheat, gram and soya is being provided free of cost to children receiving ART. This is processed by roasting/extrusion and is fortified with micronutrients and trace elements which help in improving immunity of people living with HIV. Each ration will provide one RDA as specified by WHO. The programme aims at partially meeting the nutritional needs of over 3000 children currently enrolled under the ART programme in the country. The programme has been undertaken in collaboration with technical support from several international agencies including Clinton Foundation and WFP. In the state of Tamil Nadu, under the Tamil Nadu State Aids Control Society, nutrition interventions of the programme included free nutritional supplements and nutrition counselling to PLHIV with casespecific advice to people such as pregnant women. The programme estimated to benefit over 15,000 PLHIV. As part of its efforts to increase the quality of life and life expectancy of people living with HIV and AIDS, in March 2007, the Tamil Nadu government in partnership with WFP launched the nutritional supplement support programme known as “Nutriplus programme”. In this programme, nutritional support was provided to PLHIV registered at all 20 anti-retroviral therapy (ART) centres in Tamil Nadu. (iii) Eating safely PLHIV are vulnerable to many infections because their immune system is damaged. This includes food-poisoning infections like Salmonella. Proper preparation and storage of food is a very important part of staying healthy. Proper food handling and storage minimizes the risk of food borne illnesses and is very important for people with weakened immune systems as is the case in HIV. Following food safety measures are recommended ● ●

● ● ●

●

●

Use only pasteurized milk. Never use products whose “sell by” or “best used by” labels have passed. Wash hands with soap and water frequently. Carefully wash all cutting boards after chopping vegetables. Store hot leftovers in a shallow, small container. Reheat until hot to touch throughout. Don’t keep leftovers for more than three days. When in doubt, throw it out. Avoid raw eggs.

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Wash all fruits and vegetables. Peeling eliminates some risk of bacteria.

(iv) Infant-feeding guidelines for infants born to mothers with HIV A woman infected with HIV can transmit the virus to her child during pregnancy, labour or delivery, or through breastfeeding. Mother-to-child transmission (MTCT) is by far the most significant route of transmission of HIV infection in children below the age of 15 years. In 2005 alone, 700,000 children were reported to have acquired HIV infection. HIV can be transmitted during pregnancy, during childbirth, or breastfeeding. Without intervention, the risk of transmission from an infected mother to her child ranges from 15% to 25% in developed countries and from 25% to 45% in developing countries. This difference is largely attributed to breastfeeding practices (Table 14.1). Table 14.1Estimated risk and timing of MTCT in the absence of interventions During pregnancy During labour and delivery During breastfeeding Overall without breastfeeding Overall with breastfeeding to 6 months Overall with breastfeeding to 18–24 Months

5–10% 10–15 % 5–20% 15–25% 20–35% 30–45%

It is a public health responsibility to prevent HIV infection in infants and young children, and to support optimal breastfeeding to prevent mortality and illness due to diarrhea and respiratory infections. AIDS has increased the mortality of children less than five years of age in highprevalence areas, both through direct infection and because of the reduced levels of care that a family living with HIV can provide. Although only part of this increase in mortality is the result of HIV infection through breastfeeding, it is important to have clear guidelines on infant and young child feeding, including the effects of HIV. Breast feeding is normally the best way to feed an infant. Breast feeding mothers of infants and young children who are known to be HIV-infected should be strongly encouraged to continue breastfeeding [28]. Exclusive breastfeeding is recommended for HIV-infected women for the first six months of life unless replacement feeding is acceptable, feasible, affordable, sustainable and safe (AFASS – Box 14.5) for them and their infants before that time. When replacement feeding is acceptable, feasible, affordable, sustainable and safe (AFASS),

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avoidance of breastfeeding by HIV-infected women is recommended. At six months, if replacement feeding is still not acceptable, feasible, af f o r d a b l e , s u s t a i n a b l e a n d s a f e ( B o x 14.5 ) , c o n t i n u a t i o n o f breastfeeding with additional complementary foods is recommended, while the mother and baby continue to be regularly assessed. All breastfeeding should stop once a nutritionally adequate and safe diet without breast milk can be provided [28]. Regarding infant-feeding choices, NACO [29] states: Breast feeding provides the infant with all required nutrients and immunological factors that help to protect against common infections. This protection is reduced when the child is given water or any other substance during exclusive breastfeeding. Mixed feeding, i.e. breast milk and formula feeds combined, is the most hazardous form of infant feeding. Exclusive replacement feeding is the ideal option but it may not be affordable and feasible, where safe drinking water, fuel or clean utensils are scarce. In such scenario HIV-infected women should be counselled during the antenatal period about infant-feeding choices and to make an informed decision. The mother who has chosen not to breast-feed must be able to prepare feeds hygienically and should be advised to use cup feeding and not bottle feeding. In case replacement feeding is not possible, exclusive breastfeeding for the first six months of life with early cessation is recommended. The risks of HIV transmission especially if combined with ART may be less than 0.5%, if exclusive breastfeeding is done. If family support is not present, exclusive breastfeeding may be difficult and the parent(s) may need consistent psycho-social support. When the child reaches the age of six months or earlier, breastfeeding should be stopped within two weeks while ensuring the comfort level of both mother and infant. At the same time, good quality complementary foods should be introduced, ensuring adequate amounts of energy proteins and micronutrients. HIV-infected mothers should be counselled about infant-feeding choices during pregnancy (ante-natal period) and to decide before delivery. During the post-natal period, she should be counselled again to support her decision and to note if there is a change of decision on infant-feeding options. As with the PPTCT recommendations, “HIV-positive women are counselled on feeding options in order for them to make an informed decision on how they would like to feed their infants”.

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Box 14.5 AFASS Acceptable The mother perceives no barrier, cultural or social, to replacement feeding and has no fear of stigma. She will be able to cope with pressure from family and friends to breastfeed. Feasible The mother has adequate time, knowledge, skills and other resources to prepare the replacement food and feed the infant up to 12 times in 24 hours. Affordable The mother and family can purchase formula, including all ingredients, fuel, clean water, soap and equipment, without compromising the health and nutrition of the family, and also possible increased medical costs. Sustainable Availability of a continuous and uninterrupted supply and dependable system of distribution of formula for as long as the infant needs it. Safe Replacement foods are correctly and hygienically prepared and stored, and fed in nutritionally adequate quantities, with clean hands and with clean utensils, preferably by cup.

Evidence has shown that early breastfeeding cessation is associated with increased morbidity and mortality in HIV-exposed infants. Improved adherence, longer duration of exclusive breastfeeding can be achieved in HIV-infected and HIV-uninfected mothers given consistent messages on the meaning and significance of exclusive breastfeeding and frequent, high quality counselling. HIV-infected mothers who need ARVs for their own health should have antiretroviral therapy and this is likely to decrease transmission. Mothers with severe HIV but not yet on ARVs may adopt replacement feeding but it is important that the consider AFASS criteria. HIV-positive infants benefit from continued breastfeeding. There is no doubt that breast milk can transmit HIV or that an infant’s chances of survival when living in a poor or rural community are greatly decreased by not practicing breastfeeding. The challenge is how health systems can, at scale, help individual women, whether infected with HIV or not, appreciate the inherent risks and opportunities of their environment and make appropriate decisions about how to feed their infants. For scientists, the challenge is to study and understand the evidence and possible prejudices in this crucial component of child survival. Based on these principles, a number of countries have developed guidelines for feeding young children. The national guidelines for infant and young child feeding in India [30] refers to the risk factors such as breast pathology like sore nipples or even sub-clinical mastitis during breastfeeding that increase transmission and are preventable problems through good breastfeeding and lactation management support to mothers.

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Box 14.6 All HIV-infected mothers should receive counselling, which should include provision of general information about meeting their own nutritional requirements and about the risks and benefits of various feeding options and specific guidelines in selecting the option most likely to be suitable for their situation. The manifold advantages of breastfeeding even with some risk of HIV transmission should be explained to the HIV-positive mothers.

If artificial feeding is NOT affordable, feasible, acceptable, safe and sustainable (AFASS), then only exclusive breastfeeding must be recommended during the first six months of life. These guidelines imply that till one can ensure all these 5 AFASS factors, it would not be safe to select artificial feeding by HIV-positive mothers. The danger of mixed feeding should be explained to the HIV-infected mothers. Sometimes mothers may choose to artificially feed the baby, but under some social pressures they also breastfeed the child. An artificially fed baby is at less risk than the baby who receives mixed feeding, i.e. both breastfeeding and artificial feeding. All breastfeeding mothers should be supported for exclusive breastfeeding up to six months. If the woman chooses not to breastfeed, she should be provided support for artificial feeding to make it safe. To achieve appropriate infant-feeding practices in HIV-positive mothers, capacity building of counsellors and health workers including doctors and nursing staff is mandatory to ensure either ‘exclusive feeding’, or ‘exclusive artificial feeding’ as chosen by the mother. In the absence of safe water, hygiene, and community acceptance exclusive breastfeeding should be promoted until the infant is 6-month old rather than just during the first few months of life. The continued risks of serious morbidity and mortality in infants if breastfeeding is stopped early at around six months stresses the need for continued contact and counselling with mothers during the first months of the infant’s life. Counselling will also help in guiding her decisions about feeding practices beyond 6 months. Incorrect use of commercial infant formula can result in diarrheal illness and malnutrition. (v) Exercise and PLHIV Several studies have shown that aerobic exercise improves quality of life for people with HIV. For example exercise can ● ● ● ● ●

Increase muscle mass Boost the immune system Reduce cholesterol and triglyceride levels Regulate sleep patterns Reduce stress

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Enhance self-image Regulated bowel function Increase appetite and energy levels

In early HIV infection, loss of muscle mass occurs even before any apparent weight loss. Increasing muscle mass may help increase longterm survival with HIV. It is possible to increase muscle mass, which it is metabolically active tissue, as opposed to fat, which is not. Increased muscle mass can boost the total amount of energy the body produces. In turn, elevated energy levels can enhance the immune system even more. Moderate exercise is beneficial to the immune system, by increasing T4 Helper Cells, T8 Killer Cells, and Natural Killer Cells. Immune enhancement may be due to the reduced stress levels and improved selfimage of people who exercise. Exercise can reduce cholesterol and triglyceride levels. Some HIV medications increase the amount of fat in the blood, but exercise can help protect against the associated risk of heart disease. Moderate exercise can improve mood and offer an important way of maintaining a healthy self-image. Exercise can include anaerobic exercise or resistance training includes activities such as weight lifting and working out with rubber bands. These activities are more beneficial for increasing muscle or strength. Aerobic exercise includes activities such as brisk walking, cycling, swimming, running, or vigorous dancing. A combination of both aerobic and anaerobic types of activity is best. Because aerobic activity tends to promote weight loss, individuals who have trouble maintaining their weight may want to primarily focus on anaerobic activity. Participating in lower impact aerobic activities such as walking can provide benefits without burning excess calories. Besides these popular forms of exercise like swimming, cycling, aerobics, running, and weight training (sometimes called resistance training), there are a number of movement-based exercises, such as yoga, which help maintain muscle tone and suppleness whilst also having meditative or relaxing qualities. One should be aware of over-exercising. Warning signs include fatigue and increased minor infections. In case a person feels sick (dizzy or nauseated) after a 10–15 minute warm-up period, one should go easy during work-out or stop exercising until one feels better. Some studies have also suggested exercise has beneficial effects on the immune system such as increasing CD4+ cells. Exercising to the point of exhaustion, however, has been shown to be immune suppressive. The biggest benefit of exercise for PLHIV may be the

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building and retention of muscle mass. Exercise, including working out with weights, and swimming, has been shown to improve muscle function and to build lean muscle mass in PLHIV. Such exercise reduces serum triglyceride levels and normalizes blood lipids without requiring the addition of drugs. This would be beneficial to patients who are already consuming too many drugs. (vi) Nutrition Counselling Nutritional counselling is helpful for PLHIV to make an informed choice of the right type of foods in relation to their nutritional and HIV status, and other disease conditions that they experience. When dietary counselling is combined with oral nutritional supplements, there is additional evidence for its value. Nutritional counselling has been shown to be effective; it has also been shown to influence health outcomes in HIV infection (Box 14.7). Efforts to strengthen nutrition counselling, care and support for HIVinfected persons should be balanced with efforts to alleviate the overall burden of malnutrition, regardless of HIV status. Nutrition guidelines should be appropriate to local resources, and programmatic and clinical environment with the treatment and management of the disease. Box 14.7 Effectiveness of counselling on nutritional care A study reported by Tabi et al. [31] on the effectiveness of nutritional counselling as an intervention to improve health outcomes for HIV-positive patients in Ghana, West Africa. Using secondary-analytic data of recorded monthly weights of 25 PLHIV, whose ages ranged from 21 to 60 years, with a mean of 39.4 years (sd = 10.13) were obtained and analysed. It was found that PLHIV responded favourably to nutritional counselling about protein dietary intake as an intervention to improve weight gain. Repeated measures showed a statistically significant weight gain (P = 0.008). They conclude that in the absence of ART, nutrition counselling can be an effective intervention for PLHIV in developing countries. The health and nutritional status of the patients can be improved through nutritious food, allowing them to lead longer and better quality lives. It was concluded that nutritional care and support should be essential elements of a comprehensive approach to HIV.

Nutrition counselling should be based on nutrition and dietary assessment. The purpose of this assessment is to gather information about the current nutritional status and dietary practices and to identify risk factors for developing future nutritional complications. The nutritional status assessment should include at least the measurement of weight, height and haemoglobin. This will help in the calculation of Body Mass Index or BMI. Measurement of mid-upper arm circumference can help in a crude estimation of muscle wasting.

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The dietary assessment should include information on usual eating patterns and intake, appetite and eating problems, and household food security. All medications taken on a daily basis should be noted so that nutrient interactions and/or contraindications can be identified. Nutrition counselling, care and support begin with an assessment of the specific circumstances, including the nutritional status, diet and the social and other conditions that could prevent the person from achieving adequate dietary intake. For HIV-infected persons who are asymptomatic, emphasis should be placed on the need to stay healthy by improving eating habits and the nutritional quality of the diet, maintaining weight (or gaining adequate weight), preserving lean body mass, continuing physical activity and ensuring an understanding of food safety. For individuals who are experiencing HIV-related infections and illnesses and/or weight loss, the main objective is to minimize the nutritional consequences of the infections by obtaining immediate treatment, maintaining the greatest possible food intake during acute infection, increasing food intake during the recovery period, and continuing physical activity as much as possible so as to preserve lean body mass. For individuals who have advanced disease or persistent HIV-related infections and illnesses, the main objective is to provide comfort and palliative care, with modification of the diet according to the symptoms and with encouragement for eating. For persons on ART, the focus of nutrition counselling should be on management of drug and food interactions and other side effects of treatment. Advice related to treatment and counselling on nutrition issues related to ARV and OI treatment cover the timing of pill ingestion in relation to meals, the minimizing and management of nutritionrelated side-effects of prescribed medications (e.g. nausea and vomiting), and the consequences of long-term ARV treatment for body fat distribution and metabolism. Nutrition advice and counselling should also cover the food and water requirements related to ARV drug regimens. Advice should be given on how to cope with body fat distribution and the metabolic changes underlying or new conditions that require dietary modifications, e.g. diabetes mellitus, should be monitored during follow-up care. For pregnant and lactating mothers, it is critical that counselling focuses on issues referred in the section on “infant feeding”. WFP in collaboration with NACO have developed nutrition counselling materials adopting the principles described above. These materials have been provided to all ART and ICTC centres in India. Counsellors all over the country have received training on the use of nutrition counselling materials.

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15 Vitamin A metabolism Ravinder Chadha

Ravinder Chadha, PhD, is an Associate Professor at the Department of Food & Nutrition, Lady Irwin College, Delhi University. She is engaged in teaching Public Nutrition courses to undergraduate and post graduate students. Her doctoral research work was in the area of vitamin A deficiency among school-age children.

#.

Introduction

Vitamin A plays a vital role in human metabolism, being involved in a number of regulatory and other physiological processes. Understanding the role of vitamin A in human body and its physiological processing is important for effectively correcting vitamin A deficiency which remains a public health problem throughout much of the world. The present chapter focuses on the processing of dietary vitamin A, its transport in the circulation and assessment of vitamin A status.

#.2

Discovery of vitamin A

Vitamin A was the first vitamin to be discovered. In the year 1913, recognition of the dietary requirement for vitamin A began with the independent observations of McCollum and Davis [1, 2] and Osborne and Mendel [3] that there was a factor in certain fats which was essential for growth of rats. This lipid soluble growth factor which could be found in animal fats and fish oils was called “fat-soluble A”. It was also observed by Osborne and Mendel that the green parts of plants contain relatively high amounts of “fat soluble A” activity. However, it was Steenbock [4] who concluded from a comparative study of the growth-promoting activities of white and yellow maize in 1919 that there was a definite relationship between the fat-soluble A and the yellow plant pigments. This was further substantiated by Moore [5] who demonstrated that the livers of rats given a diet deficient in vitamin A but with massive amounts of carotene (derived from yellow plant

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pigments) for 1–3 months contained very high amounts of vitamin A. The chemical relationship between β-carotene and retinol was conclusively established by the classical work of Karrer et al [6, 7] as it became obvious that carotene is converted to retinol in the animal body. Though the knowledge of the metabolism of vitamin A and carotenoids has advanced dramatically over the years it continues to be an area of active research.

15.3

Occurrence and sources

All vitamin A present in the body must be derived from the diet as humans as well as other animal species have no capacity for de-novo vitamin A synthesis. Vitamin A is a generic term to designate any compound possessing the biological activity of retinol. The active forms of vitamin A are retinol (alcohol form), retinal (aldehyde form) and retinoic acid (acid form). Nearly 90–95% of total vitamin A reserves are usually in the liver in the form of retinyl esters which is the storage form of vitamin A (Figure 15.1). In the diet, vitamin A is available in two forms, i.e. preformed vitamin A which occurs naturally only in animals and provitamin A carotenoids of plant origin. Preformed vitamin consists primarily of retinol and retinyl esters which are obtained from animal food products. Fish liver oils most notably those of halibut, cod and shark are the most concentrated sources of preformed vitamin A and are often used medicinally. Liver (goat, sheep or ox), egg yolk, butter and whole milk are good dietary sources of preformed retinol. However, synthetic vitamin is used in almost all vitamin A supplements and fortification of processed foods like sugar, cereals, condiments, fats and oils. The major commercial forms are acetate and palmitate esters which are relatively stable. Provitamin A carotenoids are present in dark green vegetables and yellow and orange fruits as well as vegetables. Dark green leafy vegetables, mangoes, carrots, papaya and red palm oil are some rich dietary sources of provitamin A carotenoids. Of more than 600 carotenoids which have been identified in nature, more than 50 possess vitamin A activity. Of these, all-trans β-carotene makes the largest contribution to vitamin A activity in foodstuffs. Others like α-carotene, γ-carotene and β-cryptoxanthin contribute to a lesser extent. These provitamin A carotenoids make up 80% of all dietary vitamin A intake consumed by most people in Asia and Africa where vitamin A deficiency is a public health concern [8]. These provitamin A carotenoids are first cleaved to retinol and then converted to other vitamin A metabolites in the body.

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15.1 Structures of vitamin A and some related compounds

To express the vitamin A activity of different food sources, the term retinol equivalent (RE) is used. On equal weight basis β-carotene has less vitamin A activity than preformed vitamin A (retinol). Other provitamin A carotenoids, like α-carotene, γ-carotene and crypotoxanthin, have only about half the activity of β-carotene. Thus, on the basis of the recommendation of FAO/WHO (1967) [9], 1 μg RE is equal to 1 μg retinol, 6 μg β-carotene and 12 μg of other carotenoids. The total amount of vitamin A in foods is expressed as μg retinol equivalents, calculated from the sum of μg preformed vitamin A + 1/6 × μg β-carotene + 1/12 × μg other provitamin

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A carotenoids. However, there is great variability between individuals in their ability to respond to dosing with β-carotene. The bioequivalence of β-carotene and other provitamin A carotenoids to vitamin A were revised by the US Institute of Medicine (US IOM) [10] in the year 2000 to 12 and 24 μg, respectively. This would make β-carotene 1/12 as active as retinol and other provitamin A carotenoids 1/24. The US IOM also introduced Retinol Activity Equivalent (RAE) to express the vitamin A activity of provitamin A carotenoids which is half the former FAO/WHO Retinol Equivalent (RE). International units (IU) which were used earlier to quantify carotenes still sometimes appear on food and supplement labels. One IU is considered equivalent to 0.3 μg retinol or 0.6μg of β-carotene. Box 15.1 Bioefficacy of provitamin A carotenoids Food-based approaches are being recognized as safe and effective in preventing vitamin A deficiency. Foods containing provitamin A carotenoids tend to have less biologically available vitamin A but are more affordable than animal products which are rich in preformed vitamin A. The provitamin A carotenoids make up 80% of all dietary vitamin among most people in those regions of the world where vitamin A deficiency is a public health concern. Also strict vegetarians of any society depend upon the provitamin A carotenoids for their entire vitamin A intake. In this context, the issue of the bioefficacy which encompasses bioavailability (fraction of the ingested amount that is absorbed) and bioconversion (fraction of the absorbed amount that is converted to retinol) of provitamin A carotenoids is of profound significance. The concept of retinol equivalent proposed by the Joint FAO/WHO Expert group (1967) which was based on very little evidence assigned β-carotene 1/6 and other provitamin A carotenoids 1/12 of the value of preformed vitamin A. Nevertheless, it was useful in assessing the equivalences of different sources of vitamin A activity. Research since the mid-90s have challenged these values and many complex factors that determine the bioavailability have been brought to light. Bioavailability of provitamin A carotenoids and also non-provitamin A carotenoids such as lycopene, lutein and others with possible role in prevention of several chronic diseases is influenced by a number of factors. The chemical structure of carotenoids, food matrix in which a carotenoid is incorporated, cooking methods, dietary fat, nutrient status (Vitamin A, protein, zinc) of the host, genetic factors and interaction among those factors influence bioefficacy of carotenoids. The effect of food matrix and processing on bioavailability of carotenoids is depicted in Figure 15.2. Very high bioavailability

Very low bioavailability

Synthetic carotenoids in oil Carptempodes oil form (Red palm oil) Yellow or green fruits Yellow or green tubers Lightly cooked yellow, orange or green vegetables or fruit juices Fresh vegetables juices (without fat) Raw yellow/orange vegetables Raw Green leafy vegetables

15.2 Bioavailability of carotenoids [11] Dietary intervention studies from Indonesia, Vietnam and China have suggested that one retinol equivalent is derived from either 26–28 μg of β carotene in vegetables or 12 μg of β Carotene in fruits. Based on research evidence from

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developing countries, US IOM recommended in the year 2000 that 1 μg of retinol is equal to 12 μg of dietary b-carotene or 24 μg of dietary α-carotene or β-cryptoxanthin. These revised conversion factors have serious implications on food based approaches to control vitamin A deficiency as rich sources of provitamin A carotenoids are needed to improve the dietary adequacy of vitamin A among vast section of population in the developing regions. However, the methodology for the accurate determination of provitamin A carotenoid bioactivity in man is still evolving and more data are needed to substantiate the present recommendations.

15.4

Metabolism and storage of vitamin A

Vitamin A available from the diet in the intestinal lumen in two forms: preformed vitamin A as retinol and retinyl esters and provitamin A carotenoids. Retinol is absorbed as such from the intestinal lumen into the mucosal cells, whereas retinyl esters are hydrolysed to retinol prior to intestinal absorption. The uptake of provitamin A carotenoids occurs via passive diffusion similar to other dietary lipids and some is possibly mediated by certain membrane transporters. The physiological processing of vitamin A is discussed in this section. The whole body vitamin A metabolism is also illustrated in Figure 15.3.

15.3 Metabolism of vitamin A [12, 13, 14]

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(a) Digestion and absorption Dietary vitamin A and its precursors are released from protein in the stomach by proteolysis. Thorough cooking and mastication facilitates the release of provitamin A carotenoids, especially in case of green leaves in which carotenoids exist within chloroplasts as pigment – protein complexes. It is important that carotenoids are released from the cellulose structures so that they are available for absorption. Released vitamin A and carotenoids aggregate with lipids and pass into the upper part of the small intestine. Dietary fat and protein and their hydrolytic products stimulate the secretion of bile which emulsifies the contents of the gut lumen and promotes the formation of lipid micelles. These micelles have lipophilic groups on their inside and hydrophilic groups on their outside which facilitates fat absorption. Bile salts stimulate pancreatic lipase and other esterases that hydrolyze retinyl esters in the enterocytes (intestinal mucosal cells). On hydrolysis, retinol is formed which is well absorbed (70–90%) by intestinal mucosal cells. In the mucosal cells, a specific cellular binding protein (CRBPII) carries the retinol to the enzyme lecithinretinol acyltransferase (LRAT) which esterifies retinol before incorporation into chylomicrons [15]. Retinol is esterified to retinyl palmitate which along with triglycerides and other fat soluble nutrients is packed into chylomicrons (chylo-the triglyceride rich absorptive lipoproteins that carry dietary fat into the body) for transport to the liver. Both retinol and carotene are absorbed from the small intestine dissolved in lipid and therefore very low fat intake or presence of diseases which interfere with absorption of lipids impair this absorption. In comparison to the preformed vitamin A, the provitamin A carotenoids as well as the non-provitamin carotenoids are absorbed unmodified by the intestinal mucosal cells. A certain proportion of these passes unchanged into the lymp and the blood. The remaining is metabolized by a specific enzyme 15, 15′-dioxygenase in the intestinal mucosal cell to form first retinal which is mostly reduced to retinol palmitate. At the stage, there is no difference between the retinol provided by diet as preformed vitamin A and as provitamin A carotenoids. Symmetrical cleavage of β-carotene molecules results in two molecules of retinal while some cleavage is asymmetrical and produces less retinal (Figure 15.4). The unchanged carotene which enters the circulation via chylomicrons is cleared by liver. Some of it is cleaved by carotene dioxygenase in liver or some other tissues giving rise to retinal and retinyl esters. As mentioned earlier, the bioactivity of â carotene and other provitamin A carotenoids is much lower than that of retinol. This is because the absorption of dietary carotene (which varies between 5% and 60%) and its conversion to retinol is not a very efficient process.

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15.4 Conversation of b-carotene into vitamin A via central and excentric cleavage [13]

The absorption of dietary carotene depends to a great extent on the nature of the food ingested, whether cooked or raw, the amount of fat in the meal and also the presence of intestinal parasites such as ascaris lumbricoides and giardia lamblia. Deficiencies of protein, zinc or presence of higher amounts of other carotenoids such as lutein in diet depress the dioxygenase activity. Further, asymmetric or excentric cleavage of β-carotene which also occurs, results in formation of certain apo-carotenals (derivatives of β-carotene) which are oxidized to retinoic acid but cannot be used as sources of retinol. (b) Metabolism of vitamin A in liver The chylomicrons carry retinol esters and carotenoids from the gut via lymph into the general circulation where they are broken to some extent to form chylomicron remnants. These remnants have most of the retinyl esters which are taken up by the liver’s parenchymal cells (hepatocytes) when they reach liver which is the major organ for vitamin A storage (>80%) in the body. There is evidence that extra-hepatic cells (in lung, intestine and kidney) take up some retinyl esters from the circulation, which are converted to retinoic acid and can be used for regulation of gene expression. In the parenchymal cells, retinyl esters are hydrolysed and much of the retinol is secreted from the cells after binding with retinol binding protein (RBP or RBP 4). (The vitamin A binding protein, referred to as RBP so far is now referred by investigators by its generic nomenclature, RBP4). Most of the retinol bound to the protein is transferred to specialized liver cells called stellate cells. These cells which comprise 7% of the liver cell numbers are mainly responsible for storage of vitamin A as retinyl esters

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mostly retinol palmitate. In case of healthy individuals this store is generally sufficient to last for several months. When liver stores are low, parenchymal cells are the major site of storage. Adipose tissue is also an important site for retinol as well as β-carotene storage (about 15–20% of the total store in case of rat [16]). The retinol present in adipose cells is taken up from chylomicron esters as in case of the liver. Further, there is secretion of free retinol from these cells which is not bound to RBP. (c) Vitamin A mobilization from liver and transport in the circulation Retinol is released from liver and is transported in the blood bound to the protein RBP4 [17]. RBP4 is a single polypeptide chain with a hydrophobic pocket within which the fat soluble retinol fits. It protects retinol against oxidation and delivers it to target tissues. RBP is mainly synthesized and secreted from liver and to a lesser extent by adipose tissue [18, 19]. The RBP – retinol complex also referred to as holo-RBP is released from liver bound to another blood protein, transthyretin (TTR) which increases its size as well as molecular weight. This is important to prevent the loss of retinol in glomerular filtrate in the kidney. RBP concentration in the plasma of well-nourished adults is 1.9–2.4 μmol / l (40–50 μg/ml) [20]. In children the value is 60% of that of adults. Certain condition such as protein-energy malnutrition, infections and parasitic infestations lower plasma RBP concentration. If retinol reserves in liver have been exhausted as is the case in vitamin A deficiency, the holo RBP cannot be formed resulting in the rise in liver apo-RBP (RBP unbound to retinol) content and fall in plasma concentration of RBP. This serves as the basis of relative-dose response test (RDR) of vitamin A status discussed in the section on assessment of vitamin A status. The specific membrane RBP receptors on target tissues take up retinol from the holo RBP complex and transfer it to an intracellular RBP. The apo-RBP (the free protein) is then released from the receptor some of which may be excreted by the kidney and the remaining is hydrolysed after reabsorption in the proximal renal tubules. Inside the cells there are many intracellular retinol binding proteins which protect retinol within the cell and direct them to specific enzymes. In the circulation, vitamin A is present in different forms. After a vitamin A rich meal a very high concentration of vitamin A can be present as retinyl esters in chylomicrons. However, in the fasting state most of the retinol present in the circulation is bound in retinol–RBP–TTR complex. In addition to this, low amounts of retinyl esters bound to either very low density lipoproteins (VLDL) or low density lipoproteins (LDL), low amounts of retinoic acid bound to albumin as well as water soluble complexes of retinol and retinoic acid are present. Provitamin A

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carotenoids may also be present in the circulation mainly bound to LDL. There are no specific carrier proteins for carotenoids. Provitamin A carotenoids such as β-carotene, α-carotene and cryptoxanthin and nonprovitamin A carotenoids such as lycopene, lutein and zeaxanthin are the common carotenoids in plasma (Figure 15.5). Their concentrations in plasma depend largely on diet. Some cells can take up retinol palmitate from circulating chylomicrons via lipoprotein receptors and some retinol may enter cells by diffusion. However, cellular uptake of retinol is mainly via membrane RBP receptors. Circulating carotenoids bound to LDLs enter cells having the LDL receptors. Even though, a very small proportion of vitamin A is present in the fasting circulation of well nourished adults as all-trans and 13-cis-retinoic acid bound to albumin

15.5 Carotenoids commonly present in human plasma

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(0.1–0.4% of retinol-RBP), it contributes significantly to tissue pools of retinoic acid[21]. These acid derivatives of vitamin A bind to various nuclear receptors in cells and are responsible for increase or decrease in the level of expression of several genes.

15.5

Functions of vitamin A and carotenoids

Vitamin A activity is very important for maintaining human health. The most well-known function of vitamin A is in vision. Historically the requirement of vitamin A for normal functioning of the visual processes was known long before the vitamin was actually discovered. However, the knowledge of functions of vitamin A has advanced dramatically in the recent years. The discovery of nuclear retinoid receptors that regulates gene expression has been a major breakthrough. The active form of vitamin A in vision is 11-cis-retinaldehyde. The acid derivatives all-trans-retinoic acid and 9-cis-retinoic acid are active in the regulation of growth, development and tissue differentiation. β-carotene and certain other carotenoids have an important role as antioxidants. The varied functions of vitamin A and its derivatives as well as of carotenes are discussed in this section. (a)Vitamin A in vision In the retina of human eye there are two types of photo (light) receptor cells – rods and cones. The rods are responsible for vision in long intensity light or dim light whereas cones respond to light of higher intensities or bright light and are also involved in colour vision. The active form of vitamin A in vision is 11-cis-retinaldehyde. In retina it is reversibly associated with the light-sensitive opsin proteins, forming rhodopsin in rods and iodopsin in cones. The number of rods in the human eyes is far more (>30 times) than the number of cones. When light strikes the retina, a number of complex biochemical changes take place, resulting in the generation of a nerve impulse. This process is referred to as phototransduction whereby the energy of photons (light energy) is converted in photoreceptor cells into a nerve signal for transmission of the message onwards towards the brain for interpretation. The retina of mammalian eye has ten layers and the photoreceptors form the outermost of these. Light has to pass through all other nine layers before phototransduction can begin. In the retinal pigment epithelium, all-trans retinol is isomerized to 11cis retinol which is then oxidized to 11-cis retinal. This is transported to the photoreceptor rod or cone cells where it reacts with protein opsin to form light sensitive rhodopsin or iodopsin respectively. When exposed to

Vitamin A metabolism

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light, 11-cis retinal is isomerized back to all-trans retinal. This conformational change results in release of retinal from the protein and generates a nerve impulse. This process is known as bleaching as it results in the loss of colour of rhodopsin. The released all-trans retinal is then reduced to all – trans-retinol and joins the pool of retinol in the pigment epithelium to complete the cycle. The all-trans retinol is then isomerized to 11-cis-retinol for regeneration of rhodopsin. The availability of the isomer 11-cis retinal of vitamin A is important for initiation of the visual cycle (Figure 15.6). In vitamin A deficiency the ability to see in dim light and the time taken to adapt to darkness are impaired. Failure to see in dim light, known as night blindness, is one of the earliest symptoms of vitamin A deficiency. Besides retinol, retinoic acid also has a role in the maintenance of a healthy eye. The pathological changes in the surface of the eye such as xerosis or Bitot’s spots are early signs of vitamin A deficiency which can be reversed by vitamin A. Vitamin A, mainly as retinoic acid, is required to maintain the surface epithelium of the eye.

15.6 The Visual Cycle

(b) Regulation of gene expression Most functions of vitamin A in the body with the exception of the visual process are under genetic control and are mediated by its acid derivatives. Control of cellular growth and differentiation is a major function of vitamin A which is regulated by all-trans retinoic acid and 9-cis-retinoic acid. These active retinoic acid isomers bind to nuclear receptors that bind to response

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elements on specific genes (nucleotide sequences in the DNA) to increase or decrease the level of expression of the gene. Many of these genes are involved in growth and differentiation, such as those involved in differentiation of the three germ layers, organogenesis and limbs development during embryogenesis. Therefore, both deficiency or excess of the vitamin during early fetal life can cause malformations in various systems of the body. There are two families of nuclear retinoid receptors: the retinoic acid receptors (RAR) bind all-trans retinoic acid or 9-cis-retinoic acid and the retinoid X receptors (RXR) bind 9-cis-retinoic acid. Each family of receptors has three major subtypes: α, β, and γ. Most, if not all, cells express at least one of these six receptors. There are several hundred genes in different tissues which have been shown to be sensitive to control by retinoids. The retinoid receptors are recognized as part of hormone receptor super family called the Steroid–Thyroid–Retinoid Superfamily with a number of receptors such as vitamin D receptor, thyroid hormone, estrogen receptor progesterone receptor and many more. To recognize response elements, these nuclear receptors must act in pairs (dimers) and a member of RXR family must be present as one of the partners for the dimer to be functional. Thus, retinoids act as regulators of several hormone response systems. (c) Cellular differentiation Vitamin A is required for maintenance of healthy epithelial tissue. Cellular differentiation is a process whereby mature epithelium is formed. Vitamin A is required to prevent the synthesis of high molecular weight forms of keratin and to promote the synthesis of glycoproteins which is an important component of the mucous secreted by many epithelial tissues. Vitamin A mainly as retinoic acid regulates cellular differentiation. In deficiency of vitamin A keratin producing cells replace mucous secreting cells in several epithelial tissues. The results in drying of the cells due to impaired mucous secretion, and the excess keratin synthesis makes the epithelial surface horny and keratinized. The same process is responsible for xerosis and keratinization of conjunctiva and cornea of the eye. (d) Immune response Once known as the “anti-infective vitamin”, vitamin A is now recognized as an important determinant of immune status. It is required for maintenance of the skin and mucosal cells which act as barrier against infection. In vitamin A deficiency, epithelial tissues loose their specialized function of

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mucous production and invasion by bacteria becomes easier. Besides this, vitamin A is involved in the development of white blood cells which play an important role in immune response. Further, vitamin A functions in Tcell mediated responses and may be involved in immunoglobulin production. Lack of vitamin A decreases resistance to infection and can increase the severity of infection as in case of measles, a common childhood infection, which becomes more serious in vitamin A deficient children. There is evidence to suggest that an oxidized retinol metabolite 14-hydroxy4, 14-retroretinol is the active molecule in the immune system but its mechanism of action is not well defined [22]. (e) Growth Vitamin A is involved in the growth of the musculo-skeletal system by modulating the growth of bones through remodeling. It has been demonstrated that both vitamin A and retinoic acid produce rapid release of cyclic AMP (adenosine monophosphate) and human growth hormone secretion [23]. A correlation between fasting plasma retinol and nocturnal growth hormone has been observed. The secretion of nocturnal growth hormone has been observed to increase after vitamin A supplementation among a group of short prepubertal children with low level of the hormone. These observations point towards the possible mechanism of the influence of vitamin A on growth. However, studies on the effect of vitamin A supplementation on early child growth in communities with widespread vitamin A deficiency have been inconsequential. The probable explanation of the negative results or lack of evidence of vitamin A supplement on growth in most studies is that growth is dependent on many nutrients, and providing only one of those may not be enough to demonstrate significant effect on growth. (f) Hemopoiesis The observations on humans and in experimental animals have repeatedly shown that iron deficiency anemia responds more completely if vitamin A is included along with iron therapy. Vitamin A deficiency might interfere with the absorption, transport or storage of iron. However, the role of vitamin A in hemopoiesis is not completely understood. There is evidence that retinoic acid is involved in the production of RBCs which are derived from stem cells after proper differentiation. This implies that vitamin A possibly controls the utilization of iron. Further, vitamin A appears to facilitate mobilization of iron stores to develop red blood cells. Studies have consistently shown that vitamin A deficiency restricts the release of iron from the

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stores which results in iron overload and, in the absence of increased absorption of iron in anemia. This can occur even in the absence of any infection. Research evidence also suggests that infection and inflammation depress iron absorption and mobilization, therefore, vitamin A supplementation improves hematological response due to reduced level of infection or improvement in health. The significance of improving vitamin A status in anemia control programme is evident. (g) Reproduction Retinol, as well as retinoic acid, is needed for successful reproduction but the precise mechanism of action is not known with certainty. Studies in animals show the requirement of vitamin A for normal spermatogenesis in male and in the prevention of placental necrosis and fetal resorption in the female. In addition, the deposition of substantial amount of β-carotene in corpus luteum also points towards its role in reproduction. There is increasing evidence that vitamin A is required for every stage in the reproductive process in the female. In experimental animals, vitamin A deficiency as well as excess has been known to induce congenital malformations. In humans it has not been demonstrated conclusively that vitamin A deficiency causes congenital malformations. However, high incidence of fetal anamolies and poor reproductive outcomes have been reported among women ingesting therapeutic doses during early stages of gestation. In communities where vitamin A deficiency is widely prevalent, there is a consensus that, vitamin A supplementation throughout pregnancy should not exceed 10,000 IU per day. (h) Carotenoids as antioxidants Historically, the biological activity of a carotene has been considered synonymous with its corresponding vitamin A activity. Of the several provitamin A carotenoids, β-carotene is described as the most active because of its higher provitamin A activity. However, research in the recent years has identified many other activities of carotenoids, of which their role as antioxidants has received special attention. Under conditions of low oxygen availability, carotenes act as antioxidants by trapping singlet-state oxygen. The excessive amount of these reactive oxygen species in vivo can cause oxidative damage of lipids, proteins and DNA. It is accepted that imbalance between oxidative DNA damage and repair contribute to the risk of cancer development. Epidemiological evidence suggests an association between intake of diets rich in βcarotene and vitamin A and a lower risk of many types of cancers [24].

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However, intervention trials with β-carotene supplements have not demonstrated its cancer prevention activity. On the contrary, increased incidence of lung cancer was observed among subjects receiving supplements [25, 26]. Thus, supplementation with large doses of specific nutrients is not advisable as it could disturb the finely balanced in vivo antioxidant system which possibly requires an optimal range of various antioxidants to ensure a balanced antioxidant status. A higher intake of fruits and vegetables provides a variety of antioxidants and other beneficial substances [27]. The non-provitamin A carotenoids viz. zeaxanthin, mesozeaxanthin and lutein are concentrated in the macula lutea in the centre of retina and are responsible for its yellow colour. The concentration of this pigment in the eyes of patients of age related macular degeneration disease is lower than those without disease [28]. This degenerative disease is responsible for loss of vision in the elderly. In the macula, lutien and zeaxanthin filter out the short wavelength blue light thereby limiting damage to the retina. Further, they have antioxidant potential and can quench reactive oxygen species generated in retina. These properties of the carotenoids form basis for their possible role in reducing the risk of macular degeneration. Dark green leafy vegetables are the richest source of dietary lutein and zeaxanthin. These carotenoids are also present in egg yolk. However, relation between the disease and dietary intake of the two macular pigments – lutein and zeaxanthin has not been clearly demonstrated. Research has shown that lutein and zeaxanthin supplementation could improve visual performance in healthy people, particularly in situations of low light intensity. The preliminary findings indicate that macular pigment is important not only in reducing risk of age-related macular degeneration but could also improve the vision of healthy people. Another non-provitamin A carotenoid, lycopene, the dominating red p i g m e n t i n t o m a t o e s , i s a l s o a n a n t i o x i d a n t l i k e β- c a r o t e n e . Epidemiological evidence suggests that tomato products and lycopene consumption reduce the risk of prostrate cancer [29]. Clinical human trials with short term tomato product or lycopene feeding have indicated reduction in the levels of oxidative damage in prostrate cancer patients as well as in smokers. However, evidence from experimental models suggests that tomato powder, but not lycopene, significantly inhibited cancer growth. This suggests that lycopene is not the only anticancer factor in tomatoes. Further research is needed to clearly understand the protective role of various components within tomatoes in reducing the risk of prostrate cancer.

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Box 15.2 Lycopene–the red pigment in tomatoes Lycopene comprises 60–64% of the total carotenoids found in raw or ripe tomatoes. Other important carotenoids are phytoene, phytofluene, neurosporene and γ carotene. β-carotene constitutes only 1–2% of the total carotenoids. Lycopene is also found in pink grape fruit, guava, papaya and water melon. All-trans lycopene is the predominant isomer present in plants, but in human tissues cis-isomers are mostly found. On heating and processing tomato products, the cis-isomers of lycopene increase thereby increasing its bioavailability. Besides lycopene, polyphenols especially quercetin and kaempferol which are also potentially beneficial anti-cancer compounds, are present in tomato products, mainly in the skin and seeds.

15.6

Recommended Dietary Allowances (RDA)

Requirements of vitamin A like those of other nutrients vary with age and physiological states such as pregnancy and lactation. The RDA are meant to prevent deficiency and to provide safe intake for majority of the population (97–98%). RDAs for vitamin A are expressed in terms of retinol equivalents (RE) per day which account for different biological activities of retinol and provitamin carotenoids. The estimates of requirements are based on the minimum level of vitamin A required to reverse completely dark adaptation failure and abnormal retinogram and to maintain adequate stores. The vitamin A intake for Indians recommended in 1989 and as proposed recently by the Expert Committee is presented in Table 15.1 along with recommended vitamin A intakes from different countries and sources. The vitamin A intake of 600 RE/day or 9.3 RE/kg for Indian adult was recommended by Indian Council of Medical Research (ICMR) (1989) [30]. Requirements for the other age groups have been established by the factorial method and body weight. The recommendations on retinol requirements for all age groups, except pregnant women, have been retained by the ICMR Expert Group (2008) constituted to revise RDAs of nutrients for Indians. The requirement during pregnancy was established on the basis of studies on vitamin A supplementation required to prevent the fall of plasma vitamin A during last few weeks of pregnancy and which also associated with improved feto-placental function. The Expert Committee proposed a requirement of 800 RE/day on this basis. The additional needs during lactation have been estimated on the basis of vitamin A secreted in breast milk of well nourished mothers. An additional intake of 350 RE/day during lactation has been recommended which is in line with the intake allowance of 50 μg/kg for infants. The vitamin A requirements of children have been derived from the requirement figures for infants (50 μg/kg) and adults (9.3 μg/kg) considering the growth rates at different ages.

850

Lactation

800 800

1000

500 700

375 400

NRC [32]

Lactation 1300 first half yr. second half yr. 1200

4–6 7–10 Male 11–51 + Female 11–51 + Pregnancy

0–1 1–3

Age group (years)

950

600 700

Female 11—51 Pregnancy Lactation

600 700

500 500

350 400

UK [33]

4–6 7–10 Male 11–14 15–50 +

0–1 1–3

Age group (years)

Lactation

Adult man 18 + Adult woman 18+ Pregnancy

0–6 months 6–12 months 1–6 7–9 10–18

Age group (years)

850

800

500

600

400/450 500 600

375 400

WHO [34]

–

Lactation

7–9 10–18 Adult man 18+ Adult woman 18 + Pregnancy

0–1 1–6

Age group (years)

–

950

800

600

600 600 600

350 400

ICMR expert group* [30]

* Proposed 2008–2009. The Expert Committee recommended that a minimum of 50% RE be drawn from animal sources to ensure adequacy among vulnerable groups like pregnant and lactating women.

500 600

400 500 600

6–10 10–12 12–15

600

350 400

0–1 1–6

Male 15–18+ Female 15–18 + Pregnancy

FAO/WHO [31]

Age group (years)

T=blA 15.1 Recommended dietary intakes of vitamin A (µg RE/day)

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The ICMR Expert Committee (2008) has proposed a revision in the conversion factor of dietary β-carotene to retinol based on many controversial evidences in this regard. For β-carotene, a conversion ratio of 1:8 has been proposed by the committee on the basis of evidence from developing countries on bioequivalence of β-carotene and retinol as well as best association and compatibility of subclinical and dietary deficiency in different regions of the world. The earlier ratio of 1:4 was considered to be too high by the Committee and the ratio of 1:12 proposed by IOM (US) too low to correlate with deficiency reported in different regions. Thus, the proposed intake of β-carotene is on the basis of 1 μg of β-carotene = 0.125 μg of retinol. No separate RDA has been proposed for β-carotene or other provitamin A carotenoids. According to IOM [10], daily consumption of 3–6 μg of βcarotene would maintain blood levels of β-carotene in the range which is associated with a low risk of chronic diseases. It is therefore advised to consume five or more servings of fruits and vegetables in the daily diet with some green leafy vegetables and deep yellow or orange vegetables and fruits to obtain sufficient amount of β-carotene and other carotenoids.

15.7

Assessment of vitamin A status

Nutritional status concerns some aspect of the state of the body as influenced by the intake and utilization of nutrients. An array of methods have been developed over the years for assessment of vitamin A status which are appropriate for detecting varying degrees of vitamin A deficiency. Measurement of reserves of vitamin A by liver biopsy is the only direct method of assessment of vitamin A status. However, this method is invasive and cannot be considered appropriate for routine assessment. There are several indicators which are used for assessment of vitamin A status at clinical and subclinical level of vitamin A deficiency [35]. An overview of these indicators is included in this section. Vitamin A deficiency reflects the state of inadequate vitamin A nutriture which begins when liver stores of vitamin A fall below 20 μg/g (0.07 μmol/g). Historically, the recognition of eye lesions attributable to severe form of vitamin A deficiency formed the basis of xerophthalmia classification by ocular signs in 1976 by the first WHO Expert Group on assessment of vitamin A status (Table 15.2). The term xerophthalmia includes all signs and symptoms affecting the eye that can be attributed to vitamin A deficiency. The second WHO Expert Group (1982) on the control of vitamin A deficiency and xerophthalmia revised the classification and established the criteria for assessing the public health significance of xerophthalmia and vitamin A deficiency based on the prevalence among children less than 6 years old in the community

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Table 15.2 Xerophthalmia classification by ocular signs [36, 37] XN XI A XI B X2 X3 A X3B XS XF

Night blindness Conjunctival xerosis Bitot’s spots Corneal xerosis Corneal ulceration / keratomalacia (involving less than one third of the corneal area Corneal ulceration / keratomalacia (involving one third or more of the corneal area Corneal scar (from X 3) Xerophthalmic Fundus

(Table 15.3). In population surveys the purpose is to determine the magnitude and severity of vitamin A deficiency in the population. Thus, clinical signs of Vitamin A deficiency, viz Bitot’s spots, corneal xerosis, keratomalacia /corneal ulceration which reflect the progressive changes due to keratinization of conjunctiva and cornea can be used for identification of those deficient in vitamin A. Table 15.3 Prevalence criteria indicating vitamin A deficiency of public health significance in a population [37, 38]. Criteria Clinical (primary) Children 2–5 years old Night blindness (X N) Bitot’s Spots (XIB) Corneal Xerosis (X2) and Corneal Ulcers (X3) Corneal Scars (XS) Women of child bearing age XN during recent pregnancy Biochemical (Supportive) serum retinol <0.70 µmol/L(20 µg/dL)

Minimum prevalence %)

>1.0 > 0.5 > 0.01 > 0.05 > 5.0 >15.0

The changes in the eye as a result of xerosis due to vitamin A deficiency which lead to development of conjunctival xerosis and Bitot’s spots are preceded by changes of lesser degree which can be detected by the conjunctival impression cytology (CIC) technique. The technique involves microscopic examination of the impressions of conjunctival cells taken on cellulose acetate strips. The normal cells when stained show sheets of small regular epithelial cells and numerous mucin secreting goblet cells. In vitamin A deficiency, epithelial cells become enlarged, separated and reduced in number. There is marked decline in goblet cells or they may be totally absent [39]. Though it is simple, relatively less invasive and inexpensive technique, the difficulty in standardization of the interpretation of conjunctival impressions has presented its wide adoption for vitamin A

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status assessment. Further, the results of CIC do not correspond very well with the results of biochemical tests of vitamin A status [40, 41]. Another limitation of CIC is that it is unsuitable for younger children (<3 years) and is unreliable in the presence of eye infections such as acute conjunctivitis and trachoma [42]. As mentioned earlier, the vision in dim light which is dependent on the availability of vitamin A to the rod cells of the retina is impaired in early deficiency. There are methods to test rod function which can be used to assess vitamin A status but they require extremely cooperative subject and are unsuitable for young children who are most at risk of the deficiency. Thus, in deficient populations a brief questionnaire on using child’s inability to see adequately in poor illumination such as at dusk using locally appropriate term(s) for night blindness is a simple method to know about the vitamin A status of a community. A dark adaptometer may be used for investigation of night blindness in the children over 2 years and among pregnant women. However, conventional laboratory based testing of dark adaptation is time consuming as a fully light adapted eye takes at least 30 minutes to become completely dark adapted. In this process, the eye becomes more sensitive to low light levels, largely because of shift from photopic vision based on cones to scotopic vision based on rods [43]. Several rapid dark adaptation tests which take 2–3 minutes have been developed which require subjects to identify a letter or to sort discs of different colors [44– 47]. These are inherently less sensitive indicators of vitamin A deficiency as in all these rapid tests measurements carried out during the first few minutes of dark adaptation mainly rely on cones instead of rods in the retina. Night blindness during the latter part of pregnancy is common among vitamin A deficient population and correlates well with other biochemical and functional indicators of vitamin A deficiency [48]. In community surveys eliciting history of night blindness is simple and the response is reliable. A cut-off of ≥ 5 % prevalence of maternal night blindness has been suggested as indicative of community vitamin A deficiency problem [49]. Further, it has been recommended that night blindness history be elicited for a previous pregnancy that ended in a live birth in past 3 years using preferably the local term for night blindness. Pupillary dark adaptation is a completely different non-invasive technique the basis of which is that, the intensity of light needed to cause pupillary contraction indicates the subject’s threshold of light visible in the dark adapted state. The pupils do not respond or constrict normally in low illumination among those who are night blind. The test required minimum cooperation from the subjects and has been successfully used for young children and pregnant women [50, 51]. The dark adaptation scores based on pupillary response respond to vitamin A supplementation and a close association has been demonstrated with serum retinol and RDR

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[50–52]. The technique is useful in correctly identifying populations having normal or deficient Vitamin a status. However, the improvement in pupillary response among vitamin A deficient individual takes upto 4–6 weeks after dosing with vitamin A [43]. Thus, its use as an indicator for assessment of interventions designed to improve vitamin A status is constrained by this long waiting period. This technique requires preparation of an area that is sufficiently dark and approximately 20 minutes are needed per individual for testing. Despite these limitations, it has advantages of being non-invasive, acceptable to target populations and is able to detect subclinical vitamin A deficiency. Serum retinol levels are homeostatically regulated and do not drop until body stores are significantly compromised. Thus, serum retinol concentration reflects on individual’s vitamin A status especially when there are limited reserves of vitamin A in the body. Serum retinol level <20 μg/dl (0.7 μmol/L) are considered deficient although the average retinol levels in well nourished populations generally exceed 30 μg/dL (1.05 μmol/L) [53]. It is now known that factors such as presence of PEM as well as infection, inflammation or trauma result in lowering of serum retinol levels due to the acute phase response to such stressful situations. However, serum retinol is the most widely used indicator for population level assessment of vitamin A deficiency as it can be analyzed by many laboratories. For accurate estimation of serum retinol, high pressure liquid chromatography (HPLC) technique is preferred. Serum retinol-binding protein (RBP) is another biochemical indicator recommended for determining whether vitamin A deficiency is a public health problem. Serum RBP is easier to measure than serum retinol as RBP can be detected with an immunologic assay which is simpler and expensive compared to HPLC analysis of serum retinol, requires very small amount of serum (10–20 μL) which can be obtained from a finger prick and serum handling is simpler as it is more stable than retinol with respect to light and temperature. However, serum RBP is also lowered in the acute phase response, protein energy malnutrition and conditions such as liver diseases and chronic renal failure. Further, the immunologic assays cannot differentiate between RBP in serum which is complexed with retinol (holoRBP) and that which is not (apo-RBP). Though, serum RBP correlates well with serum retinol concentration, no universally applicable cut-offs have been suggested. Serum RBP can therefore only be used for those populations for which the relationship with serum retinol concentration has been determined in a sub sample. The indirect methods of assessment of liver stores such as Relative Dose Response (RDR), Modified Relative Dose Response (MRDR), Serum 30day response and deuterated retinol dilution technique are a true reflection of vitamin A status than serum retinol. As mentioned earlier, when retinol

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is in shot supply, apo-RBP accumulates in the liver. As retinol becomes available, holo-RBP is released into the circulation. The amount of retinol released from liver is proportional to the extent of depletion of liver. The relative dose-response tests are based on this phenomenon. In the isotope dilution technique, a dose of vitamin A labeled with stable isotope deuterium is given. A blood sample is taken after a period of three weeks which is the time allowed for equilibration with the body reserves. The extent of dilution of the labeled tracer reflects the amount of body reserves. When the deficiency sets in, liver vitamin A levels fall over a considerable period of time before the serum retinol levels fall and much before any functional or histological changes begin to occur. Thus, these tests are useful measures of vitamin A deficiency before any clinical lesions are evident. However, the logistics of employing these techniques for vitamin A status assessment limit their use as research tests. Breast milk retinol concentration provides information about the vitamin A status of lactating mothers as well as exclusively breast fed infants. Since vitamin A is mostly present in the fat globules of milk, the concentration of vitamin A in milk is expressed per gram of fat. The borderline of deficiency in a population is suggested to be ≤1.05 μmol/L or ≤8 μg/g milk fat. The average breast milk vitamin A concentrations range from 1.75 to 2.45 μmol/L in vitamin A sufficient populations whereas in vitamin A deficient populations the average population values are below 1.4 μmol/L [54, 55]. Analysis of retinol in casual samples of milk is difficult and is considered less reliable except under ideal laboratory conditions. However, it has been used successfully to evaluate the effect of interventions to improve the vitamin A status of lactating mothers [56]. The tentative ranking of some of these biological indicators was proposed by WHO (1996) [57] for usefulness in various activities (Table 15.4). It was recommended that biological indicators are essential for evaluating the vitamin A status of a population. They are the most specific and useful for determining risk assessment, targeting programmes and evaluating their effectiveness. Wherever, it is not feasible to obtain biological indicators, demographic or ecologic indicators may be used to define whether vitamin A deficiency is a problem of public health significance in a population. Some of the most relevant of these indirect risk indicators proposed by WHO are presented in Table 15.5. A public health problem exists when the prevalence in a population of atleast two of the biological indicators of vitamin A status is below the cut-off or when one biological indicator is supported by atleast four ecological indicators (two of which are nutrition and diet related). Though dietary intake of vitamin A does not directly indicate vitamin A status, it provides useful information on the utilization of available vitamin A rich sources in a population group. However, none of the ecological indicators are sufficient to determine if the problem of vitamin A deficiency exists in a population.

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Table 15.4 Relative ranking on a population base of some biological indicators useful for various surveillance purposes [57] Indicator

Risk assessment

Targeting programmes

Evaluating effectiveness

Night Blindness Breast milk retinol (lactating mothers and breast fed infants) Serum retinol RDR / MRDR CIC

+++ ++

+++ +++

+++ ++

++ +++ +

+ +++ –

++ +++ –

Table 15.5 Ecological indicators of areas/populations at risk of vitamin A deficiency – nutrition and diet related indicators [57] Indicator Breastfeeding pattern <6 months of age ≥6–18 months of age Nutritional status (< -2SD from WHO/NCHS reference for children <5 years of age) Stunting Wasting Low birth weight (<2500 g) Food availability Market Household Dietary patterns 6–71 months old children, pregnant /lactating women Semi-quantitative/qualitative food frequency

Suggested Prevalence < 50% receiving breast milk < 75% receiving vitamin A containing foods in addition to breast milk, 3 times/week

≥ 30% ≥ 10 % ≥ 15% DGLV* unavailable ≥6 months/year <75% households consume vitamin A – rich foods 3 times/week < 75% consume vitamin A rich foods at least 3 times/week Foods of high vitamin A content eaten <3 times/week by ≥75% vulnerable groups

* DGLV – Dark green leafy vegetable Table 15.6 Illness related indicators in children of 6–71 months Indicator Immunization coverage at 12–23 months of age Measles CFR Reported diarrhea disease rate (2 week period prevalence) Reported fever rates (2 week period prevalence) Helminthic infection rates, particularly ascaris

Suggested prevalence <50% fully immunized or <50% immunized for measles ≥1% ≥20% ≥20% ≥50%

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The suggested prevalence are arbitrary, and are suggested only to assist in the relative ranking of population vulnerability. The Global Vitamin A Initiative report had suggested under-five mortality rate (U5MR) as a surrogate indicator to know whether the problem of vitamin A deficiency is likely in a population and full-scale assessment is necessary [58]. Based on the existing data it was proposed that a country with U5MR >50 is very likely to have vitamin A deficiency as a public health problem that requires immediate action [59]. Countries with U5MR between 20 and 50 may have a problem until surveys prove otherwise. Though the ecological indicators are useful in suggesting the likelihood of vitamin A deficiency as a public health problem for formal assessment of vitamin A status of the population, biological indicators must be used as they directly reflect vitamin A status.

References 1. 2. 3. 4. 5. 6.

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MCCOLLUM EV AND DAVIS M (1913). The necessity of certain lipins in the diet during growth. J Biol Chem 15, p. 167. MCCOLLUM EV AND DAVIS M (1915). The essential factors in the diet during growth. J Biol Chem 23, p. 231. OSBORNE TB AND MENDEL LB (1919). The vitamins in green foods. J Biol Chem 37, p. 187. STEENBOCK H (1919). White corn vs. yellow corn and probable relationship between the fat soluble vitamin and yellow plant pigments. Science 50, p. 352. MOORE T (1930). Vitamin A and carotene. VI. The conversion of â carotene to vitamin A, in vivo. Biochem J 24, p. 692. KARRER P , HELFENSTEIN A , WEHRLI H AND WETTSTEIN A (1930). Pflanzenfarbstoffe. XXV. uber die konstitution des lycopins and carotins. Helv Chim Aeta 13, p. 1084. KARRER P , MORF R AND SCHOPP K (1931). Zur kenntnis des vitamin A aus Fischtranen II. Helv Chim Aeta 14, p. 1431. FAO / WHO EXPERT CONSULTATION (1988). Requirements of vitamin A, iron, folate and vitamin B12. Food and Nutrition Series No. 23, FAO, Rome. FAO / WHO (1967). Requirements of vitamin A. thiamine, riboflavin and niacin. WHO Tech. Rep. Ser. No. 362. US INSTITUTE OF MEDICINE (2001). Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium and zinc. US Institute of Medicine, Food and Nutrition Board, Standing Committee on the Scientific Evaluation of Dietary Intakes. Washington: National Academic Press. BOILEAU TWM , MOORE AC , ERDMAN JW JR (1999). Carotenoids and vitamin A. In: Papas AM (ed). Antioxidant Status, Diet, Nutrition and Health. Boca Raton: CRC Press, pp. 133–158. BLOMHOFF R, GREEN MH , GREEN JB , BERG T , NORUM KR (1991). Vitamin A metabolism: new perspectives on absorption, transport and storage.

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(1994). Introduction: Overview of vitamin A metabolism and function. In : BLOMHOFF R (ed). Vitamin A in Health and Disease. New York: Marcel Dekker, pp. 1–35. GREEN MH and GREEN JB (2005). Contributions of mathematical modeling to understanding whole-body vitamin A metabolism and to the assessment of vitamin A status. Sight and Life Newsletter, 2, pp. 4–10. WONGSIRIROJ N and BLANER WS (2007). Recent advances in vitamin A absorption and transport. Sight and Life Magazine 3, pp. 32–37. WEIS S, LAI K , PATEL S et al (1997). Retinyl ester hydrolysis and retinol efflux from BFC – I B adipocytes. J Biol Chem 272, pp. 1459–1465. KANAI M , RAZ A , GOODMAN DS (1968). Retinol-binding protein: The transport protein for vitamin A in human plasma. J Clin Invest 47, pp. 2025–2044. BLANER WS , HENDRIKS HF , BROUWER A et al (1985). Retinoids, retinoid-binding proteins and retinyl palmitate hydrolase distributions in different types of rat liver cells. J Lipid Res 26, pp. 1241–1251. SOPARNO DR , BLANER WS (1994). Retinol-binding protein. In: SPORN MB , ROBERT AB , GOODMAN DS (eds). The Retinoids: Biology, Chemistry, and Medicine. 2nd edition. New York: Raven Press. SIVAPRASADARAO A , FINDLAY JBC (1994). The retinol-binding protein superfamily. In: BLOMHOFF R (ed). Vitamin A in Health and Disease. New York: Marcel Dekker, pp. 87–117. BLANER WS and OLSON JA (1994). Retinol and retinoic acid metabolism. In: Sporn MB, Robert AB, Goodman DS (eds). The Retinoids: Biology, Chemistry and Medicine. 2nd edition. New York: Raven Press. BUCK J , RITTER G , DANNECKER L et al (1991). Intracellular signaling by 14-hydroxy – 4, 14 – retroretinol. Science 254, pp. 1654–1655. DJAKOURE C , GUIBOURDEUCHE J , PORQUET D et al (1996). Vitamin A and retinoic acid stimulate within minutes cAMP release and growth hormone secretion in human pituitary cells. J Clin Endo Metab 81, pp. 3123–3126. FONTHAM ETH (1990). Protective dietary factors and lung cancer. Int J Epidemiol 19, pp. S32–S42. The Alpha – Tocopherol, Beta-carotene Cancer Prevention Study Group (1994). The effect of Vitamin E and â Carotene on the incidence of lung cancer and other cancers in male smokers. N Eng J Med 330, pp. 1029–1035. OMENN GS , GOODMAN GE , THORNQUIST MD et al (1996). Risk factors for lung cancer and for intervention effects in CARET, the â Carotene and Retinol Efficacy Trial. J Natl Cancer Inst 88, pp. 1550–1559. ORFANOS CE , BRAUN - FALCO O , FARBER EM et al (eds) (1981). Retinoids: Advances in Basic Research and Therapy. Berlin: Springer-Verlag. SCHALCH W (2004). Lutein and Zeaxanthin supplementation improves visual performance: Report on a recent DSM R&D Colloquium. Sight and Life Newsletter 3, pp. 4–7. FORD NA AND ERDMAN JR JW (2006). Lycopene intake and prostrate cancer risk. Sight and Life Newsletter 1, pp. 4–9. INDIAN COUNCIL OF MEDICAL RESEARCH (1989). Nutrient Requirements and Recommended Dietary Allowances for Indians. Report of Expert Group, 1989. Proposed 2008/2009. FAO / WHO EXPERT CONSULTATION (1988). Requirements of Vitamin A, iron, folate and vitamin B12. Food and Nutrition Series No. 23, FAO, Rome. BLOMHOFF R

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32. National Research Council, Recommended Dietary Allowances (1989). 10th Edition. Washington DC: National Academy Press. 33. Panel on Dietary Reference Values (1991). Dietary reference values for food energy and nutrients for the United Kingdom. HMSO, London. 34. WHO/ FAO (2004). Vitamin and mineral requirements in human nutrition. 2nd Edition, WHO, Geneva. 35. MACLAREN DS AND FRIGG M (2001). Sight and Life Manual on Vitamin A deficiency Disorders (VADD). Assessment of Vitamin A status. 2nd edition. Chapter 4, pp. 37–50. 36. WHO/USAID (1976). Vitamin A deficiency and xerophthalmia: report of joint WHO/ USAID meeting. WHO Technical Report Series 590: World Health Organization, Geneva, Switzerland. 37. WHO/ UNICEF/USAID/HELEN KELLER INTERNATIONAL/IVACG (1982). Control of vitamin A deficiency and xerophthalmia: report of joint WHO/UNICEF/USAID/Helen Keller International/IVACG meeting. WHO Technical Report Series 672: World Health Organization, Geneva, Switzerland. 38. SOMMER A AND DAVIDSON FR (2002). Assessment and control of vitamin A deficiency: The Annecy Accords. J Nutr 132, pp. 2845S–2850S. 39. WITTPENN JR, TSENG SCG, SOMMER A (1986). Detection of early xerophthialmia by impression cytology. Arch Ophthal 104, pp. 237–239. 40. TANUMIHARDJO SA, PERMAESIH D, DAHRO AM et al (1994). Comparison of vitamin A status assessment techniques in children from two Indonesian villages. Am J Clin Nutr 60, pp. 136–141. 41. MAKDANI D, SOWELL AL , NELSON JD et al (1996). Comparison of methods of assessing vitamin A status in children. J Am Coll Nutr 15, pp. 439–449. 42. LIETMAN TM, DHITAL SP, DEAN D (1998). Conjunctival impression cytology for vitamin A deficiency in the presence of infectious trachoma. Br J Ophthalmol 82, pp. 1139–1142. 43. CONGDON NG AND WEST KP Jr (2002). Physiologic indicators of vitamin A status. J Nutr 132, pp. 2889S–2894S. 44. VILLARD L AND BATES CJ (1986). Dark adaptation in pregnant and lactating Gambain women: feasibility of measurement and relation with vitamin A status. Hum Nutr Clin Nutr 40C, pp. 349–357. 45. THORNTON SP (1977). A rapid test for dark adaptation. Ann Ophthalmol 9, pp. 731–734. 46. FAVARO RM, DE SOUZA NV, VANNUCCHI H, DESAI ID and DE OLIVEIRA JED (1986). Evaluation of rose bengal staining test and rapid dark-adaptation test for the field assessment of vitamin A status of preschool children in Southern Brazil. Am J Clin Nutr 43, pp. 940–945. 47. SOLOMONS NW, RUSSELL RM, VINTON E, GUERRERO AM and MEJIA L (1982). Application of a rapid dark adaptation test in children. J Pediatr Gastroenterol Nutr 1, pp. 571–574. 48. CHRISTIAN P, WEST KP JR, KHATRY SK, KATZ J, SHRESTHA SR, PRADHAN EK, LE CLERQ SC and POKHRAL RP (1998). Night blindness of pregnancy in rural Nepal: nutritional and health risks. Int J Epidemiol 27, pp. 231–237. 49. CHRISTIAN P (2002). Recommendations for indicators: Night blindness during pregnancy – A simple tool to assess vitamin A deficiency in a population. J Nutr 132, pp. 2884S–2888S.

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CONGDON N , SOMMER A , SEVERNS M , HUMPHREY J , FRIEDMAN D , CLEMENT L , WU LS AND NATADISASTRA G (1995). Pupillary and visual thresholds in young children as an index of vitamin A status. Am J Clin Nutr 61, pp. 1076–1082. CONGDON N , DREYFUSS M , CHRISTIAN P, NAVITSKY R , SANCHEZ A , WEST KP JR and THAPA M (2000). Dark adaptation thresholds as an indicator of vitamin A status among pregnant and lactating women in Nepal. Am J Clin Nutr 72, pp. 1004–1009. S A N C H E Z A , C O N G D O N N , S O M M E R A , R A H M AT H U L L A H L , VENKATA S WAMY PG , CHANDRAVATHI PS and CLEMENT L (1997). Pupillary threshold as an index of population vitamin A status among children in India. Am J Clin Nutr 65, pp. 61–66. DE PEE S and DARY O (2002). Biochemical indicators of vitamin A deficiency: Serum retinol and serum retinol binding protein. J Nutr 132, pp. 2895S–2901S. World Health Organization (1985). The quantity and quality of breast milk. Geneva. NEWMAN V (1992). Vitamin A and breastfeeding: a comparison of data from developed and developing countries. Wellstrart International, San Diego, CA. RICE AL , STOLTZFUS RJ , DE FRANCISCO A et al (2000). Evaluation of serum retinol, the modified relative–dose response ratio and breastmilk vitamin A as indicators of response to postpartum maternal vitamin A supplementation. Am J Clin Nutr 71, pp. 799–806. WHO (1996). Indicators for assessing vitamin A deficiency and their application in monitoring and evaluating intervention programmes. WHO, Geneva. Vitamin A Global Initiative (1998). A strategy for acceleration of progress in combating vitamin A deficiency: consensus of an informal technical consultation, 18–19 December 1997. UNICEF, New York. SCHULTINK W (2002). Use of under-five mortality rate as an indictor for vitamin A deficiency in a population. J Nutr 132, pp. 2881S–2883S.

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Vitamin A deficiency: prevention and control Sheila C. Vir

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

16.1

Vitamin A – an essential micronutrient

Vitamin A is essential for regulating a number of key biological processes in the body and contributes to the normal functioning of the visual system, growth and development, maintenance of epithelial cellular integrity, immune function, and reproduction [1]. Vitamin A is known to be involved in maintaining immuno-competence by helping to maintain the lymphocyte pool and playing a role in T-cell-mediated responses [2, 3]. Neither humans nor animals can synthesize or survive without vitamin A. It is therefore vital that the micronutrient vitamin A is provided in the diet in sufficient amounts to meet all the physiological needs. Key functions of vitamin A are summarized in Table 16.1. Table 16.1 Functions of vitamin A [4] Vision Cellular differentiation and morphogenesis Immune response Haemopoiesis Growth Fertility

16.2

Photopic and colour, scotopic Gene, transcription Non-specific, cell-mediated Iron metabolism Skeletal Male and female

Consequences of vitamin A deficiency

Dietary vitamin A is consumed from animal sources or fortified food items as preformed retinyl esters or from plant sources as provitamin A carotenoids. Vitamin A and its precursor carotenoids are fat-soluble compounds.

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Approximately, 5–10 g of fat in a meal is sufficient to ensure absorption of vitamin A and its precursor [5, 6]. Vitamin A (retinol) being fat soluble is stored in body organs when intake is in excess of physiological need – 90% of stored vitamin A is in liver [1]. From liver, vitamin A is released into circulation in association with retinol binding protein (RBP) and transthyretin, a protein complex that transfers vitamin A to tissues sites and becomes available for use by cells throughout the body, including those of the eye. Liver stores form an important buffer against variations in the intake of vitamin A and its precursors. When intake surpasses physiological requirements, the excess vitamin A is stored and liver reserves increase. On the other hand, when dietary vitamin A intake is less compared to body requirements, liver stores are drained to maintain serum retinol at the normal level of above 0.7 μmol/l [6, 7]. Because of prolonged periods of low intake of vitamin A, and its usage by tissues or breastfeed, liver stores get depleted of the vitamin. With such depletion, the vitamin is actively recycled through the liver and among specific tissues and results in partially adapting to the diminishing availability. This adaptation and recycling mechanism maintain relatively constant blood levels until body stores become depleted below a critical point. The level of depletion at which physiological functions begin to be impaired is not entirely clear [1]. The time required for vitamin A deficiency to precipitate depends on the amount of vitamin A (or precursor) ingested, the extent of pre-existing liver stores, and the rate at which vitamin A is being utilized by the body. A child who routinely consumes marginal or poor intake of vitamin A will have very limited stores. In such children, any further reduction in intake of vitamin A, either as a result of a change in diet or because of impaired absorption (as in gastroenteritis), or a sudden increase in metabolic demand (febrile state notably measles or growth spurt) will cause rapid use of limited reserves of vitamin A resulting in depletion of the vitamin. Additionally, reduced synthesis of retinol binding proteins (RBP) in protein-deficient or severely malnourished children impairs vitamin A utilization of the available stored vitamin A, even when liver stores are high [7]. In vitamin A deficiency, keratin-producing cells replace mucus-secreting cells in many epithelial tissues of the body. The integrity of epithelial barriers and the immune system are compromised before the visual system is impaired. This is the basis of the pathological process termed xerosis that leads to the drying of the conjunctiva and cornea of the eye followed by destruction of the cornea and blindness. As indicated in Fig. 16.1, with a decline in vitamin A status, systemic consequences of vitamin A deficiency (VAD), including increased mortality, begin to occur even before the appearance of appreciable rates of clinical xerophthalmia [6].

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16.1 Vitamin A status and clinical implications [6]

Public health consequences that can be attributed to vitamin A deficiency are defined as vitamin A deficiency disorders or VAD disorders (VADD). The term VAD disorders was introduced in 2002 at the XX International Vitamin A Consultative Group (IVACG) meeting and is defined as health or physiological consequences attributable to VAD, whether clinically evident (e.g., xerophthalmia, anemia, growth retardation, increased infectious morbidity and mortality) or not (e.g., impaired iron mobilization, disturbed cellular differentiation and depressed immune response) [6]. The mortality risks increases from the stage when vitamin A is depleted in tissues and plasma but there is no clinical sign of deficiency. The spectrum of vitamin A deficiency disorders (VADD) has been diagrammatically presented as in Fig. 16.2 [8]. In children, vitamin A deficiency causes xerophthalmia and results in blindness. Xerophthalmia is the general term applied to all ocular manifestations of impaired vitamin A metabolism, from night blindness through complete corneal distribution. VADD therefore covers what was previously referred to as “subclinical manifestations”.

16.2 Spectrum of vitamin A deficiency disorders [8]

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Xerophthalmia remains the most specific and readily recognized clinical manifestation of vitamin A deficiency, and has served as the definitive criterion for assessing vitamin A status. Ocular manifestations are the most easily identifiable signs of an overt vitamin A deficiency. Table 16.2 presents the xerophthalmia classification [8]. The stage XIB (Bitot’s spot) is not always responsive to improvement in vitamin A status. However, up to the stage of corneal xerosis (X2) prompt treatment with large doses of vitamin A can result in full restoration of sight without any residual impairment [4]. Ulceration/ keratomalacia marks progression of the disease. Ulceration which involves less than one-third of the corneal surface (X3A) generally spares the central pupillary zone, and prompt therapy ordinarily preserves useful vision. More widespread involvement (X3B), usually results in perforation, and loss of eye globe and prompt therapy may still save the other eye and the child’s life. Table 16.2 Xerophthalmia classification [8] XN X1A X1B X2 X3A X3B XS XF

Night blindness Conjunctival xerosis Bitot’s spot Corneal xerosis Corneal ulceration / keratomalacia (involving less than one third of the corneal area) Corneal ulceration / keratomalacia (involving one third or more of the corneal area) Corneal scar (from X3) Xerophthalmic fundus

Vitamin A deficiency in children also limits growth, weakens innate and acquires host defenses, exacerbates infection and increases the risk of death [9]. The health consequences of vitamin A deficiency in women of reproductive age contributes to increase in morbidity and mortality during pregnancy and early post-partum. Vitamin deficient night-blind women in pregnancy are associated with higher risks of severe anemia, wasting malnutrition, and reproductive and infectious morbidity [10]. Severe VAD during pregnancy or maternal VAD is also associated with increase in mortality in the first months of life [9].

16.3

Epidemiology of vitamin A deficiency

Vitamin A deficiency, a public health problem, results from a chronic low dietary intake of vitamin A due to social and economic factors which adversely influence regular availability, access and consumption of vitamin A rich foods. Table 16.3 presents the recommended nutrient intake of vitamin A. In addition to low dietary intake, other factors which contribute to and exacerbate VAD are increased requirements for vitamin A during infections or malabsorption due to the absence of fat in the diet [12].

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The type and amount of vitamin and pro-vitamin ingested, absorbed, transported, stored and metabolized determines the extent of inadequacy of vitamin A [7]. Unrelated disease states can also sometimes dramatically alter each of these factors and, in turn, the individual’s vitamin A balance. For example, gastroenteritis affects both the types and amount of food given and the child’s appetite while the shortened transit time in this diseased situation further decreases absorption of any vitamin A that is Table 16.3 Dietary vitamin A reference intakes for children from birth to 6 years of age (a)

FAO Basal requirement Safe intake Estimated average requirement (EAR) (b) RDA(c) (a)

(b)

(c)

Age groups < 1 year µg

1–3 years (µg)

4–6 years (µg)

180 350 –

200 400 210

200 400 275

–

300

400

Basal requirement is defined as the minimum daily intake of vitamin A needed to prevent the appearance of clinical signs of vitamin A deficiency (xerophthalmia) and to permit normal growth. Safe intake is defined as the amount of vitamin A needed to meet basal needs and other vitamin A dependent functions and maintain a minimally adequate liver vitamin A store of 20 µg/g for the median person plus 2 sd; thus safe intake meets needs for 97–98% of all healthy people. EAR is defined as the amount of vitamin A needed to meet basal needs and other vitamin A dependent functions and maintain a minimally adequate liver vitamin A store of 20 µg/g in half of all healthy people. RDA is defined as the EAR + 2 sd; thus, the RDA meets the needs for 97– 98% of all healthy people.

ingested. If a child is already protein-deficient, transport and storage could decrease while fever could result in increasing the metabolic needs. The key underlying epidemiological traits that tend to characterize most situations where vitamin A deficiency occurs as a public health problem are as follows [1, 7].

16.3.1 Ecological, social and economic factors Consumption of vitamin A and duration of consumption is influenced by the availability of foods rich in vitamin A activity that are grown and available in specific seasons at a reasonable cost. Fruits and vegetables are sources of vitamin A which are in the form of provitamin A carotenoids and represent the major source dietary vitamin A in the developing world, among which β-carotene is the most bioavailable. Food sources of pro-

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vitamin A carotenoids include dark green leafy vegetables such as spinach and amaranth, yellow and deeply coloured orange vegetables and fruits such as carrot, ripe mango, papaya, yellow sweet potato, pumpkin, chillies. These need to be converted into retinol before they can provide protection from vitamin A deficiency. Carotene needs dietary fat or oil to be absorbed. On the other hand, vitamin A from animal foods such as milk, cheese, yogurt, butter, eggs, liver and small fishes are rich sources of retinol and can be directly used by the body. A number of process steps, dependent on normal physiological functions, convert provitamin A forms to retinol. Absorption and bioconversion of dietary β-carotene and other provitamin A carotenoids into retinol are a part of a complex process which is influenced not only by the amount of carotenoid consumed in a meal but a number of factors – these factors are incorporated into the mnemonic SLAMENGHI: species of carotenoid, molecular linkage, amount of carotene consumed in a meal, matrix in which carotenoid is incorporated, effectors of absorption and bioconversion, nutrient status of the host, genetic factors, host related factors and interaction between the other factors [13–15]. Therefore in addition to availability of fruits and vegetables, the actual conversion to retinol is critical. In the past, the molar retinol equivalency of dietary β-carotene and other pro-vitamin A carotenoids was assumed to be 6:1 and 12:1, respectively [15]. The food composition and database in meals and food supplies was accordingly calculated. Further evidence from research findings resulted in increasing the ratios to 12:1 for dietary β-carotene and 24:1 for other pro-vitamin A carotenoids [16, 17]. It has been estimated that in the undernourished populations, carotenoid bio-conversion may be even less efficient from mixture of vegetables and fruits and the rate of conversion may be very poor with a high conversion ratio of about 21:1. [15]. The implications of such poor ratio of conversion imply a significant increase in the requirements of fruits and vegetables to meet the dietary vitamin A requirement of population who are dependent on these sources. Vegetables and fruits are often seasonal and require abundant water supplies and/or moderate temperature to grow. In regions and countries, with long periods of water shortage and relatively constant hot temperatures, regular food sources of vitamin A are often inadequate resulting in higher possibility of having high prevalence of vitamin A deficiency.

16.3.2 Child feeding practices Child feeding practices play an important role in the epidemiology of vitamin A deficiency. Children of both well-nourished and poorly nourished populations are born with limited hepatic store of vitamin A at birth. Liver

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stores at birth are sufficient to supply the infant’s vitamin A requirements for only a few days, even when mother is well nourished during pregnancy [18]. Breast milk provides retinol in a readily absorbable form. Clinical symptoms of vitamin A deficiency rarely occur in breastfed infants during the first year of life in populations with endemic vitamin A deficiency [9]. It is well-documented that breast milk affords protection against VAD in infants who are predominantly breastfed even in situations when breast milk vitamin A content is low. The concentration of vitamin A in breast milk is influenced by maternal vitamin A intake and status as well as the fat content and stage of lactation [18]. Colostrum secreted in the first 4– 6 days post-partum and transitional milk from about 7–21 days of lactation contain much higher concentration of vitamin A than mature breast milk. The practice of discarding of colostrum in some developing countries therefore deprives the newborns of concentrated source of vitamin A. In situations, when a mother is deficient in vitamin A or the child is bottle fed or the child is given skimmed milk or whole milk diluted with water, deficiency of vitamin A often results since the body stores of vitamin A in infant gets depleted resulting in subclinical vitamin A deficiency and consequent health risks. Discontinuation of breast milk or introduction of complementary feed at six months with poor content of vitamin A as well as reduction in breast milk fed deteriorate vitamin A status of young children. Low routine consumption of milk, egg, yellow fruits and vegetables, dark green leaves or meat/fish in the first 12 months of complementary feeding have been reported to be three times more likely to be xerophthalmic than matched control given these foods [19]. The problem of subclinical depletion therefore has been observed to increase significantly between 6 months and 3 years of age when a child is introduced to complementary food and the breast milk quantity gradually continues to diminish. Unless special effort is made, family diet often do not contain adequate vitamin A to meet the demands of growing child and for adequately replacing the amount that was provided by breast milk in early part of infancy. The situation is further worsened by the fact that the diet of young children is often small in quantity and frequently contains less fat resulting in dietary fat being not available for the absorption of vegetable source of provitamin A. Additionally, vitamin A status of children in developing countries is often adversely influenced by the poor vitamin A status of mother who produces breast milk low in vitamin A.

16.3.3 Infection and worm infestation Infants in developing countries are often exposed to conditions of frequent infections or disease and increased catabolism which deteriorate vitamin

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A status. In young children, the frequency, duration and severity of infections contribute directly or indirectly to vulnerability to vitamin A deficiency. Infection induces vitamin A deficiency through a variety of ways depending on the vitamin A status of the host at onset, cause, duration and severity of infection. Infections not only lessen appetite but adversely influence absorption, conservation and utilization of vitamin A. Frequent acute bacterial infections damage mucosal surface required for absorption. Infectious illness, such as diarrhoea, measles or severe respiratory infections result in increased demands and urinary losses of vitamin A. Serum retinol levels therefore may reduce as a result of infection resulting in malabsorption due to diarrhoea or intestinal pathogens, impaired release or accelerated depletion of hepatic retinol reserves, increased retinol utilization by target tissues or increased urinary losses. Lowered levels of retinol or hyporetinolemia may adversely affect immune competence, which could exacerbate or predispose children to infection [20]. In situations of disease, vitamin A deficiency tends to precipitate significantly following the peak prevalence of diarrhoeal and respiratory diseases. Measles is reported to severely deplete vitamin A stores, leaving a child more vulnerable to disease such as pneumonia, diarrhoea and xerophthalmia. Frequency of diarrhoeal and respiratory infections is therefore associated with vulnerability to vitamin A deficiency [21]. Measles is estimated to precipitate as much as 25–50% of cases of blinding xerophthalmia in Asia and Africa [7]. Low availability of vitamin A from milk combined with higher requirement due to chronic infection in infants contributes to lowering liver stores, especially failing to accumulate beyond early infancy [11]. Protein energy malnutrition is an important contributory cause of VAD since it interferes with storage, transport and utilization of vitamin A [7]. Intestinal worms, soil transmitted helminthes (STHs), i.e. round worm, hook worm and whipworm in pre-school children directly compete for vitamin A intake and contribute to VAD [22]. It is estimated that 230 million children of 0–4 years globally are infected with STHs. Roundworms are the most prevalent STH reported in preschool children and cause significant vitamin A malabsorption [23]. Roundworms live in the gut and need vitamin A to grow and this results in competition for the nutrient resulting in VAD. In Nepal where prevalence of both VAD and STH is high, children with xerophthalmia are reported to have three times the load of roundworm infection compared to uninfected control group [24].

16.3.4 Age VAD can occur in individuals of any age. However, it is a disabling and a potentially fatal public health problem for preschool children. Clinical

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symptoms of vitamin A deficiency rarely occur in predominantly breastfed infants during the first year of life even in populations with endemic vitamin A deficiency [9]. VAD affects children of the preschool age group because of low intake of vitamin A and great susceptibility to infections as well as due to an increased requirement for the micronutrient vitamin A to support the rapid growth during this period. VAD related blindness is most prevalent in children under 3 years of age and is associated with Protein energy malnutrition or PEM [1]. The prevalence of mild xerophthalmia (XN, XIB) has been found to increase with age through the fifth year of life and possibly beyond, since children in high risk population continue to be exposed to diet lacking vitamin A or pro-vitamin A rich food items. No estimates for school aged children exist. In older children of school age, the prevalence of mild xerophthalmia, notably Bitot’s spots, may be highest, although this is considered to possibly be a reflection of past rather than current vitamin A status [1].

16.3.5 Sex There is no consistent, clear indication in humans of a sex differential in vitamin A requirements during childhood [1]. In most societies or cultures, the risk of severe blinding xerophthalmia (corneal ulceration and keratomalacia) is equal in both sexes; moreover, improvement in vitamin A status generally reduces mortality equally in both sexes.

16.3.6 Season In many areas of the world sources of vitamin A (and of food in general) are in short supply during the hot and dry season. During such specific seasons, high rate of infections such as measles and diarrhoea are reported. Both these factors are important seasonal aspects influencing vitamin A status.

16.3.7 Cluster Vitamin A deficiency and xerophthalmia tend to cluster within countries and within specific families and neighborhoods possibly since the dietary and health practices responsible for vitamin A deficiency are shared by most members of the same community [1, 7]. Clustering of risks appears to intensify within smaller disadvantaged groupings. Survey findings from Africa, South and South-East Asia reveal a consistent 1.5- to 2.0-fold risk of xerophthalmia among children in villages where other children have the condition [25, 26]. There is a 7-

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to 13-fold higher risk of xerophthalmia in families where siblings have clinical signs of deficiency compared to children of those families where siblings present with no such signs of VAD [25]. The occurrence of clinical vitamin A deficiency tends to cluster rather than being evenly distributed and such clustering of vitamin A deficiency cases primarily applies to clinical eye signs. Such clustering is also a reflection of convergence of a number of risk factors that lead to depletion of vitamin A stores in the surrounding child population and of these a few individuals who are exposed to additional causal factors possibly develop clinical deficiency of vitamin A. These factors responsible for clustering are important with reference to prioritizing families and communities for implementing treatment and preventive actions.

16.4

Vitamin A deficiency (VAD) – a public health problem

Table 16.4 presents details of the prevalence criteria indicating VAD to be a public health problem within a defined population. Vitamin A status of preschool children is particularly crucial and ideally childhood prevalence criteria are recommended to be restricted to children 2–5 years of age. There has been a review and modifications suggested in the level of cutoff presented earlier [6, 27]. The revised proposed criterion of IVACG 2001 includes a clinical prevalence criterion of the prevalence of night blindness during pregnancy in the past three years. This information has been observed to be simple and practical to collect [6, 28]. Table 16.4 Prevalence criteria indicating VAD within a defined population [6] Criteria Clinical Children 2–5 years old Night blindness (XN) Bitot’s spots (X1B) Corneal xerosis (X2) and corneal ulcers (X3) Corneal scars (XS) Women of childbearing age XN during most recent pregnancy Biochemical Serum retinol <0.70 μmol/L (20 μg/dL)

Prevalence (%)

>1.0 >0.5 >0.01 >0.05 >5.0 >15

The status of VAD can be assessed by two biochemical measure such as serum retinol concentrations and serum retinol binding protein or RBP [29]. Serum retinol concentration of <20 μg/dL (0.70 μmol/L) is an indicator of subclinical VAD and requires high precision analysis by high performance liquid chromatography (HPLC). Serum retinol concentration

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reflects an individual’s vitamin A status, particularly when reserves of vitamin A are limited. However, the limitation of the indicator serum retinol level is that it is affected by infection and protein energy malnutrition. Prevalence of deficiency, assessed by serum retinol concentration below the conventional cut-off of 0.70 μmol/L, of more than 15% among preschool children 6–71 months of age is considered to represent a public health problem [6]. Table 16.5 Prevalence of VAD in children ≥1 year of age of serum values ≤0.70 µmol/L [1] Level of public health problem

Prevalence

Mild Moderate Severe

≥2 to <10% ≥10 to <20% ≥20%

HPLC is considered the only laboratory technique that is reliable for routine measurement of serum retinol. When HPLC measurements are not available, assessment of VAD is recommended to be based on clinical criteria. The clinical signs of xerophthalmia (Greek term xeros meaning “drying” and ophthalmia meaning “of the eye”) as well as the early stages of the condition such as squamous metaplasia can be measured by impression cytology or impaired dark adaptation that precedes complaints of night blindness (poor vision at dusk). XN is often difficult to detect in younger children while Bitot’s spot (X1B) in older children are often remnants of earlier deficiency. In assessing the presence or absence of XN in a child, it is recommended to use one or more locally appropriate terms (often translated as chicken eyes or chicken blindness). In northern India and Nepal, the term commonly used is rathondi meaning blindness of night while in South East Asia, terms used are matang manak, kurap, harapan, etc. In well-nourished populations, history of night blindness during pregnancy is consistently reported to be below 3%. As indicated in Table 16.4, a minimal prevalence of 5% XN in these women is the cut-off value recommended for labelling presence of VAD in the population [28]. Maternal night blindness or a woman’s history of experiencing night blindness (XN) at some point during last live-birth pregnancy is a good indicator of VAD in the wider population. As indicated in Table 16.6, in poor rural regions, where xerophthalmia in children constitutes a public health problem, night blindness in women during pregnancy is also commonly reported [28]. It is therefore recommended to study the prevalence of night blindness in women of reproductive age who have had a live birth in the past three years [29]. This indicator is proposed to be even more accurate than questioning parents about XN in their preschool-age children [6].

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Table 16.6 Prevalence estimates of xerophthalmia in preschool children and maternal night blindness during pregnancy by country Country

Xerophthalmia in children (%)

Blindness during pregnancy (%)

Nepal (a) India Philippines Zambia

3[30] 1.1[32] 0.4–0.7[33] 6.2[35]

16.2[31] 12.1[32] 8.6[34] 11.6[35]

(a)

pre-national vitamin A program

The clinical and biochemical indicators for assessing VAD presented in Table 16.4 are subject to limitations. WHO therefore recommends that at least two indicators be used for assessing the vitamin A status of a population [1, 27]. In the absence of direct clinical and biochemical criteria to assess VAD, it is proposed that under-5-year mortality rate (U5MR) be used as a “surrogate” indicator for VAD in a population. Population of countries with high U5MR invariably has been proven to have significant VAD [30–36]. Any country or localized population with U5MR >50 is likely to have vitamin A problem unless proven otherwise and therefore this indicator is used for screening VAD as a public health problem at the national level and for ensuring actions are taken immediately for addressing vitamin A deficiency.

16.5

Public health significance of vitamin A deficiency disorders

Vitamin A deficiency is a major public health nutrition problem in the developing world. It is among the “top ten” health problems contributing to the global burden of disease and childhood mortality [31–36]. In 1995, VAD was reported to be a public health problem in 78 developing countries [1], and VAD was reported to be widespread in periequatorial regions of the world. In 2000, VAD was considered to be a public health problem in 118 countries [32–37]. The extent and severity of VAD is most widespread across large areas of south and south-east Asia and Sahelian and sub-Saharan Africa. The highest prevalence of clinical VAD occurs in Africa, while south East Asia has the highest number of children affected. In early 1990s, it was estimated that VAD causes blindness in 250,000– 500,000 children [33–38] and was a major factor contributing to 1–3 million child deaths [34–39]. A region wise global data on prevalence of VAD (Table 16.7), reported in 2002, estimates that 127.2 million preschool children are vitamin A deficient and of these about 4.4 million children under the age of five are affected by clinical xerophthalmia [8]. This global estimate excludes a number of countries who were unable to assess the true level of deficiency due to technical and financial constraints.

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Table 16.7 Global prevalence of preschool child vitamin A deficiency and xerophthalmia, with numbers of cases, by region [8] Region

Population <5 years (× 103 )

Africa Eastern Mediterranean South/Southeast Asia Western Pacific Region of the Americas Total

103,934 59,818 169,009 122,006 47,575 502,494

(a)

Vitamin A deficient (a)

Xeropthalmia

%

No (× 103)

%

No (× 10 3)

32.1 21.2 33.0 14.0 17.3 25.3

33,406 12,664 55,812 17,128 8,218 127,273

1.53 0.85 1.20 0.18 0.16 0.88

1,593 510 2,026 220 75 4,424

Defined by serum retinol <0.70 µmol/L or, occasionally, abnormal conjunctival impression cytology

As presented in Table 16.7, 33.0% of VAD children live in South and South East Asia, 32.1% in Africa and 21.2% in eastern Mediterranean region. Table 16.8 indicates that the largest number of vitamin A deficient children are estimated to live in India (35.3 million) followed by Indonesia (12.6 million) and China (11.4 million). The geographical distribution roughly matches with ecological indices of poverty and undernutrition. As is evident from the data, a far greater numbers of children show no external signs of VAD, but live with dangerously low vitamin A stores, which indicate that the child population is vulnerable to infection and reduced immunity to fight Table 16.8 Prevalence of preschool child vitamin A deficiency and xerophthalmia, with numbers of cases, in selected countries of the six regions [8] Region

Population <5 years (× 10 3)

Africa Ethiopia 11,032 Kenya 1,812 Eastern Mediterranean Pakistan 23,793 South/Southeast Asia Bangladesh 15,120 India 114,976 Indonesia 22,006 Western Pacific China 97,793 Philippines 9,800 Other countries 5,959 Region of the Americas Brazil 15,993 Gautemala 1,816 European Region Macedonia 152 (a)

Vitamin A deficient (a) % No (× 10 3)

4,462 4.80

61.2 2.00

Xeropthalmia %

No (× 103 )

40.6 530

6,752 89

24.0

5,710

0.24

57

30.8 30.8 57.5

4,649 35,355 12,653

0.62 1.56 0.34

94 1790 75

11.7 38.0 16.2

11, 442 3,724 964

0.17 0.07 0.44

170 7 26

13.7 13.4

2,187 244

0.13 0.00

20 0

29.5

45

0

0

Defined by serum retinol < 0.70 µmol/L or, occasionally, abnormal conjunctival impression cytology.

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common childhood diseases. These children have a markedly increased risk of illness and death, particularly from measles and diarrhoea. VAD is estimated to be an underlying cause of at least 650,000 early childhood deaths due to diarrhoea, measles, malaria and other infections each year [8]. Besides children, there is increasing evidence that VAD is a problem among women in the reproductive age group. Night blindness is common among women in the latter half of pregnancy, affecting 10–20% of pregnant women in South and Southeast Asia. The condition appears to be 25 times more prevalent in pregnant women than in preschool children [10]. It has been estimated that nearly 20 million pregnant women in the developing world have low vitamin status and almost 6.2 million are clinically night blind [8]. In the past VAD was viewed as a public health concern primarily for addressing preventable blindness, and therefore earlier in many countries actions for improving vitamin A status was a part of blindness prevention programme. Since 1982, research findings have increasingly stressed on the significance of vitamin A in the broader context of child health and survival. These were based on the results of epidemiological investigations and community-based studies launched in late 1970s into the role of VAD in child mortality. One of the earliest study was from Indonesian where children with mild xerophthalmia, but no other obvious nutrition stress, were reported to be 2–3 times more likely to develop respiratory infections or diarrhoea and more likely to die than children without eye signs [41, 42]. Between the period 1986 and 1993, eight population-based intervention trials in South-East Asia, South Asia and Africa further supported this finding. It was found that vitamin A supplementation, achieved by periodic high potency dosing (200,000 IU for over 12 months children and lower dose IU for 6–12 months), weekly low potency dosing (15,000 IU) or food fortification could reduce child mortality by 6–54% [43–51]. Meta-analyses of the findings of the study concluded that in areas where vitamin A deficiency is prevalent, child mortality is reduced by 23–34% after vitamin A intervention [52–55]. The pooled estimate is 23% reduction in the risk of all cause mortality in children 6–59 months with vitamin A supplements [53]. The impact of vitamin A on lowering case fatality by measles was estimated to be about 50% [8], while the risk of fatality from diarrhoea and dysentery was lower at about 40%. A recent analysis has estimated about 50% reduction in case fatality from diarrhoea and measles among vitamin A recipients [56]. The impact of vitamin A supplementation on risk of mortality from respiratory infections, unrelated to measles, is reported to have no significant influence [57, 58]. The effect of vitamin A on infant and child morbidity is not conclusive. It has, however, been indicated that

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vitamin A possibly benefits infant survival in undernourished populations depending on the age of administering the dose, supplementation method used, nutritional status and dominant disease pattern [51]. Three reported trials of vitamin A supplementation in the neo-natal period in low-income countries indicates that neonatal vitamin A supplementation is associated with reduced mortality. A pooled analysis of all studies from South Asia indicates 21% reduction in mortality in babies younger than 6 months [37]. Similarly, in chronically undernourished population, vitamin A deficiency is considered to pose a health risk to women during pregnancy and lactation. VAD during pregnancy is associated with anemia, wasting, undernutrition and other morbid symptoms [29, 59, 60]. The risk groups are therefore children from age of six months to six years, pregnant and lactating women while high priority risk groups are children with xerophthalmia, measles, diarrhoea, severe protein–energy malnutrition, children with acute or prolonged diarrhoea and with acute lower respiratory infection.

16.6

International focus on prevention of vitamin A deficiency

A number of events since 1970 drew attention to the problem of vitamin A deficiency [61]. Recognizing the gravity of the situation of xerophthalmia, the 25th World Health Assembly urged intensification of activities in 1972 to prevent needless loss of sight. Xerophthalmia was recognised as one of the three important causes of preventable blindness [62]. This was followed by a WHO meeting at Hyderabad, India and World Food Conference on the subject [61], which resulted in recommendations and commitment of the participating governments to reduce the problem of vitamin A deficiency. From 1974 to 1990, a committed scientific community worked extensively to remove existing gaps in knowledge related to addressing vitamin A deficiency through public health interventions [2, 61]. In 1980s, the focus was on VAD and its serious impact on xerophthalmia. It was reported that at least 5 million children in Asia develop xerophthalmia and every year 250,000 of them go blind [63]. In 1984, the emerging evidence of protective role of vitamin A in child health and survival was followed by the resolution of the 37th World Assembly (WHA 37.18) for prevention and control of vitamin A deficiency and xerophthalmia. The wording of this resolution is of historical significance since in the political arena vitamin A deficiency was for the first time recognised to result in health consequences beyond

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xerophthalmia and blindness [61]. The overall strategy proposed included long-, medium- and short-term measures. New impetus for reduction of VAD was provided by results of intervention trials which had indicated the relationship of vitamin A status with child survival [53]. The remarkable impact of vitamin A supplement on child mortality increased the significance of prevention of vitamin A deficiency at the World Summit for Children in 1990 and at the follow-up International Conference of Nutrition in 1992. The significance of vitamin A was recognised in 1992 by the Fifty-fifth World Health Assemblies which directed WHO to intensify its efforts to control the impact of vitamin A deficiency on child health, blindness and survival since the problem of vitamin A deficiency was estimated to be responsible for as many as one out of every four child deaths in regions and countries. The experiences from different countries proved that long-term goal of VAD prevention programme should be to ensure adequate dietary intake of vitamin A and elimination of all form of vitamin A deficiency in children between six months to five years who are at the greatest risk of deficiency. The most cost-effective child health and child survival strategies for vitamin A elimination included a combination of strategies – comprising breast feeding, dietary diversification, food fortification and vitamin A supplementation. WHO-UNICEF established a “Mid Decade Goal” to be achieved by the end of 1995: to ensure that at least 80% of all children under 24 months living in areas with inadequate vitamin A received adequate vitamin A through a combination of breastfeeding, dietary improvement, fortification and supplementation. As part of the global call to action, the UN Special Session on Children in 2002 set as one of its goals the elimination of vitamin A deficiency and its consequences by the year 2010 [64]. Universal supplementation of children 6–59 months with vitamin A is recommended to be included in the health package in all countries where U5MR exceeds was 70 deaths per 1,000 live births, an internationally accepted proxy indicating a high risk of deficiency among children under five [65].

16.7

Intervention strategies for preventing vitamin A deficiency disorders (VADD)

Vitamin A supplementation and vitamin A fortification have been recognised to have robust evidence to improve child nutritional status and recommended to be included in the package of nutrition interventions in countries with high burden of undernutrition [37]. With emerging information, it is evident that elimination of VAD as a public

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Public health nutrition in developing countries

health problem is one of the major interventions for improved child survival. To successfully combat VAD, WHO recommends vitamin A supplement intervention as a short-term measure and establishment of proper infant feeding practices as a long-term sustainable solution [1]. The strategy to achieve the goal of elimination of VAD is to ensure that young children living in areas where the intake of vitamin A is inadequate receive the vitamin through a combination of breastfeeding, dietary improvement, food fortification, and supplementation.

16.7.1 Promotion of breastfeeding Promotion of breastfeeding is an integral component of a comprehensive strategy to combat VAD. Colostrum and early breast milk are concentrated sources of vitamin A and for the first 6–12 months infants depend on readily absorbable vitamin A provided in breast milk. Mothers whose vitamin A intake is adequate produces breast milk with vitamin A concentration that meets their infants’ needs for at least the first six months of life [66]. Breast milk is a critical dietary source of vitamin A and therefore is important in the protection of xerophthalmia in children. Mature breast milk of healthy women contains 600–700 μg of vitamin A per litre [18]. Over 90% of vitamin A content is derived from highly bioavailable esters. A breastfed infant of a vitamin A adequate mother, with an intake of about 725 ml milk per day, consumes about 435–500 μg dietary vitamin A [67]. In developing countries with high prevalence of malnutrition, vitamin A concentration in milk has often been reported to be half of that reported from well-nourished population of women [67]. In well-nourished societies, therefore, body vitamin A stores of children continue to improve with age while in situations where mother is deficient in vitamin A, the amount provided through breast milk is reduced. However, despite reduction in concentration of vitamin A in developing countries, breast milk provides clinically protective amounts to infants especially when exclusively breastfed for the first 6 months. The significance of breast milk in protecting infants from xerophthalmia is evident from studies in situations of early cessation of breastfeeding. The concentration of vitamin A in milk is influenced by the vitamin A status of the mother, stage of lactation and fat content of milk [68]. The average vitamin A concentration in mature breast milk of women in developing countries is much lower—about 300 μg/L and colostrum concentration of vitamin A is 50 μg/dL [11]. In well-nourished women, the concentration of vitamin A tends to decrease in the first month and remains relatively stable during the remaining period of lactation in well-

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nourished women [69]. In case of women in developing countries with marginal intakes of vitamin A, milk vitamin A concentration shows a progressive decrease with the lowest levels at three months [70, 71]. The extent to which infants are estimated to meet their vitamin A requirements from breast milk is presented in Table 16.9 [18]. Although these are approximate estimates, the information reveals that in “high” milk intake group, exclusive breastfeeding is enough to result in vitamin A stores to accumulate even if the breast milk concentration is low (<30 μg/dl) or adequate (50 μg/day) but not if deficient with less than 20 μg/dl. Table 16.9 Estimated vitamin A intakes compared with requirements assuming different values for breast milk volume and vitamin A concentration [18] Age Breast Low breast milk intake (b) (month) milk Milk Vitamin % of retinol(a) volume A intake require(ml) (µg) ments(c)

Average breast milk intake(b) High breast milk intake(b) Milk Vitamin % of Milk Vitamin % of volume A intake require- volume A intake require(ml) (µg) ments(c) (ml) (µg) ments (c)

0–2

714

3–5

Def.

457

91

30/73

Low Adeq.

228

137 76/182

46/110

Def.

515

103

34/82

154 257

51/123 86/206

71

24/57

106 177

35/85 59/142

Low Adeq. 6–8

Def. Low Adeq.

(a) (b)

(c)

355

784

776

143

48/114

214 357

71/171 119/286

157

52/126

235 392

78/188 131/314

155

52/124

233 388

78/186 129/425

959

191

64/153

288 479

96/230 160/ 383

1, 022 204

982

68/163

307 511

102/246 170/409

196

65/157

295 491

98/236 163/392

Deficient (Def.) <20 µg/dl, Low <30 µg/dl, Adequate (Adeq.) >50 µg/dl Low intake –2 sd below mean; average intake, mean intake in developing countries; high intake +2 sd above mean Requirement to build stores (300 µg/day)/basal requirement (125 µg/day)

It is evident that along with promotion of breastfeeding, effort needs to be directed to increase the consumption of foods rich in vitamin A by mothers in developing countries who are reported to be often deficient in vitamin A due to consuming diets low in vitamin A during periods of high requirements. High fertility with prolonged breastfeeding further reduces vitamin A stores in mothers [11].

16.7.2 Dietary diversification Promoting consumption of food rich in vitamin A is the long-term solution to address vitamin A deficiency. Local foods rich in vitamin A need to be identified and effort needs to be made to promote consumption of vitamin A rich food

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Public health nutrition in developing countries

items to build stores in infants, young children and women in the pre-pregnancy or pregnant stage since this population group is at the highest risk of VAD and implications of deficiency are serious at this stage. The richest source of vitamin A is found in foods of animal origin such as liver, meat, eggs and dairy products. Vitamin A is also found in plants. The best dietary sources are dark green leafy vegetables (DGLV) including spinach, cassava leaves, amaranth, baobab leaves and red sorrel. Equally rich are deep yellow and orange fruits such as carrot, sweet potato, pumpkin, mango and papaya. Red palm oil, widely used in plants in Africa, is another good source of vitamin A. A certain amount of fat and protein is also necessary in the diet for the body to be able to absorb and transport the vitamin A in these foods. Improved dietary intake of vitamin A rich food requires an adequate, affordable and diverse supply of food sources of vitamin A through out the year. A number of efforts made in the past have demonstrated positive impact on increasing market availability and affordability of inexpensive source of fruits and vegetables through introduction of horticultural activities at micro level. Such actions at household or community level are feasible in situations of adequate water availability and suitable humidity and land fertility. Animal foods, though excellent sources of vitamin A, are not available to the population at risk in developing countries due to economic and social constraints. Introduction of foods rich in vitamin A in the complementary feed of a child is critical for preventing VAD. Soft yellow fruits and vegetables, dark green leaves, eggs and other food sources of vitamin A need to be routinely fed to children after 6 months, along with continuation of breastfeeding. In many developing countries, a regular supply of such food items at an affordable cost is not feasible. Moreover, availability and accessibility to vitamin A rich food items at family level is constrained not only by cost but poor availability of vitamin A rich foods in certain seasons and the effort required to clean and cook dark green leafy vegetables (DGLV). A number of countries have experimented with innovative approaches to increase production and consumption of foods rich in vitamin A activity. Increase in production and consumption of vitamin A rich foods has been demonstrated through introduction of home or community gardening complemented with intensive nutrition education and social marketing [72, 73]. Social marketing project of Thailand concentrated on promoting one single vitamin A rich source vegetable – the ivy gourd [74]. Promotion of ivy gourd in Thailand was used as an image representing other vitamin A rich vegetables. Lessons learnt from these projects emphasized the need to focus efforts to identify and selectively propagate DGLV and other B-carotene rich foods, promote acceptability of such foods as well as influence use of such food items in family diet

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practices. Additionally, it is important to promote appropriate cooking methods in the traditional diets to ensure maximal retention of nutritive value [74, 75]. Changes in food consumption patterns require complex efforts to influence deeply ingrained family habits and cultural norms. An effective communication strategy to achieve the long-term goal of sustained behaviour change is critical. Messages and communication strategy, specially designed to address mother’s specific concern about feeding selected vitamin A rich foods to children, is crucial. Long-term shift in fact requires consistent efforts and monitoring of impact over several years. Demonstration sessions have been shown to be effective for convincing community regarding how to prepare local foods with inclusion of vitamin A rich food, especially for children. As a rough guide, a handful of fresh green or red varieties of amaranth (40 g) or drumstick leaves (35 g) or a medium-sized mango (100 g) provides the daily requirements for toddlers and preschool children [7]. A study undertaken in India [76] indicated that using a conversion ratio of 1:6 for β-carotene to retinol, a child less than 2 years needed about one table spoon of cooked dark green leafy vegetables (DGLV) per day to meet daily vitamin A requirements. Similarly, it has been estimated that a pregnant woman/nursing mother required about 3 table spoon of cooked DGLV per day for meeting the recommended dietary allowance for vitamin A. According to this study, it has been recommended that a family of five persons needs to procure and cook about 250 g of DGLV (cooked one cup) on a daily basis for the entire family. Based on the revised proposed factor for converting carotenoids into retinol of 12 or 21 μg of β-carotene to 1 μg of retinol for a mixed fruit and vegetable diet [11], the estimated amount of DGLV required to meet the RDA will increase at least two- to threefolds. Biotechnology approach is being increasingly used to increase β-carotene and/or increase bioavailability of vitamin A and pro-vitamin A carotenoids from plant foods comprising commonly eaten cereals and vegetables such as rice, sweet potato, corn etc. New technologies are being introduced for processing red palm oil, a rich source of carotenoids, so that over 80% of the carotenes present in crude palm oil is retained [77].

16.7.3 Fortification of food with vitamin A Food fortification is a highly effective strategy to correct low intake of vitamin A in daily diet. Food fortification is being introduced in increasing number of countries, and holds great hope for long-term

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control of vitamin A deficiency. Fortification of commonly consumed foods such as sugar, cereals, oils, milk, margarine, infant food and various types of flour is being implemented in a number of countries [78]. Oil is considered an ideal food for vitamin A fortification for two primary reasons – fats in oil assists in the absorption of vitamin A and oil fortification process is relatively inexpensive. In Brazil, vitamin A added to oil is well absorbed and has been demonstrated to significantly increase plasma retinol and liver vitamin A stores [79]. A model for oil fortification is expected to emerge from the ongoing efforts in West Africa [80]. The technology for fortifying sugar with vitamin A, developed in Guatemala in mid-1970s, is now well established and the technology of fortification of sugar with vitamin A as well as iron has also been successful. An effectiveness study has demonstrated improved vitamin A status with fortification of sugar in Guatemala and other Central American countries [81]. Guatemala cost-analysis study revealed that critical targeting and central processing conditions contributed in making fortification two to four times more cost-effective in reaching beneficiaries with adequate amounts of vitamin A than v i t a m i n A c a p s u l e d i s t r i b u t i o n o r e ff o r t s t o p r o m o t e d i e t a r y diversification [82]. Sugar fortified with vitamin A, zinc, and iron either alone or in combination is being marketed in Brazil. In South-East Asia, vitamin A fortified monosodium glutamate (MSG) is widely promoted and is reported to improve breast milk and serum retinol concentrations as well as growth and survival of preschool children in Indonesia and Philippines [83, 44]. Despite successful biological impact, MSG fortification is not a national programme [81]. Fortification initiatives in any country are dictated by the cost, expertise, infrastructure, policies and political will. Development and marketing of finished products sometimes takes several years to reach all at-risk children and their families. It has been recommended that successful fortification programmes in a country should be complemented with administration of vitamin A supplements to the high-risk population group. It is estimated that in approximately 40 of the vitamin A supplementation priority countries, vitamin A fortified foods are available but the extent of its usage is not known [80].

16.7.4 Provision of high dose vitamin A supplement High dose Vitamin A supplement (VAS) While dietary and food-fortification strategies are essential, it is not feasible to implement such interventions quickly or widely in those developing countries where VAD is most severe. Administration of routine vitamin A

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supplements is critical to prevent occurrence of vitamin A deficiency in situations where dietary intake of vitamin A is inadequate and the scope for rapidly improving the situation through dietary means is low for many years, e.g. in situations of chronic poverty, chronic shortage of food including food sources of vitamin A or fat [7]. Periodic high-dose vitamin A supplement (VAS) is intended to protect against VAD and its consequences by immediately improving the body reserves of vitamin A. As a result, efforts directed to eliminate VAD have turned to regular administration of supplement as a low cost, highly effective means of rapidly and sustainably improving the vitamin A status and health of children [38]. For children living in deficient population, the periodic supply of highdose vitamin A supplement (VAS) has been accepted as a swift, simple, low-cost, high-benefit intervention. VAS has produced remarkable results, reducing mortality by 23% overall and by up to 50% for acute measles sufferers and that of diarrhoeal disease mortality by about 33% [9, 46, 84, 85, 86]. Administration of vitamin A supplement is also recommended to be used in conditions for treatment of those with signs of acute xerophthalmia as well as in situations where high-risk individuals need to rapidly improve vitamin A status, e.g. children with infections such as diarrhoea or measles or in emergency situations such as drought or feeding of refugees who are dependent on relief rations. The administration of vitamin A supplement along with measles vaccine to infants has been reported not only in improving serum retinol levels but also to result in improving sero conversion of measles [87]. High potency vitamin A supplement has been introduced as a child survival tool since 1990s. At the global level, vitamin A supplement programme was accelerated in 1993. Two forms of vitamin A supplement preparations of high potency, oil based and water miscible, are used (Box 16.1). Water miscible VAS preparations are not recommended for public health programmes. Vitamin A supplementation has been listed among the key interventions achievable on a large scale that have proven potential to reduce the number of preventable child deaths each year [37] and is therefore recognised as a critical intervention for achieving the Millennium Development Goal 4 (MDG-4) pertaining to child survival, particularly in countries with high under-five mortality and /or vitamin A deficiency prevalence rates. In order to have substantial impact on child survival, all children between the ages of six and 59 months in the target countries are recommended to receive high dose vitamin A supplements every 4–6 months.

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Box 16.1 Vitamin A supplement high dose preparations Preparations of high-dose vitamin A supplement are supplied as retinyl palmitate, retinyl acetate or retinol. The most widely available commercial form is retinyl palmitate [66–72]. A dose of 200,000 IU is equivalent to 110 mg of retinyl palmitate, 69 mg retinyl acetate, or 60 mg retinol. As long as recommended doses are administered, the chemical form is not important. Vitamin A preparations for supplementation programme are diluted with high-quality vegetable oil, usually peanut oil. Addition of vitamin E (40 mg) for 200,000 IU of vitamin A acts as an antioxidant to stabilize the product and to enhance the absorption and storage of vitamin A by the body. Water-miscible preparations of vitamin A high-dose supplement are not considered suitable [88, 89]. Water-miscible emulsified and dry preparation of retinol are reported to be ≥ 10 times more toxic as compared to oil-based preparations of retinol. Oil-based preparations are preferred for oral administration of vitamin A. Vi t a m i n A s u p p l e m e n t p r e p a r a t i o n s , e s p e c i a l l y i n l i q u i d f o r m , a r e recommended to be stored in a dark bottle (or an aluminium container) to shield from light since the chemical stability and therefore the biological activity of vitamin A is affected by temperature and sunlight and other sources of ultra violet light. Vitamin A supplement preparation is sufficiently stable and requires no cold chain. The estimated shelf-life of oil-based solution of vitamin A properly stored in unopened opaque container is estimated to be at least 2 years. Once a container has been opened, potency is gradually reduced. Liquid vitamin A preparations from properly stored containers should be used within 6–8 weeks of opening. Although such preparations beyond the designated periods are less potent, they remain safe and often contain adequate vitamin A for therapeutic use [66]. Partial protection against the loss of potency is acquired when the oil-based VAS solution is formulated in capsules. VAS is available as gelatin capsules which can be swallowed by children at least 36 months of age or adults. For younger children, the nipple on the capsule is cut off or the capsule pricked with a pin, and the contents squeezed into child’s mouth. The high dose retinol gel capsules (in single doses of 200,000 IU or lower dose capsules of 100,000, 50,000, 25,000 and 10,000 IU) are available for public health programme [65]. The cost of a single capsule is US$0.02 and US$0.04 per child can prevent and correct the deficiency. Vitamin A is used as oily solution rather than in form of capsules in only 9 countries – India, Nigeria, Mali, Brazil, Bangladesh, Iran, Mexico, Guatemala, Nicaragua and Iran [65]. Indian government procures vitamin A supplement in flavoured syrup form mixed with Arachidonic oil [90]. Vitamin A is supplied in India as oil-based syrup in dark brown coloured bottles of 100 ml. The concentration of supplement is 100,000 IU/ml. A spoon measuring 2 ml is supplied with each bottle. A spoon to the upper level measures 2 ml (200,000 IU) while the half level marking measures up to 1 ml (100,000 IU). The cost of 100 ml or 50 doses of VAS of 200,000 IU is approximately one US dollar or each dose of vitamin A supplement costs 2 US cents. The timely distribution of vitamin A preparation to field requires a wellfunctioning storage system at central warehouse. Linking with supply of primary health care and maternal and child health services is practical. Unopened containers of both liquid and capsules retain over 90% activity for six months at 30°C. Vitamin A supplement preparation is recommended NOT to be kept below zero degree centrigrade [66]. Vitamin A supplement storage does not require any special storage measures such as cold chain. It should be stored in a cool dark room protected from sunlight.

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For individuals one year of age and older, administration of 200,000 IU of vitamin A supplement (VAS) provides adequate protection for 4– 6 months, the exact interval depending on the vitamin A content of the diet and rate of utilization by the body. The recommended appropriate dose interval for high dose VAS is 4–6 months, although it is indicated that 3-month interval is safe [66]. The recommendation is to scale up twice yearly vitamin A supplementation for children aged between six months and five years to achieve at least 70% coverage on a recurrent basis [80]. The VAS doses for various age groups recommended in the IVACG meet 2001 are presented in Table 16.10. Table 16.10 Recommended schedule for routine prophylactic high-dose vitamin A supplementation in vitamin A deficient populations [91, 92] Population

Amount of vitamin A to be administered

Time of administration

Infants 0–5 months

150,000 IU as three doses of 50,000 IU with at least a 1-month interval between doses 100,000 IU as a single dose every 4–6 months 200,000 IU as a single dose every 4–6 months

At each DTP contact (6, 10, and 14 weeks) (otherwise at other opportunities) At any opportunity (e.g., measles immunization) At any opportunity

400, 000 IU as two doses of 200, 000 IU at least 1 dose apart And / or 10, 000 IU daily or 25,000 IU weekly

As soon after delivery as possible and not more than 6 weeks later And / or during the first 6 month after delivery

Infants 6–11 months Children 12 months and older Postpartum women

Additional dosage is required for children with clinical signs of vitamin A deficiency as a part of treatment package for those children suffering with severe acute malnutrition or infection such as measles and diarrhoea (Table 16.11). Children with concurrent vitamin A deficiency and measles can suffer serious complications and immediate vitamin A therapy is therefore recommended to reduce the risk of excessive measles case fatality. Similarly in situations of diarrhoea episode or severe acute malnutrition, additional vitamin A supplement dose administration is recommended. Table 16.11 presents the recommended treatment dosage for children and women 13–49 years [92]. Recent studies report that pregnant and breastfeeding women in a poor population have high prevalence of night blindness and biochemical vitamin A deficiency and likely adverse impact on both mother and her infant [92–96]. Prophylactic doses of vitamin A supplement for lactating women have been recommended [86]. Earlier the VAS dose recommended was a single dose to mothers in the first 4–6 weeks postpartum. WHO

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Table 16.11 Vitamin A treatment regimens [92]

(a)

Infants and children (a)

Vitamin A dose (IU)

Young infants (0–5 months) Older infants (6–11 months) Children (males: 12 months or more; females 12 months to 12 year and > 50 years) Women (13–49 years) Xerophthalmia: night blindness and/or Bitot’s spot Active corneal lesions (rare)

50,000 100,000 200,000 10,000 every day or 25,000 every week for at least 3 months 200,000 on days 1, 2 and 14

Schedule – severe malnutrition, day 1; measles, days 1 and 2; xerophthalmia, days 1, 2 and 14. Severe malnutrition: kwashiorkor or weight for height below –3 sd (NCHS)

recommended revised dosage for women in vitamin A deficient areas to be increased to two doses of 200,000 IU vitamin A – first dose of 200,000 IU at delivery and the next dose within 6 weeks postpartum [92, 97]. This recommendation ensures that infants receive the necessary immune boosting protection of vitamin A for the first six months of life. For fertile woman, independent of the vitamin A status, 10,000 IU is the maximum daily supplement recommended at any time during pregnancy [92–97]. For women with xerophthalmia, a treatment dosage of 10,000 IU every day or 25,000 IU every week for at least 3 months is recommended [98]. The efficacy of VAS appears to be 90% in preventing any stage of xerophthalmia for six months in children [9] despite projected dosage absorption of only 30–50% in developing countries. During periods of reduced dietary intake or increased need, a gap of 4–6 months is estimated to provide nutrition reserve for use. Protection with massive dose of VAS against hyporetinolemia (serum retinol <20 μg/dL or <0.70 μmol/L) may be less sustained as serum retinol remains elevated for only up to 2 months following high-potency VAS [9]. Vitamin A supplement (VAS) – delivery strategy The goal of VAS is universal coverage of children 6–59 months [65]. “Adequate coverage” in a country is defined as reaching ≥ 70% of children age 6–59 months with VAS on two occasions, 4–6 months apart while “insufficient coverage” is defined as countries reaching ≥70% of children ages 6–59 on one occasion while poor coverage is defined as countries reaching <70% children with VAS on any occasion [99]. The coverage threshold of 70 percent represents “the minimal coverage at which countries can expect to observe reductions in child mortality comparable to those measured in large scale vitamin A supplementation trials in the community” [65]. Administering vitamin A supplement is a

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simple action, especially in situations where vitamin A capsules (VAC) are used. One of the greatest challenges for vitamin A programme is to find sustainable cost-effective mechanisms for delivery to achieve the goal of adequate VAS coverage. Innovative ways of VAS administration strategy was launched in 1988 when the 41st World Health Assembly committed WHO to the goal of global eradication of poliomyelitis by 2000 in ways “which strengthen national immunisation programmes and health infrastructure” [100]. Linking provision of vitamin A supplement during National Immunisation Day (NID) along with polio vaccine was considered a cost-effective delivery system since target group of children for polio were the same and the nation wide campaign aimed to reach the unreached that were also at risk of vitamin A deficiency. Moreover, it was apparent that it was logistically easy to introduce VAS during NIDs since no refrigeration or special storage effort was required and training involved was relatively simple. VAS administration was piggybacked to the ongoing national NID programme and a field guideline on distribution of vitamin A supplements with NID was developed [101, 102], which facilitated a number of countries to link vitamin A supplement administration to Polio NIDS towards achieving the goal of elimination of vitamin A deficiency by 2000 which was one of the goals committed by member countries at the World Summit for Children in 1990 and the International Nutrition Conference in 1992 [103, 104]. In 1998, 75 percent of 118 countries where VAD is a known or suspected public health problem conducted NIDs and of these 89 countries (75%) included vitamin A supplementation in their NIDs [38]. Moreover, administration of VAS along with polio vaccine during NIDs was valued and welcomed by community. VAS was found to act as incentive to mothers and care-givers to take children to immunization sites. However, based on country-programme experiences, linking VAS administration with polio vaccine administration also was of concern to public-health experts since it was observed that the extra planning and management support that was required for VAS possibly compromised the performance of Polio NIDS [105, 106]. Moreover, since NID was organised normally only once annually, a special strategy for the additional dose or second dose was required. Several countries, including Bangladesh and Myanmar, took the lead and organised additional specific periods such as “vitamin A week” or “vitamin A months” when high dose vitamin A supplements were distributed. This resulted in organization of “Micronutrient day” or “Vitamin A days” six months after the annual NID in various countries including Bangladesh, Nepal, Niger and the Philippines [38].

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Following Polio NIDS being gradually discontinued in many countries, the lessons learnt were applied to link VAS with routine immunisation with high degree of success. In fact, WHO strategy which was introduced in 1988 for integration of delivering vitamin A supplement through Expanded Programme on Immunisation (EPI), as a cost-effective strategy for the control of vitamin A deficiency in a community, was revived [91]. Providing the doses of VAS to children on the days of routine immunisation services offered a long-term solution and this was the strategic shift made by many countries. Box 16.2 presents details of emergence of such a strategy in Cambodia [107]. Box 16.2 Cambodia experience – linking vitamin A and immunisation programme [107] The national vitamin A program was initiated in Cambodia in 1994; in 1995 National Immunisation Days (NIDs) for polio began. While NIDs were being organised, it was recognised early on that it would be good for vitamin A capsule (VAC) distribution to “piggy back” on to the NIDs. The National Vitamin A Working Group, consisting of members from Ministry of Health / Departments of Nutrition, Polio Eradication and Expanded Program for Immunisation (EPI), UNICEF, WHO and HKI agreed to conduct a pilot to see how well-distribution of vitamin A high dose capsules (VACs) with NIDS would work. Results of the pilot were very promising and led to the country adopting VAC distribution linked to NIDs as one of the main strategies for distribution of VAC. By 1996 VAC distribution became fully integrated into NIDs. Distribution of VACs through NID-linked strategy continued until the end of 1997 after which the NIDs for polio ended. It was then decided that VACs would be distributed through routine immunisation services. In 1998, Cambodian government took steps to distribute vitamin A capsules (VACs) to children aged 6–59 months through the following channels: ●

●

●

Routine immunisation outreach activities – this was carried out by healthcentre staff who visited 10–20 villages, approximately three to four times per year for immunization services. The outreach team was expected to carry supply of VACs at least twice yearly, around the months of March and November. VAC distribution on sub-national immunisation days (SNIDs): special supplemental campaigns such as SNIDS. Measles outbreak response.

Following the success of this strategy, VAC distribution was integrated into the National Immunisation Program (NIP) and is currently being distributed twice a year to children 6–59 month of age through routine immunisation outreach.

Like Cambodia, many other countries such as Thailand, Bhutan and Afghanistan adopted the sustainable approach of integrating vitamin A supplement administration with the ongoing routine child immunisation programmes or to the routine Maternal Child Health (MCH) programmes [108]. However, in many countries immunisation contact was suitable to reach only under ones and the first opportunity to administer VAS along with measles vaccine at around 9 months of age was found to be

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effective [65]. The delivery system, however, was not adequate to reach children 12–59 months twice annually. Overall coverage achieved through, traditional VAS linked to immunization sessions routine services, remained low due to poor access and utilization of services and an inability to reach older children. It was recognised that regular outreach and events were required to be organised to protect children from the life-threatening effects of VAD. In 1997, a consultation of experts was organised to discuss ways to rapidly increase acceptance and adoption of countries of VAS as a critical child survival intervention [65, 109]. A number of delivery strategies emerged and innovative approaches were launched for vitamin A programmes such as Child Health Days or Child Health Nutrition biannual months. The experiences of West and Central Africa have demonstrated that VAS to children is effectively delivered by institutionalization of Child Survival/Health Days. The twice yearly distribution of VAS through existing permanent institutions in the region is considered sustainable [110]. Figure 16.3 indicates that by 2004, the strategy of Child Health Days were used by 23% of the countries, 15% organised special micronutrient events while 26% administered VAS on polio national or sub-national immunisation days [65].

16.3 Proportion of total delivery attempts in 2004, by strategy [65]

VAS administration events required significant planning, strong logistical support and special allocation of resources and it was considered cost-effective to add additional important child-health activities linked to vitamin A administration. Deworming of preschool children was often linked to vitamin A administration (Box 16.3).

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Box 16.3 Vitamin A plus programme – integrating vitamin A distribution with deworming [22] It is estimated that as many as 230 million children aged 0–4 years are infected with soil-transmitted helminthes (STHs). Roundworms are the most prevalent STH infection in preschool children and cause significant vitamin A malabsorption. Worm infections contribute to vitamin A deficiency. Worm infections and vitamin A deficiency are public health problems in the same geographical areas. The target groups for vitamin A and deworming are very similar. Both VAS and deworming is administered twice a year. However, the main difference in the target age group is important. Vitamin A supplements are given from age of six months while deworming tablets are given from age of one year, i.e. the target group for vitamin A supplement is 6–59 months whereas the target group for deworming is 12–59 months. One of the two following deworming drugs are recommended – Albendazole (400 mg tablet – half tablet for 12–23 months and one tablet for 24 months and older) or Mebendazole (500 mg tablet – one tablet for 12 months and older children). Integrating administration of deworming and VAS programme is not only effective in terms of impact and increasing coverage of both supplements and deworming drug but is also noted to result in increasing community’s trust in health personnel since deworming is extremely popular due to its immediate and highly visible effect. Such vitamin A plus programme has been successfully implemented in Nepal, DPR Korea and Cambodia.

The integrated programme concept resulted in the intervention package of health services termed as “vitamin A plus” package and efforts were made for the integrated delivery of child survival package [65]. Table 16.12 presents a summary of components of vitamin A plus package of 15 countries. In some countries, the first dose for children 6–12 months was continued to be given with measles administration and a special period was allocated as Health-Nutrition week or fixed biannual “Child Health Months” for reaching children twice a year with VAS and other additional interventions [111]. Rapid improvement in the coverage of second and subsequent doses of massive dose of vitamin A administration was achieved with biannual fixed month approach, with an estimated cost of about $0.25 per delivered dose [112, 113]. The success, to a large extent, was achieved due to appropriate strategies for ensuring timely and regular supply of vitamin A supplements, integrating distribution with public health care system, a well-planned social mobilisation effort and a strong monitoring and supervision system. Vitamin A supplement promotion and training For the sucess of VAS programme, communication and social mobilisation is essential. An effective communication strategy with rigorous audience focus, with consistent message across the entire broad geographic areas, is critical for improvements in VAS coverage. Communication efforts must be complemented with an appropriate delivery system, which takes into consideration consumer perspective for distribution such as timing and location, information on product advantages and on the simple “where”

X X

X

X X X X X X

X X X

X

X X X X

X X

X

Zambia

X

X X

X X X

X

X X

X X

X

X

X X

X X

X X

X X

X

X

X

IEC

X

X

X

Iron supplementa- Iron suppltion (pregnant ementation women) (LBW infants)

X

Ivermectin treatment (onchocerciasis)

TT = tetanus toxoid; IEC = information, education and communication; IEC focuses on infant and young child feeding and the promotion/testing of iodised salt in the cited countries. Bangladesh plans to pilot the inclusion of birth registration in upcoming child health packages. Mosquito net distribution in the Philippines is limited to remote areas where malaria is endemic.

X

X X X

Deworming Immunisation Mosquito TT vaccination Growth nets (mothers) monitoring

X X X

Under-5 supplementation

Bangladesh Cambodia Congo, Democratic Republic of the Ethiopia Ghana Korea, Democratic People’s Republic of Lao People’s Democratic Republic Nepal Nigeria Philippines Swaziland Tanzania, United Rep. of Uganda

Country

Table 16.12 Components of child health day packages in recent years [65]

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and “when” of distribution is useful when built in as part of the message. Additionally, commitment by service providers is critical for program success. Special effort needs to be made to address concern and fear of frontline workers of the safety of distribution of high dose vitamin A supplement. The communication strategy needs to address the issue of the serious consequences of children administered extra doses of VAS and the significance of adhering to the dosage schedule. It is important to set up a monitoring and feedback mechanism for communication strategy and actions at the smallest administrative level. Such a strategy is crucial not only for fixing problems but in keeping the providers motivated. In case of VAS administration programme, simple rapid household survey could be useful to get information on the knowledge of five “Ws” at family level – what are the vitamin A supplements, where and when do you get them, who are they for and why do you want them. Moreover, feedback on the sources of information about vitamin A as well as whose opinion on VAS administration is of significance to the family has been proposed to be useful for re-visiting and modifying communication strategy [120]. For effective implementation of VAS administration, training of health persons and other stakeholders is critical. Training needs to stress on the significance of VAD on child survival, the methods to be adopted for identifying and enlisting all beneficiaries at risk of VAD, understanding of comprehensive strategy comprising breastfeed, dietary diversification, fortification and supplementation, treatment and prevention protocol of the supplement for preschool children and mothers, recognizing signs and symptoms of deficiency, treatment schedule to be followed for children with xerophthalmia, diarrhoea, measles and severe malnutrition. In addition, training needs to address programme issues with reference to logistics management, communication strategy and monitoring, as well as recording mechanism to be followed. It is critical that training emphasizes on the safety of VAS and the importance of adhering to the recommended doses of VAS as well as the need to take cautions for preventing over dosage which could cause toxicity (see Box 16.4). Monitoring VAS programme The system for monitoring of administration of VAS needs to be designed with the objective to provide information on the “effective coverage”, i.e. the proportion of children receiving two annual doses of vitamin A [65]. Recording of VAS in special tally sheets or within the maternal and child health or immunization programme has been streamlined in many countries by recording the information in the existing health or nutrition record systems such as growth charts,

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Box 16.4 Safety of administration of vitamin A supplements to infants and children The recommended high doses of vitamin A supplements for children and mothers are perfectly safe [97]. Clinical Toxicity due to hypervitaminosis does not result from public health intervention programmes [114]. Virtually no risk has been observed when prophylactic vitamin A doses, two doses of 200,000 IU separated at least by one month interval is administered to 1–6 years old. About 200 cases of hypervitaminosis are estimated to occur annually compared to an estimated 3 million preschool children who develop VAD each year and are exposed to an increased risk of morbidity, mortality with 250,000–300,000 becoming blind [115]. Administration of excessive amount of vitamin A supplement can lead to toxicity or hypervitaminosis. The manifestations of toxicity depend on age of the individual, hepatic function, dose and duration of vitamin A administration and the vitamin A status. The adverse effects of periodical vitamin A supplementation are occasional in the range of 1.5–7.0% [114]. The symptoms reported are mild and transient [114]. The side effects experienced are loose stools, headache, irritability, fever, nausea, vomiting which disappear practically in all children within 24–48 hours. In neonates and young infants under the age of six months, vitamin A supplementation has been associated with an increased incidence of transient bulging of fontanelle that resolves within 24–72 hours. The recommended postpartum two doses of vitamin A of 200,000 IU are reported to be well tolerated [97]. Toxicity, acute or chronic, has been reported with the abuse of vitamin A supplements. Signs and symptoms of acute vitamin A toxicity (single ingestion of 25,000 IU per kg body weight or 500,000 IU consumed over a short timeappear within 8–24 hours after ingestion and include manifestations such as nausea, vomiting, diarrhoea, changes in behaviour, increased intracranial pressure causing headache, diplopia, papilloedema and bulged fontanelle in infants and skin changes etc [116–118]. Chronic hyper vitaminosis A results from long term intake of moderate vitamin A doses (about 4000 IU/kg body weight or over >18000 IU) daily for 6–15 months. The symptoms are low grade fever, headache, fatigue, irritability, anorexia, loss of weight, gastrointestinal disturbances, hapatosplenomegaly, skin changes, anemia, hypercalcemia, pseudotumor cerebri, etc [58–60]. Toxicity is reversible by discontinuing vitamin A but may take several weeks. During pregnancy, the recommended vitamin A supplement is recommended to be limited to 10,000 IU .This level of daily consumption is safe and beneficial. Vitamin A supplement exceeding 10,000 IU/day, especially in early pregnancy, may cause major birth defects and are considered harmful [119].

family-held immunisation cards and health records. Record keeping of VAS administered is considered essential not only for monitoring coverage but also for serving as an effective tool to intensify efforts to ensure full coverage as well as for avoiding dose duplication and potential side effects. Box 16.4 presents details regarding the issues pertaining to safety of administration of vitamin A supplements to infants and children. For measuring progress of vitamin A supplementation programme, indicator used is the percentage of children between the ages of 6 and 59 months receiving two annual doses of vitamin A, 4–6 months apart. Only a few countries carry out coverage surveys immediately following VAS distribution using methods similar to those developed to track

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immunisation coverage [65]. Data on number of children receiving vitamin A distribution from one distribution to the next is more easily available than information on specific children receiving two doses per year which denotes “effective coverage” or full protection to children. In the absence of such data, assumptions for two doses of vitamin A administered are being derived from the information available regarding percentage coverage of children in a population for at least one high dose of VAS in the past six months. Efforts are ongoing to improve the recording system with a view to overcome the constraint and facilitate direct monitoring of two dose coverage [56]. Progress in vitamin A supplementation coverage Assessment has been undertaken in a total of 103 countries [66]. These countries were identified as priority countries for vitamin A supplementation – 61 countries with high U5MR, 35 additional countries with relatively low U5MR but elevated prevalence of VAD and another seven countries which continued to consider vitamin A deficiency as a public health problem. It was estimated that only 26 of the 103 priority countries attained effective coverage levels in 2004, i.e. reached at least 70 percent children with two rounds of VAS. There was a sharp increase reported in the global coverage with two doses of VAS during the years 1999–2004. In 1999, globally only 16% of children were fully protected with two annual doses which increased to 58% in 2004, 72% in 2005 and a drop to 62% was observed in 2007. The reduction in overall percentage coverage observed in 2007 was attributed to the drop in percentage coverage reported from India with the introduction of policy in the year to extend VAS coverage to children over 3–6 years in the national VAS programme instead of focusing on only 6 months to three years (Fig. 16.4). It is evident from reported data that despite such an accelerated progress since 1999, further effort is required to reach every child with VAS twice a year and sustain universal coverage for as long as the need is evident.

16.4 Global (a) one-dose and two-dose coverage trends, 1999–2007 [56,70] (a)

Global coverage calculations exclude China

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Administration of VAS to women at the contact during delivery or at the contact with mother during newborn’s first immunization with BCG has been reported to be rather low. By 2004, post-partum administration of VAS has been reported to be operational in only two-thirds of the 103 countries identified as priority countries for addressing VAD [56] and only 12 countries exceeded 50% coverage: Azerbaijan, Benin, Cape Verde, Egypt, Honduras, Marshall Islands, Morocco, Myanmar, Oman, Sao Tome and Principe, Tajikistan and Vietnam. Analysis of success of VAS programme reveals that the success and continuity of the programme depends greatly on political commitment, vitamin A supplies being available regularly at peripheral level, c o m m u n i t y a w a r e n e s s a n d d e m a n d . Ti m e l y p r o c u r e m e n t a n d distribution of VAS supply is critical. Procurement involves adequate resources, timely purchase of appropriate quantities of VAS supplies according to the size of the target population and appropriate logistic system for effective distribution. Determination of supply requirement needs to be assessed on the basis of population age group and percentage coverage planned with preventive dosage of VAS. An additional supply of VAS is required for special conditions such as xerophthalmia or clinical VAD, measles, diarrhoea, severe protein–energy malnutrition. Indicators for assessment – elimination of vitamin A deficiency. For assessing, the virtual elimination of VAD, the following indicators have been proposed (Table 16.13). Table 16.13 Core indicators for assessing progress towards the goal of virtual elimination of VAD [6, 92–96, 98] Functional indicator (a) Night blindness (children 24–71 months of age) Biochemical indicators Serum retinol <0.70 µmol/L (children 6–71 months of age) or Breast milk retinol <1.05 µmol/L or <8 µg/g milk fat (a)

(b)

Prevalence goal < 1% <15%(b) < 10%

Other clinical indicators of xerophthalmia, i.e. conjunctival xerosis with Bitot’s spots (X1 B) <0.5%; corneal xerosis/ulceration/keratomalacia (X2, X3A, X3B) <0.01%; corneal scars (XS) <0.05%, where known to occur can also be used to assess progress towards eliminating VAD and especially towards eliminating vitamin A. The prevalence criteria in 2001 was proposed to be raised from >5% to >15%.

The big challenge for prevention and control of VAD is to effectively implement the well-integrated mix of interventions that including foodbased approach to improve overall dietary supply and quality, improving infant and young child feeding practices, ensuring food fortification

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reaching the most deprived population section and universal coverage of young children with vitamin A supplementation for prevention of VAD. For elimination of VAD, integrated efforts for VAD control need to be combined with overall maternal and child public health measures to reduce infections and improve mother’s nutritional status.

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17 Vitamin A prevention and control programme in India – past efforts and current status Sheila C. Vir and Richa Singh Pandey

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India. Richa Singh Pandey, MD (Community Medicine), has several years of experience in the field of public health and nutrition. Dr. Singh is currently a nutrition specialist with UNICEF (India). Prior to joining UNICEF, she worked on an important newborn care project with Saksham Study group of Johns Hopkins–King George Medical College Collaborative Centre and as a consultant with UNICEF on maternal child health and nutrition issues.

17.1

Vitamin A deficiency status in India

Vitamin A deficiency (VAD) has been recognised as a major public health problem in India since 1960s. Surveys carried out in the southern and eastern parts of the country during this period had revealed that at least 30–50% of all children in the preschool age group suffered from eye manifestations as a result of deficiency of vitamin A [1]. It was estimated that about 12,000–14,000 children became blind in the country as result of keratomalacia caused due to severe deficiency of vitamin A. Studies of the past two decades indicate a substantial reduction in severe VAD problem and a reduction in ocular signs caused due to deficiency of vitamin A (Table 17.1). Such a decreasing trend observed in the

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Table 17.1 Reported prevalence of VAD in India Year 1971–74 1975–79 1988–90 1995 1998 1998 1998 1998 2000 2000

Prevalence (%) 2.0 2.0 0.7 1.4 0.21 0.11 0.05 0.05 0.7–2.2 1.2–4.0

Criteria Nutritional blindness(a) [2] Bitot’s spot(c) [3] Bitot’s spot(c) [4] Bitot’s spot(a) [5] Bitot’s spot(b) [6] Corneal xerosis(b) [6] Keratomalacia(b) [6] Corneal opacity(b) [6] Bitot’s spot [7] Night blindness [7]

prevalence of VAD coincides with the implementation of the National Vitamin A Prophylaxis Programme in the entire country in the early 1970s under the Fourth Five Year Plan [1]. No national survey on prevalence of VAD has been undertaken in the country. The Ministry of Human Resource, however, has compiled data of three major surveys and developed a national database on clinical signs of xerophthalmia [6]. The emerging national profile on prevalence of VAD indicates a wide variation in VAD prevalence in 26 states/union territories (Table 17.2).VAD surveys within a state report a wide intra-district and cluster to cluster variation in VAD prevalence in preschool children [8]. Despite reduction in clinical signs of VAD, subclinical deficiency of vitamin A continues to be widespread. This is evident from the data presented in Table 17.3 [9–11]. Subclinical VAD as measured by serum retinol levels, below 0.7 μg/dl [9–11], in children below 6 years is reported to be between 34% and 60% while the corresponding clinical VAD prevalence is found to be rather low. The data available from the Indian Council of Medical Research (1999) from 5 districts indicate an average prevalence rate of 1.84% night blindness, 1.12% Bitot’s spot and 0.15% corneal scars [12]. These survey findings confirm vitamin A deficiency disorders (VADD) is a public health problem in India. The primary cause of widespread VADD in preschool children is low dietary intake of vitamin A and carotenoids by infants and children (Table 17.4) [6, 13, 14]. The average intake of vitamin A by preschool children is reported to range between 106 and 214 mg with almost 80 percent have intakes less than 50 percent of the recommended dietary allowance (RDA). Such low intake of vitamin A combined with recurrent infection result in poor vitamin A status of preschool children.

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Table 17.2 Prevalence (%) of vitamin A deficiency signs in 26 states/union territories (UTs) of India [6] State/UT

Bitot’s spot

Haryana Mizoram Himachal Pradesh Nagaland Punjab Tripura Rajasthan Dadra Nagar Haveli Chandigarh Daman & Diu Delhi Goa Bihar Gujarat Sikkim Maharashtra Orissa Kerala Arunachal Pradesh Karnataka Assam Tamil Nadu Manipur Andhra Pradesh Meghalaya

0.04 2.97 0.01 0.35 0.12 0.02 0.22 0.38 0 0.05 0.05 0 0.14 0.20 0.19 0.72 0.86 0.25 0.34 0.77 0.45 3.11 0.14 0.79 0.18

Madhya Pradesh

2.62

Table 17.3 Prevalence of vitamin A deficiency in children in the state of UP [9–11] Districts

Prevalence of Bitot’s spot (%)

Plasma retinol (% <0.07 µg/dl)

Plasma retinol (% <0.35 µg/dl)

Dehradun Badaun Mainpuri L.Kheri Bahraich Hardoi Sitapur Rai Bareilly Unnao

0.02 0.0 0.96 0.46 5.6 – – – –

– – – 55.8 – 38.8 50.0 33.8 44.8

– – – 4.2 – 4.1 3.0 4.2 12.7

Lucknow

–

59.7

12.6

476

Public health nutrition in developing countries Table 17.4 Intake of vitamin A (IU/day) [6,13,14] Vitamin A intake (IU/day)

1-3 years

4-6 years

RDA

400

400

201 50 106 26.5 129 32.3

214 60 127 31.8 166 41.5

(1998) 2002 2006

intake % RDA intake % RDA intake % RDA

Maternal VAD is reported to be common in India. Clinical reports published during 1960s indicated problem of night blindness in pregnant and lactating women [15, 16, 17]. Night blindness during pregnancy has also been reported in the nutritional surveys undertaken in India in the last decade [6, 18, 19]. Studies from the National Institute of Nutrition indicated 4% of pregnant women belonging to low socio-economic status had night blindness during the third trimester while all the pregnant women surveyed had low serum retinol levels <30 g/dl [19]. The data of the DWCD and the National Family Health Surveys 2 [6, 18] confirm that maternal night blindness (Table 17.5) is prevalent and that there is wide variation from state to state [7, 18]. Nutrition survey among tea estate women workers in Assam state in 2008 also reveals that 16.3 percent women during the last pregnancy had a history of night blindness [20]. The high prevalence of maternal night blindness is a proxy indicator of vitamin A deficiency in a community. A percentage prevalence rate of over 5 percent maternal night blindness indicates VAD to be a public health problem in the population surveyed [21].

17.2

Measures taken for prevention and control of VAD

Recognizing vitamin A deficiency to be a public health problem, efforts have been made in India since 1970s to control the deficiency. Promotion of diets rich in vitamin A including promotion of exclusive breastfeeding to infants in the first six months and appropriate complementary feeding from six months onwards have been recognised to be the long-term solution to overcome VAD. Role of food fortification of dairy products and fats and oils in controlling VAD has been considered important. Efforts are being directed to identify suitable food vehicles for vitamin A fortification. Higher priority is being accorded for ensuring access to vitamin A fortified foods by economically deprived population. Appreciating the slow progress in dietary intervention measures, intensive efforts are continuously being made to strengthen the vitamin A supplement (VAS) administration programme for preschool children and establish a suitable VAS delivery

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Table 17.5 Prevalence of clinical vitamin A deficiency [6, 18] State/UT Delhi Haryana Himachal Pradesh Chandigarh Jammu & Kashmir Punjab Rajasthan Madhya Pradesh Uttar Pradesh Bihar Orissa West Bengal Arunachal Pradesh Assam Manipur Meghalaya Mizoram Nagaland Sikkim Goa Gujarat Maharashtra Andhra Pradesh Dadra & Nagar Haveli Daman & Diu Karnataka Kerala Tamil Nadu Tripura WHO cut-off for public health problem

Bitot’s spot (%) [7] 0.05 0.04 0.01 0 0.12 0.22 2.62 0.14 0.86 0.34 0.45 0.14 0.18 2.97 0.35 0.19 0 0.20 0.72 0.79 0.38 0 0.77 0.25 3.11 0.02 > 0.5%

Maternalnightblindness opacity [18] 3.8 1 3.8 18.5 0.8 14.7 19.7 14 19.4 18.7 11.6 20.2 6.9 8.5 23.9 14.6 21.1 21.6 2.2 10.9 9.7 5.3 6.3 2.1 3.7 Do not exist

mechanism to ensure each preschool child receives at least two doses of VAS six months apart in a year. This chapter primarily focuses on the vitamin A supplementation component of the VAD programme.

17.3

Vitamin A supplementation programme

In India VAS programme implementation commenced in 1970 and it was the first country to launch the VAS administration programme. The evolvement of the VAS programme in the last three decades, with reference to policy and delivery mechanism model, can be broadly divided into the following three phases: ● Phase I – Launch of Vitamin A Prophylaxis Programme for Prevention of Nutritional Blindness, 1971 ● Phase II – Revision of Policy in 1991 and Integration of Vitamin A Programme with the child survival efforts

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Phase III – Acceleration of vitamin A programme — establishing effective biannual VAS Delivery Model, 2000

(a) Phase I – National Vitamin A Prophylaxis Programme for Prevention of Blindness In India, the National Programme for Prevention of Vitamin A Deficiency was launched by the Ministry of Health and Family Welfare in 1971 as nutritional blindness prevention programme under the Fourth Five Year Plan [1, 22]. It was estimated that such a programme will prevent vitamin A deficiency which was contributing to about 20% of all cases of blindness [23]. The most important rational approach to address the problem of VAD was to increase the dietary intake of vitamin A. Such an approach was viewed as a time-consuming complex process which would delay in preventing children from going blind. Urgent measures were required. Administration of massive dose of vitamin A supplementation (VAS) was the solution proposed to prevent VAD and associated blindness [1]. The national programme initially focused on children residing in only seven states of the country where VAD prevalence was considered high [22]. Later, the programme was extended to all other states. Under the programme children 1–5 years received 2 ml of syrup providing 200,000 IU of vitamin A, once in six months. The dosage and frequency was based on clinic-based studies by Srikantia and Reddy in 1969 and 1970 [24, 25]. These studies concluded that oral administration of 300,000 IU of oil soluble preparation of vitamin A was associated with less toxicity and also sustained normal serum retinol levels for a period of six months. It was observed that in situation where dietary intakes were very poor, the levels were maintained for a period of 3–4 months [26]. Extensive field trials were undertaken involving 2500 preschool rural children who were administered 300,000 IU vitamin A in oil once a year over a period of five years. The prevalence of ocular signs of vitamin A deficiency was reduced by 75% from a baseline of 10%. No new cases of corneal lesions were reported during the study period [27]. Based on these trials, it was recommended that all children at risk be given vitamin A supplement of 200,000 IU biannually to prevent blindness. Such a dose was considered appropriate to prevent blindness and was not expected to completely build up the stores and prevent vitamin A deficiency. Based on these recommendations of the dosage, a meeting of state officers was organised in June 1970 and an operational plan for the national VAS programme was developed. The vitamin A programme was launched in 1971. In view of the limited resources, the programme was initially confined to such areas where prevalence of vitamin A deficiency was believed to be high. The programme in the first year aimed at covering all children 1–3 years. Later under the

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programme, all children of 1–5 years were recommended to be provided with six monthly dosage of 200,000 IU vitamin A. Initially 1.6 million children in 7 states of the country were covered [22]. The technical information issued by the Maternal Child Health (MCH : No.2) stated “As coverage of the entire age group and avoidance of any repeated administration of the drug are of great importance, it is desirable to fix a specified period for administering the programme. For example, the primary health centre/urban MCH centre may decide to cover all eligible children during the month of September 1970 and complete the administration of the drug during the period of one month; the administration of the next dose to these children as well as new children to be included, would then have to be done in March 1971 only” [1]. Vitamin A, specially prepared for the programme, contained 100,000 IU per ml of syrup. A spoon of 2 ml was supplied with each 100 cc bottle of vitamin A solution .The Maternal and Child Health and Family Welfare Organization was responsible for the implementation of the programme through the primary health centres. The Auxiliary Nurse Midwife (ANM) and other paramedical working in primary health centres were responsible for administering the VAS concentrate to children in rural centres, under the supervision of medical officers. In urban areas, the programme was instructed to be administered at child welfare clinics of urban family planning centres. For effective coverage and to avoid repeated administration, it was recommended that the distribution be done during a fixed time period, on a “crash” basis instead of spreading it over prolonged periods. An interim evaluation was undertaken in two states, Karnataka and Kerala, after the children had received at least two massive doses of vitamin A. The coverage was 75–90% of the expected number of children and there was 75% reduction in the prevalence of conjunctiva signs of vitamin A deficiency in children who had received two doses of vitamin A [22]. The results demonstrated the administration feasibility of VAS on large scale and indicated that massive dose of vitamin A could be administered as a public health programme without requiring any significant additional inputs. On the basis of these findings, the vitamin A programme was later extended to several states. In 1975, the Department of Family Welfare of the Government of India assigned the task of a comprehensive evaluation of the vitamin A massive dose programme to the National Institute of Nutrition in 1975 [3]. The programme was evaluated in 1976. Thirteen states where the programme was in operation for a minimum period of two years at the time of evaluation in 1978 were selected [22]. These 13 states were Andhra Pradesh, Bihar, Gujarat, Haryana, Karnataka, Kerala, Orissa, Madhya Pradesh, Maharashtra, Rajasthan, Tamil Nadu, Uttar Pradesh and West Bengal. The

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evaluation was finally conducted in only 8 states between January and July 1978 and the 5 states that were excluded for various reasons were Bihar, Madhya Pradesh, Haryana, Tamil Nadu and Uttar Pradesh. About 69,000 children were covered and the incidence of Bitot’s spot was assessed age-wise to study the impact of the massive dose of vitamin A and to evaluate the operational aspects. The findings revealed that the programme guidelines of “crash programme approach”, particularly with respect to administering VAS during the fixed months of the year, were not followed in many primary health centres, except in two of the eight states, i.e. Andhra Pradesh and Karnataka. Vomiting was reported to be the side effect of commonly encountered by almost all 33 workers of 42 sub-centres interviewed while diarrhoea and fever were reported occasionally. All workers mentioned such side effects were observed in children under two years and were transitory. These symptoms “subsided by itself” [3]. Recording of information on vitamin A dose administered was poor except in Karnataka where separate record registers were provided. Massive dose of vitamin A supplements were reported to be well accepted by community and effort to create awareness was considered essential. The study identified several operational problems including problems in supply of vitamin A, poor knowledge of the programme amongst functionaries, reliance on clinic rather than extension approach and low community awareness. (b) Phase II – Reformulation of policy and its implementation The Government of India in September 1988 constituted a Task Force [28] to study various operational issues of the National Prophylaxis Programme for Prevention of Blindness Due to Vitamin A deficiency (NPPVAD) and propose measures for increasing VAS coverage. It was observed by the Task Force that NPPVAD was implemented as a part of the Maternal and Child Health (MCH) programme of the health sector but was a low priority programme. It was estimated that only 30-million or 30% of the children in the vulnerable age group of 1–5 years were being covered under the programme. For improving VAS coverage, as per the direction of the Task Force, a study on the supply stock situation of vitamin A concentrate dose manufactured and supplied under the NPPVAD was undertaken [29]. The supply study reported that in 1985, the projected consumption of vitamin A in the country was 90 million mega units (MMU) and of this only 11.76 MMU was for vitamin A prophylaxis programme while the rest was allocated for use as additive to vanaspati, cattle and poultry feed and other pharmaceutical uses. Following report of the production and supply of vitamin A in India, it was proposed by the Task Force on 8th May 1989 to

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link VAS administration with Universal Immunisation Programme or UIP (including the first dose of vitamin A administered at the time of measles vaccine and the second with DPT booster). It was envisaged that such a system for VAS delivery would result in achieving a high coverage with VAS in preschool children without causing any additional pressure on the existing infrastructural and operational costs. With such a strategy of linking VAS with UIP, it was projected that by 1995, the requirement for vitamin A supplement would increase significantly to 25 MMU from 10 MMU. It was recommended that the existing technology for the production of vitamin A supplement therefore be updated to meet the increase in supply requirement and VAS be made available at a reasonable controlled price. The price of syrup was then estimated to be Rs 28 per 100 ml or about 56 paise (1.2 US cents) for one mega dose of 200,000 IU (equivalent to 110 mg vitamin A Palmitate or 66 mg of vitamin A acetate). The guidelines issued by WHO in 1988 for improving coverage of vitamin A dosage by linking with Expanded Programme Immunisation or EPI [30] gave an impetus to the decision of the Task Force of the Ministry of Health and Family Welfare, Government of India to consider linking vitamin A massive dose programme with the Universal Immunisation Programme (UIP). The World Summit for Children in 1991 drew the attention of global leaders for urgently addressing the problem of VAD and for directing efforts to rapidly improve the vitamin A supplement coverage of preschool children for reducing child mortality and improving child survival [31]. The Government of India revisited the NPPVAD which had been in operation in the entire country since the Fourth Five Year Maternal Child Health (MCH) Plan. The Ministry of Health and Family Welfare in 1990, in collaboration with UNICEF, constituted an expert Task Force under the chairmanship of Commissioner MCH [33]. The Task Force primarily debated on the issue of inclusion of infants 6–12 months as beneficiaries of VAS programme, proposing a suitable delivery system for administering VAS to infants, overall management of NPPVAD and proposing the treatment dosage for clinical cases of VAD. The Task Force took into consideration the increasing evidence that vitamin A supplement administration (VAS) influenced child survival and that the impact of VAS was not limited to mere prevention of nutritional blindness. The protective effect of vitamin A supplement during episodes of measles and the advantages of administering massive dose of vitamin A supplement at 9 months along with measles vaccine was reviewed [30]. The Task Force agreed to include children 6–11 months in the vitamin A programme and administer VAS dose of 100,000 IU. For administering VAS to infants, the contact with infants during measles vaccination at 9 months was considered practical. The combined VAS-measles vaccine administration

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policy was further supported and influenced by the findings of the National Institute of Nutrition (NIN) which observed that seroconversion rates of measles vaccine were significantly improved (84%) when vitamin A supplement was co-administered with vaccine compared to low rate (63%) under routine field conditions of immunization. This combined schedule was reported to be effective in improving serum retinol levels [33]. Such a strategy was found to be beneficial, safe and feasible. In 1991, based on the recommendations of the Task Force, a new revised “Policy on Management of Vitamin A Deficiency” was formulated [34] and issued by the Ministry of Health and Family Welfare of the Government of India (Box 17.1). Box 17.1 Policy on management of vitamin A deficiency 1991 [34] “Administration of massive dose of vitamin A to preschool children at periodic intervals is a simple, effective and most direct intervention strategy. This is a short term strategy. Under the massive dose programme every infant 6–11 months and children 1–5 years is to be administered vitamin A every 6 months. Priority is to be given for coverage of children 6 months – 3 years since the highest prevalence of clinical signs of vitamin A deficiency is reported in these age group. The recommended schedule is as follows: 6-11 months – 1 dose of 100, 000 IU 1-5 years – 200, 000 / 6 months A child must receive a total of 9 oral doses of vitamin A by its 5th birthday. The contact with an infant during administration of measles vaccine between the age of 9–12 months is considered a practical time for administrating the vitamin A supplement – 100, 000 IU for infants. A camp approach may be used for administering vitamin A to children 1–3 years and 3–5 years. However, the DPT /OPV booster in mid 2nd year to a child is a suitable time for the 2nd dose of vitamin A. Wherever ICDS programme is functioning, AWW should be involved in the distribution and administration of vitamin A. Treatment dose – all children with clinical signs of vitamin A deficiency must be treated as early as possible. Treatment schedule is to administer 200,000 IU of vitamin A immediately after diagnosis. This must be followed by another dose of 200,000 IU 1–4 weeks later. Children with eye lesions must be treated immediately with vitamin A even if they are being refereed for special care. Vitamin A syrup concentrate, as per the Policy, be made available at primary health centres and sub-health centres in the form of flavoured syrup at a concentration of 100,000 IU/ml or 100,000 IU capsule only for 6-11 months (fixed dose 100,000 IU vitamin A capsules is referred in the Policy). For children 1–5, vitamin A only in syrup form is recommended. Vitamin A solution bottle, once opened, is advised to be utilized within 6–8 weeks. The Policy also focuses on promoting consumption of vitamin A rich food. Breastfeeding, including feeding of colostrum is emphasized. Feeding of locally available β -carotene (precursor of vitamin A) rich food such as green leafy vegetables and yellow and orange vegetables and fruits like pumpkin, carrots, papaya, mango, oranges etc along with cereal and pulse to a weaning child is stressed and should be promoted. In addition, whenever economically feasible consumption of milk, cheese, paneer, yogurt, ghee, eggs, liver, etc. is advised to be promoted.

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The Policy emphasizes on the dietary measures – promotion of breastfeeding, including feeding of colostrum, and foods rich in vitamin A as well as recommends universal coverage of children 6 months to 5 years with six monthly high dose vitamin A supplements (Box 17.1). A total of nine doses of VAS are instructed to be administered by the fifth birthday while priority for administration of VAS is instructed to be given to children between 6 months and 3 years. The Policy recognizes that the contact with infants during measles immunization is a practical approach for providing the first dose of vitamin A to a large number of children 6– 11 months. The policy also defines the vitamin A supplementation schedule for treatment of VAD cases. India VAD programme Policy does not include prophylactic VAS administration for women in the reproductive age. During pregnancy and lactation, the need for regular dietary intake of vitamin A rich foods by pregnant and lactating mothers in mproving diet is emphasized. The public health strategy focuses on bringing about changes in dietary practices of the population through education and horticultural interventions. The Policy does not refer to any interventions even for treatment of maternal VAD. However, treatment of individual women with night blindness and Bitot’s spot is addressed by daily supplements of a much smaller dose of VAS of 5000–10,000 IU vitamin A per day a period of 4–6 weeks. With the emerging evidence that vitamin A content of breast milk is influenced by the maternal vitamin A status, it has been proposed that diagnosis and management of VAD be considered to be a part of routine antenatal care [35]. In 1992, the Policy guidelines for the administration of VAS to preschool children, including infants at nine months, were incorporated as one of the major activities of the Child Survival & Safe Motherhood (CSSM) Programme [36]. The VAS administration under the CSSM Programme focused only on children of 9 months to 3 years and children over 3–5 years were excluded in the operational plan. The CSSM Programme guidelines emphasized that the first dose of vitamin A (100,000 IU) be administered at nine months along with measles vaccine while contacts with children at 18 months for the DPT/OPV booster dose was considered an appropriate time for the second dose (200,000 IU). Remaining 3 doses of VAS of 200,000 IU each were to be given at six monthly intervals to children 18 months to 3 years. Treatment dose recommended in the Policy was included in the CSSM Programme. Additionally, therapeutic doses of VAS were recommended to be administered to those suffering from diarrhoea, measles and acute respiratory infections presenting with signs of vitamin A deficiency. Later, these guidelines on VAS administration that were issued under the CSSM Programme continued to be implemented under the Reproductive and

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Child Health (RCH) programme which was launched with the modification of the CSSM programme [8]. Under the CSSM and later under the RCH programme, six bottles of vitamin A supplement (VAS) syrup of 100 cc were supplied for a population of 5000, as part of “drug kit A” of the government. This was supplied every six months i.e. a total of 12 bottles of 100 cc per 5000 population per year using the following calculation (Box 17.2). The VAS supply projection was based on the assumption that a subcentre would have an average population of 5000. The supply estimated was inadequate since the population covered by the subcentre was often as high as 7000–8000 for the high population states of Uttar Pradesh, Bihar, Madhya Pradesh, Orissa, Rajasthan, etc. The VAS programme implementation was monitored as a part of the RCH programme monitoring system. However, it was observed that the record of VAS administration was maintained for only the first dose of VAS which was administered to infants along with measles vaccine. Box 17.2 Estimation of Vitamin A supplement supplied in Kit A under CSSM/RCH programmes 1. 2. 3. 4. 5. 6.

Subcentre population = 5000 Birth rate (BR) = 25/1000 live births Infants born per year = BR × subcentre population = 25/1000 × 5000 = 125 Children between 1–2 year = 125 Children between 2–3 years = 125 Requirement of 100 cc VAS Syrup bottles (a) Requirement of doses for children 9-12 months = 125 × 1 ml = 125 ml (b) Requirement of vitamin A doses for children 1–2 yrs = 125 X 2 ml × 2 times a year = 500 ml (c) Requirement of vitamin A doses for children > 2–3 yrs = 125 × 2 ml × 2 times a year = 500 ml (d) Total requirement = 125 + 500 + 500 = 1125 ml

7. Total bottles required = 1125/100 ml = 11.25 = 12 bottles

The strategy of linking first dose of VAS with measles vaccine administration proved practical [8, 38]. The national coverage for VAS increased to 48.9% as against the all India measles coverage of 55.2% [37]. Sixteen states reported the coverage of over 55% for both measles vaccine and vitamin A administration indicating that the linkage of administrating VAS with measles vaccine was effective in reaching children 6–12 months. On the other hand, coverage of children 1–3 years with the second and third dose continued to be as low as 3 percent – in fact the drop out rate from the first to the third dose was reported to be 91% [7]. In 1998, studies conducted in Madhya Pradesh and West Bengal highlighted the constraints in vitamin A programme with regard to inadequate and irregular supply of VAS, poor logistics management

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and monitoring. The study of Madhya Pradesh also reported that only 28% children had ever received vitamin A syrup [39]. The findings of national and state surveys revealed that the strategy of integrating vitamin A supplementation into routine health services of RCH had improved the coverage of children only within the first year of life .Once children were immunized, there was no contact of children with the health system except when children were sick. It was therefore evident that a mechanism was required to reach children with VAS during the critical years of preschool children. A delivery approach for VAS that would reach out to a much larger number of children under 5 years was apparently essential to attain the levels of population coverage that would result in achieving the full potential of benefits of vitamin A supplement on child survival [8, 9, 39]. A need for an establishment of a reliable delivery mechanism to reach children with the six monthly dosage of VAS was considered critical. The challenge for the success of VAS programme was to address programme issues such as irregularity in supply of vitamin A, poor orientation of the functionaries who were providing the services to the population, lack of supervision and lack of inter-sector coordination between the health functionaries and the Integrated Child Development Services (ICDS) functionaries. (c) Phase III – Emergence of VAS Delivery System Models In mid 1990s, there was a global level effort to revive the VAS programme by linking VAS administration with polio NIDs (National Immunisation Days). In July 1998, a Joint WHO /UNICEF statement [40] encouraged all countries where VAD was a public health problem to include policy of administration of age appropriate VAS dosage to children during NIDs – an integration of “two powerful child survival tools”. Between October 1999 to March 2000, VAS administration linkage with polio vaccine was administered in two states, Orissa and Uttar Pradesh [41, 42]. Linking vitamin A with Pulse Polio Immunization (PPI) provided different experiences. In Orissa, where a systematic effort was made to link VAS administration with PPI, the coverage rates were high. The risk of immediate side effects such as fever, nausea and vomiting reported from Orissa was about 3% for children administered vitamin A dose along with oral polio vaccine. This incidence of illness reported in children with combined VAS and polio administration was similar to those who received only vitamin A or received neither VAS nor OPV [8, 41]. In the state of Uttar Pradesh, the coverage of VAS showed a wide variation and the poor coverage was attributed to poor logistic support as well as poor organization, training and absence of monitoring mechanism [8]. The

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National Consultation on vitamin A held in September 2000 recommended not linking VAS administration with polio vaccine administration in the country and alternative strategies to be explored for improving VAS coverage [43].The strategy of administering VAS along with measles vaccine at 9 months was recommended to be continued. The significance of ensuring VAS supplementation during the second half of infancy was considered critical for the reported benefits on child health [35]. In early 2000, a number of delivery strategies were experimented for vitamin A supplement (VAS) administration such as intensive campaign approach as well as the biannual delivery strategy [8]. The early trials of the biannual strategy in the two fixed months of the year (June and December), undertaken in the state of Uttar Pradesh, were reviewed by the expert working group of the Tenth Five Year Plan. The biannual strategy model was considered appropriate for up scaling the vitamin A programme in the country under the Tenth Five Year Plan [44]. It was stated in the Plan that the administration of 2nd to 5th doses of vitamin A be linked to routine immunization days in the two fixed months of the year. A number of states launched the biannual strategy with modifications introduced by the state governments in the operational plan. Between 2001 and 2008, the fixed month biannual strategy programme was reported to have been established in at least 10 states – Assam, Bihar, Chattisgarh, Gujrat, Jharkhand, Karnatka, Madhya Pradesh, Orissa, Tamil Nadu, Uttar Pradesh. In September 2007, all children upto 5 years and not only upto 3 years were instructed by the Government of India to be covered under the VAS Programme in the entire country [45]. The instruction of the government to include children over 3–5 years under the RCH-2 was revived (earlier also stated in the Vitamin A Management Policy of 1991 of the Government of India [34] which included all children 6 months to 5 years) since reaching all preschool children was considered critical for improving child survival. The biannual strategy of vitamin A programme emphasizes on the organization of six-monthly VAS administration sessions in fixed period of the year along with community mobilization. As per the biannual strategy, two months, six months apart are identified as VAS months, when vitamin A doses are to be administered. All states follow the RCH guidelines and administer the first dose to infants only at nine months. However, the strategy for administering the first dose differs. Some states continue to administer the first dose along with measles vaccine while others adopt the strategy of giving all the nine doses to children 9 months to 5 years in the fixed designated months. Vitamin A supplementation is administered through the existing network of primary health centres and sub-centres under the Reproductive and Child Health Programme 2 [46– 48]. The female multipurpose worker (Auxillary Nurse Mid-wife or ANM)

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and other paramedics of the health centres are responsible for administering vitamin A concentrates universally to children in the 9–59 months of age. The services of frontline workers of Health and ICDS (ASHAs or Accredited Social Health Activist who is a community volunteer under the National Rural Health Mission and anganwadi workers or AWW of ICDS) are utilized for the implementation of the programme. In some states, the VAS programme has been successfully used as a stand alone programme while in a few as an entry point to address other important child nutrition issues such as iodised salt promotion, campaign for identifying severely undernourished etc [46–48]. The bi-annual events require a significant amount of planning, logistical support, training, monitoring and coordination with other sectors to enable health systems to reach marginalized communities at least twice a year with VAS and a basic package of services. Effective district planning and implementation include defining roles of the primary stakeholders and developing their capacity to execute their roles, ensuring timely supply of VAS, effective communication and social mobilisation, establishing a monitoring mechanism. The Tenth Plan recommendations that the two months (pre-summer/ pre-winter period) in a year, 6 months apart should be taken up for VAS distribution for coverage of children has resulted in accelerating the adoption of the biannual strategy. The state implementation plans focus on the enumeration of children under five years, ensuring VAS supply and appropriate logistic management, publicity of VAS distribution during the specific months through mass media as well as peripheral health workers, organization of regular training and orientation sessions and establishing a system for the maintenance of records of VAS coverage. Successful demonstration of biannual VAS in various states has resulted in incorporation of this strategy in the ongoing Eleventh Five Year Plan by the Government of India [49]. Details of the process and impact of establishment of a biannual strategy VAS Programme are evident from the details presented for a state of northern India, Uttar Pradesh.

17.4

Establishment of the biannual fixed month strategy – an overview of a state initiative

The efforts made to accelerate the vitamin A supplementation (VAS) programme through the launch of the biannual strategy in the state of Uttar Pradesh is presented at the time of launch of the biannual strategy, Uttar Pradesh, the largest state in India had a population of approximately 190 m, a high infant mortality rate (67/1000 live births), under-five mortality rate (96/1000 live births) and a very high incidence of malnutrition (>42% in <3 years children). Poor infant feeding practices, frequent infections like diarrhoea and acute respiratory infections (ARI) and micronutrient

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deficiency (vitamin A, iron, iodine) contribute significantly to malnutrition, morbidity and mortality in children. For evidence-based planning of VAD elimination programme in the state as well as for seeking high political support, a survey was undertaken in 1999 in the four regions of the state to estimate the prevalence of vitamin A deficiency [50]. A total of 46,544 children between 2 and 6 years were surveyed for night blindness and 58,216 children 6 months to 6 years were examined for the assessment of Bitot’s spot. The study revealed a very high presence of clinical vitamin A deficiency in the state as indicated in the Table 17.6 below. The incidence of Bitot’s spot with conjunctival xerosis was reported to be much higher than the public health level cut off of 0.5%. The survey findings confirmed that VAD is an important public health problem in the state (Table 17.6). The coverage of children who were reported to have received vitamin A supplementation (VAS) was reported to be one of the poorest in the country – only 14.3 % of the population ever receiving the first dose. Coverage with subsequent 2nd to 5th dose was extremely low with dropout for 3rd dose being 91% [51]. The national survey findings of 1998–99 [18] also revealed that the supplementation with vitamin A doses was very low with only 10% children reported to have received at least one dose of vitamin A supplement. It was noted that the primary coverage was in the age group of 9–12 months with estimated 68.1% infants receiving VAS during measles vaccination. Coverage with 2nd to 5th dose was reported to be almost negligible. Table 17.6 Prevalence of Bitot’s spot and night blindness in children in the state of Uttar Pradesh [6] District

Year when study was conducted

Bahraich 1999 Badayun 2001 Mirzapur 2001 Etawah 2001

No. of children surveyed 2–6 6 moths years to 6 years

Prevalence of Bitot’s spot (6 months to 6 years)

11989 11509 12120 10926

5.6% 9.17% 10.5% 1.9%

14250 14686 14940 14340

Prevalence of night blindness (2–6 years) 3.4% 4.7% 9.7% 7.1%

Prevalence of malnutrition (weight/age) – 74.9% 56.7% 49.4%

The high prevalence of clinical vitamin A deficiency and low coverage with VAS led to the launch of a pilot project in one of the districts – Bahraich district [51]. Twice yearly administration of VAS in a campaign mode was considered appropriate. The biannual strategy model focused on a one week intensive drive for improving vitamin A coverage of children 9 months to 3 years. The intervention package, besides VAS administration, focused on the administration of measles vaccines to infants 9–12 months and promoting appropriate complementary feeding practices. For promotion of complementary feeding, ANMs of health system were trained to check and

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record the practice of feeding semi-solid food to infants that was being followed by caregivers or mothers at the time of VAS and measles vaccine administration. Using a standardized recording registers, the mothers were also questioned regarding the composition and frequency of feeds and breastfeeding practices being followed. Following the analysis of this information, ANM was advised to counsel the caregivers on appropriate infant and child feeding practices along with advice to incorporate vitamin A rich food and additional 1–2 tea spoon of fat in the portion of diet being fed to a child. For launching the pilot project, children 9–36 months were enumerated by ANMs in the special registers provided for the project. A district operational plan for one week drive was developed with travel plans of each ANM to visit the 4–7 sub-centre villages with a population of about 6000–7000. In addition, VAS administration plans to reach urban children through the staff of district hospital was also worked out. Supply requirements of vitamin A, measles vaccine, etc were estimated and supplied. For measles vaccine, appropriate actions were taken for the cold chain. Social mobilisation drive for informing community of the importance of VAS and measles and the system to be adopted for monitoring vitamin A administration was planned by the health department [52]. This was followed by imparting training to ANMs and supervisors of the health department of the district. Training focused on creating data base of beneficiaries, calculating supply requirements (VAS, measles vaccine, monitoring registers and counselling printed materials), logistic management and skills in counseling on feeding and administrating VAS and measles vaccine. The health staff was also trained for organising community mobilisation drives. Community participation was ensured by undertaking intensive awareness generation activities in the district. A week long campaign, six months apart, in the months of December 2000 and June 2001 was organised. Technical, financial and logistic support for the above campaign was provided by UNICEF. The first round in December 2000 was carried out only in rural areas while the second round in June 2001 was organized both in rural and urban areas. As a result of the biannual strategy, vitamin A supplementation coverage increased from 10% in 1998–99 to 83.5% in December 2001 and measles vaccine coverage increased from 23% to 43.5% in two rounds in the district [52]. The lessons learned from the pilot project were synthesized. The campaign approach was found effective but not considered a sustainable approach for the state since the health sector manpower was occupied most of the time with pulse polio campaigns. The campaign mode for VAS administration was therefore dropped and a shift was made in the strategy [53]. The two fixed months – June and December, six months apart, were designated as the child health and nutrition months (in local language Bal

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Swasthya Poshan Mah or BSPM). The VAS programme was referred as the BSPM programme. Administration of VAS was spread out in the entire month and not limited to a week. The VAS administration was linked to the routine immunizations plans of these two months. The first dose of VAS of 9–12 months was administered along with measles vaccine throughout the year while vitamin A supplement to children >1–3 years was administered only in the two fixed BSPM months in the outreach immunisation sessions as per the routine immunisation (RI) micro-plans. Effort was also made to cover all children 9–12 month of age in these BSPM months if they had missed their first dose of vitamin A supplement during the RI sessions in the preceding six months. The biannual BSPMs were also viewed as opportunity to deliver a package of the following set of interventions for improving child health and nutrition. ●

● ●

Management of severely malnourished children (grade III and grade IV) Promotion of Infant and Young Child Feeding (IYCF) Promotion of consumption of iodised salt and organizing salt testing events at community level

The BSPM programme in the state was launched in December 2003.The two years gap in implementation of the programme, following completion of the pilot project, was due to frequent intensive pulse polio drives in the state during this period. Between 2003 and 2005, the biannual BSPM was implemented in only 18 of the 70 districts of the state with the support of UNICEF, MI and USAID/MOST. These districts were located in three distinct regions of the state comprising 180 administrative blocks with a population of 37 m and 2.5 m children (between 9 and 36 months). The programme was taken to scale in 2006 in the entire state and was included in the State Plan of Implementation of the National Rural Health Mission (NRHM) from 2007 onwards. Health and Integrated Child Development Services (ICDS) programme of district, block and village level were responsible for implementation of the BSPM activities. For maximising reach and increasing VAS coverage, an operational plan was developed using the strategy diagrammatically presented in Figure 17.1. The health sector was assigned the task of administering VAS to children while the ICDS sector with responsible for identification, listing and mobilization of beneficiaries to the VAS-immunization site. The job responsibilities of each of the two primary sectors for performing the following primary actions for the implementation of the BSPM activities was clearly defined (Box 17.3).

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17.1 Biannual child health and nutrition strategy

Box 17.3 Role of the two primary departments Health department ●

●

●

●

●

Block medical officer to prepare and share a copy of the RI microplan with the Block ICDS officer. Health Supervisors to ensure that ANMs visits RI session sites as per her microplan. ANMs to supplement first dose of vitamin A along with measles vaccine to all the children who have missed it during the routine immunization sessions through out the year. ANMs to administer second to fifth dose of vitamin A to >12-36 months children during the biannual months only (since 2007, children up to five years are reached with VAS). Compilation of ANMs report at block and further compilation of block reports at district level after completion of biannual rounds. District data to reach Directorate within one month following BSPM month (i.e. in first week of February and August).

Role of ICDS during BSPM months ● ●

●

●

●

Survey and identification of children under three and pregnant mothers by AWW Listing of under threes by AWW for following health services ■ Vitamin A supplementation ■ Routine Immunization and ■ Referral of severely malnourished children. Block ICDS officer to share the list of enumerated beneficiaries with Block Medical Officer AWW to undertake social mobilization and IEC activities for increasing VAS coverage. AWW to intensively promote exclusive breastfeeding for six months, introduction of complementary feeding after six months and consumption of iodised salt during the biannual rounds. AWW to support ANM on outreach immunization days for administration of vitamin A supplementation and routine immunization to children 9 months to 3 years (since 2007 up to 5 years).

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17.4.1 Identification and listing of beneficiaries through conducting biannual survey ICDS is the largest programme in the country having a village based worker for providing essential nutrition and health services to the community with support of health department. Under the ICDS programme, community surveys are expected to be undertaken twice a year. For identification of VAS beneficiaries, the timings of the biannual surveys were reorganized to April and October of the year to proceed the fixed months of the BSPM. The list of beneficiaries of each village was prepared and shared by block (about 100–125 villages per block) officer of ICDS (Child Development Project Officer – CDPO) with the Block Medical Officer of the Health sector.

17.4.2 Vitamin A supplement (VAS) supply VAS supply requirement based on population estimates was calculated using a bottom-up approach for district and (average 10–12 blocks per district) the state (Box 17.4). VAS supply distribution from district level to block primary health centre (about 1,00,000 population) and to the health subcentres was undertaken at least 2–4 weeks prior to the BSPM months. Each ANM was advised to carry at least two bottles of vitamin A supplement to the village on the administration day. VAS supply from 2003 to 2007 was entirely supported by UNICEF and MI.

17.4.3 Microplan development and sharing The health subcentre in India caters to a population of 5000 (5–6 villages with about 1000 persons/village) and is the smallest administrative unit of the health infrastructure. The subcentre is manned by an auxillary nurse mid-wife (ANM), a female health worker, who provides a gamut of preventive and curative services to the community residing within the subcentre area. As per the visit plan, the health worker visits each of the sub-centre villages at least once in a month for provision of health services, including routine immunization. In the state of Uttar Pradesh, Wednesday of every week is fixed for RI and the Wednesdays are known as the “RI days” of the state. The RI microplans present field visit plan on RI day for each of the ANMs of the block. The RI micro-plans at the block level is a therefore a compilation of field visit plans of each of the ANMs (about 20–30 ANMs in each block) for conducting RI sessions in the assigned sub-health centre area comprising 5–7 villages/hamlets (population 5000–7000). The RI micro plans present details of the specific outreach areas being visited by ANM for undertaking

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Box 17.4 Vitamin A supply estimation for a district with population of 1,00,000 1. 2. 3. 4. 5.

Total population Birth rate Total no. of infants (0–1 year) Total no. of 9 months–12 months (25% of total infants) Total no. of children in age groups 1–2 year, 2–3 year, 3-4 year and 4-5 year 6. Vitamin A supply calculation (in ml) (a) 9 months-12 months requiring first dose (1 ml/child × 625 children) (b) 1-2 years requiring 2nd–3rd dose (2ml/child/dose × 2500 children × 2 doses) (c) 2-3 years requiring 4th and 5th dose (2 ml/child/dose × 2500 children × 2 doses) (d) 3-4 years requiring 6th and 7th dose (2 ml/child/dose × 2500 children × 2 doses) (e) 4-5 years requiring 8th and 9th dose (2 ml/child/dose × 2500 children × 2 doses) (f) Total volume of vitamin A required for children 9 months-5 years (625 ml + 10000 ml + 10000 ml + 10000 ml + 10000 ml) (g) Adding wastage of 10% to the total requirement (10% × 40625 ml) (h) Total requirement of VAS for 9 months-5 years (40625 + 4063) 7. Therefore, total number of 100 cc vitamin A bottles required for a district with population of 100,000 (44687/100)

100,000 25/1000 live births 2500 625 2500 (for each of the four age groups) 625 10000 ml 10000 ml 10000 ml 10000 ml 40625 ml

4063 ml 44687 ml 447 bottles

primary health care activities, including RI activities, on each of the Wednesdays and Saturdays of the months. The plan includes the details of sites within a village/hamlet being used as “immunisation sites” for administering vaccines. The RI plan also includes information on the link ICDS frontline worker who coordinates with ANM and community for execution of the RI activities, population of the village and date of immunization. The RI microplan for the biannual BSPM months forms the basis for administration of VAS on the RI days (Figure 17.2). It is therefore critical that the RI micro plans of the BSPM months are shared with the ICDS sector for effective coordination and management of the BSPM Programme.

17.4.4 Communication and social mobilisation An effective, well defined, sustainable and replicable communication and social mobilisation strategy is pre-requisite for improving vitamin A coverage and influencing correct dietary and feeding practices. Education and social mobilisation activities are an integral component of the BSPM

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17.2 RI microplan for a sub-centre

programme. Communication and social mobilization activities were planned to be undertaken by the ICDS system throughout the fixed biannual BSPM months of June and December. In the BSPM programme, ICDS frontline worker were entrusted with the responsibility of mobilizing beneficiaries to the RI site for administration of VAS and immunisation. The communication messages focused on creating demands for services as well as promotion of infant and young child feeding. Standardized messages on vitamin A, iodised salt and Infant & Young Child Feeding were displayed at the selected sites. Rallies by school children, wall painted slogans, placards, banners and posters were used for these communication and social mobilisation activities. Two days prior to the VAS administration on RI days, intensive social mobilisation activities were conducted by organising rallies in the village or organising public announcements as well announcements in primary schools, ICDS centres etc (Figure 17.3). The pulse polio programmes had demonstrated that such intensive social mobilisation actions, 1–2 days prior to the vaccination days were important actions for timely creation of awareness and mobilizing community to visit the vaccination sites. A set of information and communication materials (posters, banners, folders, inserts, calendar) containing technical details about biannual strategy, vitamin A supplementation, iodised salt, infant and young child feeding were developed and distributed in the entire state. These proved to be extremely useful in disseminating correct standardized messages in the community.

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17.3 Village-level implementation of biannual activities

17.4.5 Capacity building health and ICDS staff For execution of the BSPM activities, a joint training of health and ICDS sectors was considered critical. Intensive training was undertaken for state, district, block and village functionaries of joint health and ICDS teams. Faculty members of the departments of Community Medicine of the nine State Medical Colleges were designated “State Observer-cum-Monitoring Trainers” or (SOMTs) and were trained as master trainers for the state level BSPM activities. SOMTS in turn selected eight persons as “Block Core Trainers” from the health and ICDS sectors at block level. These block trainers undertook the joint training health and ICDS functionaries (ANM and ICDS Anganwari Worker or AWWs) with supervision support of SOMTs. Prior to the BSPM months, a rapid re-orientation training was undertaken for the managers and functionaries of both the sectors. Training materials were developed by the State Government. Important amongst these was a joint training module which was used for training programme managers as well as functionaries. Based on the performance and feedback, training content was continuously modified. Special effort was made to train all functionaries on the importance of following the VAS recommended age-wise schedule and cautions to be taken for preventing overdose administration. Management of side effects, if any, formed part of the training. During 2006, the training on biannual strategy was taken to scale in the entire state. Approximately 1650 Health & ICDS district and block programme mangers and approximately 6500 block

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health and ICDS functionaries were trained for implementation of the BSPM strategy.

17.4.6 Supervision and monitoring The activities during the biannual rounds were monitored by the introduction of a supervision format for monitoring joint VAS -RI sessions by functionaries of both the health and ICDS sectors. Additionally, an external monitoring system was also established for monitoring programme inputs in 18 districts of the first phase of implementation. A team of SOMTs monitored biannual activities at both planning and implementation stage. Using a standardized methodology, the monitors provided information on the BSPM processes such as identification of beneficiaries through biannual surveys and use of special ICDS survey registers provided, administration of VAS as per the schedule. In addition, status of the availability of health sub-centre RI micro-plans for the BSPM months and sharing of these microplans with the ICDS systems was also monitored by SOMTs.

17.4.7 Establishment of VAS Coverage Record System In December 2004, effort to institutionalize an effective monitoring system was made by introducing child centered recording and monitoring system for the biannual VAS administration. A total of 25,000 special biannual child centered registers were supplied for recording data by health workers at the village level on VAS, treatment doses for clinical VAD cases, administration of measles vaccine, and for recording status of introduction of complementary foods at nine months. Data was planned to be computed in specially developed block and district level formats. Training on developing skills for completing these registers and formats was imparted not only to district managers and programme functionaries but to the data computing persons attached to the 70 districts of the state. The impact of using such a system had a positive impact on the VAS coverage in June 2005 but the childcentered recording system was not considered sustainable. Experimenting with an alternative monitoring mechanism was considered essential.

17.4.8 Impact of the programme in selected districts The impact of the biannual BSPM programme on VAS coverage in the first two years, December 2003 to December 2005, was evaluated by an external agency [54]. The intensive programme inputs in 18 districts resulted in increasing the coverage of vitamin A supplements of children 9–12 months to 63% while the coverage of 2nd to 5th dose increased from almost nil to 62% (Figure 17.4). The process of evaluation also presented a very significant positive impact on skills for undertaking village survey and identifying

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beneficiaries and knowledge of health and ICDS functionaries regarding age-wise correct doses of vitamin A supplements for preschool children. The BSPM strategy, with defined responsibilities of health and ICDS sectors, resulted in appreciating their roles in complementing the efforts for achieving the common objective of improving child nutrition, survival and development. This was reflected in improvement in functional collaboration between health and ICDS sectors. BSPM was also demonstrated to be a good example of using VAS administration as an entry point for operationalising a comprehensive child health and nutrition programme.

17.4 VAS coverage-18 intensive Phase I districts

The VAS programme strategy linked to RI was reported to result in improving not only VAS but improving RI coverage and streamlining RI sessions. The development and availability of RI micro-plans at block level steadily increased and by the fourth BSPM round, 94% blocks were reported to have RI micro-plans as compared to 65.1% at the beginning of BSPM activities in 18 districts of the first phase (Figure 17.5). The percentage of immunisation/ outreach session held increased from 60% to 82%. Iodised salt consumption increased from 6% to 49%. A total of 59,889 children were identified as severely undernourished and were followed up for management.

17.5 Impact of BSPM on RI microplan availability between 2003 and 2005

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17.4.9 Scaling up the biannual VAS delivery system in the entire state Based on the experience and positive outcome of the implementation in 18 districts, the BSPM initiative was taken to scale in the entire state in 2006 of over 190 million population comprising 70 districts with estimated 12 million children <3 years. The coverage of infants with the first dose of VAS in the state increased from 9.4% to 43% and of 2nd to 5th dose from nil to 37% (Figure 17.6). In 2007 the BSPM strategy was included in the State Programme Implementation Plan for the Rural Health Mission (State PIP–NRHM).

17.6 VAS coverage statewide

17.5

Elimination of vitamin A deficiency – future direction

VAS Programme is an integral part of the RCH-2 Programme of the National Rural Health Mission (NRHM) 2005–2011. The biannual strategy for improving coverage of VAS is a sustainable model which can be effectively taken to scale. Reaching preschool children in both rural as well as urban regions is crucial and a suitable sustainable VAS programme design needs to evolve to reach the unreached urban children. For the implementation of VAS administration in rural and urban regions, streamlining of the procurement of adequate quantity of VAS supply remains a challenge. Higher priority and political commitment for implementation of the vitamin A supplementation programme, along with commitment to improve production and access to vitamin A fortified foods is essential to eliminate vitamin A deficiency in India and making a significant difference in survival rate and quality of life of children in the country.

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References 1. Fourth Five Year Plan, Family Planning programme. Technical information: MCH No. 2. Maternal and Child health Scheme for Prophylaxis against Blindness in Children caused by Vitamin A Deficiency. Indian Council of Medical Research (1971–74). 2. Text Book of Human Nutrition (1996). Oxford and IBH Publishing Company, New Delhi. 3. National Nutrition monitoring Bureau Report (1991). National institute of Nutrition, Hyderabad. 4. BAGCHI K (2001). In: Benefits and safety of administration of vitamin A to pre school children and pregnant and lactating women. Kapil, U and Srivastava VK (eds), Ministry of Health and Family Welfare and All India Institute of Medical Sciences, New Delhi; p 67. 5. WHO (1995). MDIS-Micronutrient Deficiency information System, World Health organization. MDIS Working Paper # 2. Global Prevalence of Vitamin A Deficiency. 6. Department of Women and Child Development, Government of India, India, Nutrition Profile, 1998. 7. CHAKRAVARTHY I (2001). Indian Scenario of Prevalence of Vitamin A Deficiency. In: Benefits and safety of administration of vitamin A to pre school children and pregnant and lactating women. Kapil U and Srivastava VK (eds), Ministry of Health and Family Welfare and All India Institute of Medical Sciences, New Delhi; p 100. 8. VIR S . Linkage of vitamin A massive dose supplement administration with pulse polio immunization – an overview. In: Benefits and safety of administration of vitamin A to pre school children and pregnant and lactating women. KAPIL U AND SRIVASTAVA VK (eds), Ministry of Health and Family Welfare and All India Institute of Medical Sciences, New Delhi; pp. 60–68. 9. AWASTHI S (2000). DEVTA project. Uttar Pradesh – Personal Communication. 10. Draft report of District nutrition Project, ICMR 1998–99. 11. SRIVASTAVA VK (1999). Vitamin A status of preschool children in Baharaich district, Uttar Pradesh, Study for Government of UP. 12. Indian Council of medical research (1999). District nutrition Project, draft report (1). 13. National Nutrition monitoring Bureau Report (2002). National institute of Nutrition, Hyderabad. 14. National Nutrition monitoring Bureau Report (2006). National institute of Nutrition, Hyderabad. 15. DIXIT DT (1966). Nightblindness in third trimester of pregnancy. Ind J Med Res u, pp. 791–795. 16. MANDAL GS, NANDA KN and BOSE J (1969). Nightblindness in Pregnancy. J. Obstet Gynecol. 19, pp. 453–458. 17. VENKATACHALAN PS (1962). Maternal nutritional status and its effects on the newborn. Bull. World Health Organ 26, pp. 193–201. 18. National Family Health Survey (NFHS) 2, 1998–99. International Institute of Population Sciences, Mumbai. 19. BHASKARAN P and KRISHNASWAMY K (2002). Vitamin A supplementation strategies – India status. In: Benefits and safety of administration of vitamin A to pre school children and pregnant and lactating women. Eds Kapil, U and Srivastava

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Public health nutrition in developing countries VK, Ministry of Health and Family Welfare and All India Institute of Medical Sciences, New Delhi, pp. 45–58. VIR S (2008). Addressing child malnutrition in tea gardens of Dibrugarh district, Assam. UNICEF consultancy report. SOMMER A and DAVIDSON FR (2002). Assessment and control of vitamin A deficiency: the Annecy Accords. J Nutr 132, no. 9S, pp. 2845S–2849S. VIJAYARAGHAVAN K and N PRAHLAD RAO (1978). National Programme for the Prevention of Vitamin A Deficiency – An evaluation. National institute of Nutrition, Indian Council of Medical research, Hyderabad. Indian Council of Medical Research (1974). Annual Report, p 75. SRIKANTIA SG and REDDY V (1970). Effect of a single massive dose of vitamin A on serum and liver levels of the vitamin. Amer J Clin Nutr 23, pp. 114–118. SRIKANTIA SG (1969). Prevention of vitamin A deficiency, world. Rev Nutr Diet 31, pp. 95–99. PREIRA SM and BEGUM A (1969). Prevention of vitamin A deficiency. Amer J Clin Nutr 22, pp. 858–862. SUSHEELA TP (1969). Studies on serum vitamin A levels after a single massive oral dose. Ind. J med Res. 57, pp. 2151–2152. Task force, Government of India (1988) constituted by the Ministry of Health and Family Welfare, government of India, New Delhi. National prophylaxis programme for prevention of blindness due to vitamin A deficiency. MANNAR MGV (1989). Production and supply of vitamin A in India. Report prepared for the Ministry of Health and family Welfare, Government of India, 1989. WHO (1988). Expanded programme on immunisation update - vitamin A: Time for action. World Summit for Children (1990). World Declaration on the survival, protection and development of children and plan of action for implementing the World Declaration on the survival, protection and development of children in the 1990s. World Summit for children, United Nations. New York, 30th Sept, UN, 1990. Ministry of Health and Family Welfare (GoI). Communication No. M 12015/ 6188-MCH III. 9th March 1990. Task force on vitamin A programme, Minutes of the Task Force (1990). Chaired by Deputy Commissioner MCH. BHASKARAN P and VISWESWARA RAO K (1997). Enhancement in seroconversion on simultaneous administration of measles vaccine and vitamin A in 9 months old Indian infants. Ind. J. Paed. 54. Ministry of Health and Family Welfare, Government of India (1991). Policy on Management of Vitamin A Deficiency. REDDY V (2002). Benefits and safety of vitamin A supplementation during pregnancy and lactation page 16-25. In: Benefits and safety of administration of vitamin A to pre school children and pregnant and lactating women. Eds KAPIL , U and SRIVASTAVA VK , Ministry of Health and Family Welfare and All India Institute of Medical Sciences, New Delhi. Ministry of Health and Family Welfare, Government of India. Child Survival and safe Motherhood Programme, 1992. Ministry of Health and Family Welfare, Government of India. Evaluation of Immunization 1998–1999, 2000. UNICEF (1998). Integration of vitamin A supplements with immunization policy and programme implementation: report of a meeting, UNICEF, New York, 12– 13 Jan 1998.

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(1996). Linking periodic dosage of vitamin A with universal immunization programme – An Evaluation. National Institute of Nutrition, Indian Council of Medical Research, Jamai Osmania PO, Hyderabad 500007. WHO / UNICEF (1998). Joint Policy and Operational Questioning relating to vitamin A and EPI / NIDs. Joint statement, WHO / UNICEF, Geneva, 1998. National institute of Nutrition (2000). Impact of vitamin A supplementation delivered with OPV as a part of immunization campaign in Orissa, India. ICMR/ WHO/UNICEF and MI. Directorate of Family Welfare, government of UP (2000). Vitamin A given during pulse polio immunization campaign. Dec 1999 to Jan 2000. KAPIL U and SRIVASTAVA V (2002). Benefits and safety of administration of vitamin A to pre school children and pregnant and lactating women. Ministry of Health and Family Welfare and All India Institute of Medical Sciences, New Delhi. 10th Five Year Plan. Planning Commission, Government of India, 2002–2007. Policy on Management of Vitamin A Deficiency 1991(No Z 28020/30/2003CH,Government of India, Ministry of Health and Family Welfare, Child Health Division dated 2 nd Nov 2006). VIR S, PRASAD LB , JAIN A , SINGH R , ATEGBO EA , HETTIARATCHY N AND SCHULTINK W (2007). Vitamin A Supplementation Programme an effective entry point for addressing Malnutrition in the State of Uttar Pradesh, India. Abstract – Consequences and Control of Micronutrient Deficiencies – Science, Policy and Programme – Defining the Issues, 16–18 April, 2007, Istanbul, Turkey. G SINGH , S VIR , V AGUAYO , U NARAYAN . Child health and nutrition months significantly improve vitamin A supplementation coverage in Uttar Pradesh, India (TU 33) in program/abstracts. Micronutrients, health and development: evidence based programme, 12–15 May 2009, Beijing, china, micronutrient Forum. SAXENA S, SAXENA V AND NAMSHUM N. Challenges of addressing vitamin A deficiency in India (TU 40), in program / abstracts. Micronutrients, health and development: evidence based programme, 12-15th May 2009, Beijing, china, micronutrient Forum. Government of India, Ministry of Women and Child Development (2006). Report of the working group on integrating nutrition with health, 11 th five year plan (2002–2012). SRIVASTAVA VK (1999). Vitamin A status of preschool children in selected districts in UP. Report submitted to UNICEF. Department of Women and Child Development, Government of Uttar Pradesh and UNICEF, 1997. Nutritional Profile of Women and Children in Uttar Pradesh. GUPTA SB , SALUJA DBS , VIR S, SAXENA V , HASAN MZ , SRIVASTAVA VK (2001). Child Health and Nutrition week: Intervention coverage with vitamin A supplement and measles vaccination. Training manual. Department of Health and Family Welfare, Government of UP and UNICEF (Lucknow Field Office). Government of Uttar Pradesh and UNICEF (2003). Biannual vitamin A supplementation programme in Uttar Pradesh, Bal Swasthya Poshan Mah. MOST, India (2004). Coverage evaluation of vitamin A supplementation in Uttar Pradesh, Academy of Management Studies. Department of Health and Family Welfare (2008). State Programme Implementation Plan, National Rural Health Mission (NRHM).

18 Iodine metabolism and indicators of iodine status Madan M. Godbole and Rajan Sankar

Madan M. Godbole is Professor and Head of the Department of Endocrinology at Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow. Research fields including brain development, breast cancer and stroke in relation to iodine/thyroid hormone. He is a Fellow at National Academy of Medical Sciences. Rajan Sankar is the Regional Manager and Special Adviser in South Asia for the Global Alliance for Improved Nutrition (GAIN). Prior to this, he was a Project Officer in UNICEF, India Country Office and Regional Technical Advisor of the Micronutrient Initiative. Dr. Shankar was the Head of Thyroid Research Centre at the Defence Research and Development Organisation in Delhi.

18.1

Introduction

Iodine is a constituent of thyroid hormone (TH) and is an essential micronutrient for normal growth, development and function. Iodine deficiency (ID) causes an enlargement of the thyroid gland, physical function and mental retardation. Mild to moderate ID results in loss of intelligence points, learning disabilities and poor human resource development. The former being the tip of the iceberg and latter constitutes the invisible bulk of the pyramid [1]. National governments are putting in place universal salt iodization (USI) as a major vehicle to prevent the problem of IDD [2]. Salt-iodization levels and urinary iodine excretion are the most commonly used parameters for process and impact assessment of USI and IDD elimination. The serum thyroid stimulating hormone (TSH), thyroglobulin (Tg) and ultrasound measurement of thyroid gland volume have been validated as secondary parameters for monitoring the success of the salt iodization program and elimination of IDD [3–4]. Countries with strong monitoring and evaluation machinery in place have been able to overcome the problems pertaining to major obstacles of USI such as poor quality of salt, inadequate iodization,

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503

losses during transportation, humidity, logistic problems and poor public and administrative awareness [5]. The understanding and choice of impact assessment parameters is governed not only by administrative decisions and economics of scale, but also by the choice of survey methodology and selection of target groups like school children, pregnant and lactating mothers. The clear understanding of iodine metabolism through the humanlife cycle and various factors that may affect iodine metabolism and thyroid hormone synthesis during pregnancy, neonatal, childhood, adolescence and adult life is of prime importance.

18.2

Metabolism – iodine absorption and transport

Iodine present in foods as iodides is readily absorbed from the gastrointestinal tract. Other forms of iodine in food is converted into the iodide ion in the gut lumen, and >90% is rapidly absorbed in the upper-small intestine. Fifteen percent of ingested iodine is taken up by the thyroid gland within 24 hours of ingestion, and the excess is excreted by the kidneys in urine [6]. Urinary-iodine excretion per day reflects the iodine-nutrition status of a population and is the most widely used parameter for monitoring the impact assessment of intervention protocols. However, it is not used to assess an individual’s iodine-nutrition status. The only direct test of thyroid function employs a radioactive isotope of iodine as a tag for the body’s stable form of iodine. Most often the test involves the measurement of the fractional uptake by thyroid of a tracer dose of radio iodine. The isotope quickly mixes with stable endogenous pool of body iodine in the extracellular fluid and begins to be removed by two major organs thyroid and kidneys. As this process continues the plasma levels of tracer iodine decreases exponentially. The low levels are reached by 24 hours and inorganic radioactive iodine becomes virtually undetectable in plasma after 72 hours of administration. In contrast, thyroid content of radioactive iodine increases rapidly in early hours, and then decreases until a plateau is reached. The proportion of administered radioactive iodine ultimately accumulated by thyroid is a reflection of the clearance of iodine by thyroid and kidney. The normal thyroid clearance rate (TCR) is approximately 0.4 L/h and the renal clearance rate (RCR) is 2.0 L/h, so that radio iodine uptake (RAIU) generally approximates 20% of the administered dose and indicates the rate of thyroid hormone synthesis and by inference the rate of thyroid hormone releases into the blood [7]. These considerations of iodine metabolism make the measurements of these parameters of value for assessment of iodine nutrition status of an individual. Several factors have made many of these tests, except measurement of urinary iodine, less frequently used. However, understanding the measurement of iodine status using these methods is important since

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these various methods are valuable in the interpretation of the situational analysis of iodine deficiency and its correction due to many confounding factors that clinicians and epidemiologist may confront in management of regular program monitoring and evaluation [6–7].

18.3

Iodine requirement and intake

The daily dietary intake of iodine varies widely throughout the world, depending on the iodine content of soil and water and on dietary practices. Even in a single area, iodine intake varies among different individuals and in the same individual from day to day. Availability of adequate amount of exogenous iodine to allow sufficient thyroidal uptake for formation of normal quantities of thyroid hormone is a pre-requisite for normal growth and development and maintenance of good health in adults. Taking into account daily loss of about 10–20 μg and 100–150 μg through fecal and urinary routes, at least 100 μg is required daily to eliminate any signs of iodine deficiency. This requirement is enhanced during pregnancy and growth, as indicated in Table 18.1. Table 18.1 Recommended daily intake (µg/day) Adult During pregnancy children

18.4

150 250 90–120

Iodide trapping, organification, coupling, TH synthesis and release (Figure 18.1)

Iodine ingested in inorganic and organic forms from dietary sources is rapidly and efficiently absorbed by the gastrointestinal tract. In the body, iodine remains in the form of iodide (I –) that is confined largely to extracellular compartment. Iodide concentration in plasma is very low and is completely filterable, reabsorbed passively and a specialized mechanism is required for its uptake by thyroid cells. This process called iodide trapping is accomplished by a membrane protein, the sodium-iodide symporter (NIS). The transport of iodide is an active process dependent on the presence of sodium gradient across the basal membrane of the thyroid cells. Update of 2Na+ ions result in the entry of one iodide atom against an electrochemical gradient. The iodide transport system generates an iodine gradient of 20–40 over the cell membrane. Iodide from both intracellular and extracellular pools within thyroid gland participates in series of reactions that lead to the synthesis of thyroid hormones. Iodide get oxidized to produce intermediates that get rapidly incorporated in tyrosine moieties of thyroglobulin, a matrix protein to form

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hormonally inactive monoiodotyrosines (MITs) and diiodotyrosines (DITs), by a process termed as organification. Oxidation of thyroidal iodide is mediated by the heme containing protein thyroid peroxidase (TPO). Iodotyrosines formed by oxidation and organic binding are precursor of hormonally active iodothyronines namely Triodothyronine (T 3) and Tetraiodothyronine (Thyroxine; T4). The coupling reaction that catalyzed by TPO either two DITs or one MIT and one DIT through an ether linkage to produce T4 and T3. Thyroglobulin (T g) is required for TH synthesis and is considered a sensitive indicator for measuring iodine status. This matrix protein is required for the efficient formation of T4 and T3 and is found in a ratio of 20:1 in human T g molecule and alterations indicate a disease state making Tg as an attractive biomarker.

18.1 Synthesis and release of thyroid hormone, T4-Thyrroxine, T3-Tetraiodothyronine, DIT-Diiodotyrosine, MIT-Monoiodotyrosine, TSH-Thyroidstimulating hormone, Tg-Thyroglobulin, TPO-thyroid peroxidase

18.5

Storage and availability of throid hormones (TH)

The high homeostatic value of thyroid hormone economy relates to large storage capacity of hormones and extremely restricted turnover of ~1% per day in thyroid gland. This large reservoir provides long-term protection against cessation of TH synthesis and sporadic iodine deficiency. Considering that normal thyroid gland weighing 20 g contains

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approximately 5 mg of T4, the protection offered can be sufficient to maintain euthyroidism for at least 50 day period [16]. Thus low-circulating levels of Tg indicates long-term depletion of iodine. The value of circulating levels of Tg as biomarker is still to be validated with adequately large sample size in view of questionable contribution of peripheral hydrolysis of Tg.

18.5.1 Thyroid hormone release The higher T4/T3 ratio in T g compared to thyroidal secretion indicates that in addition to synthetic mode, T3 is also produced by T4 deiodination by two enzymes type 1 and 2 deiodinases. Because of the decreased iodine supply and in the DIT/MIT ratio, the T4/T3 ratio decreases in human Tg molecules in thyroid glands of operated iodine-deficient subjects. Excess amount of iodide first increases and then decreases the organification within thyroid cells resulting in reduction in yield of organic iodine with increasing doses of iodide. This effect known as Wolff-Chaikoff Effect, has been used to treat the hyperthyroid patients and has been cited in support of so-called ill effects of excess iodine [8].

18.5.2 Thyroid hormones in plasma A wide variety of iodothyronines and their derivatives exist in plasma. The iodine economy is closely related to metabolic transformation of thyroid hormone in peripheral tissues. The levels in peripheral tissues determine the biologic potency and effects. The knowledge of pathways of thyroid-hormone metabolism is fundamental to understand the physiopathology of iodine-deficiency disorders and consequences for impact assessment of intervention programs. Of the thyroid hormones, T4 is highest in circulation and is the only hormone solely synthesized by thyroid gland. On the other hand, 80% of T3 comes from the peripheral tissues and only 20% comes from synthesis in thyroid gland. Only trace amount of other iodothyronines, iodotyrosines and conjugated products are found in plasma and the released iodine from deiodination is recycled to maintain iodine economy. Iodotyronines remain in circulation bound to thyroid binding globulin (TBG) (80%), transthyretin (TTR), thyroid binding peralbumin (TBPA) and albumin. Maintenance of large quantity of major Iodothyronines in circulation in spite of poor solubility in water is possible due to their association with high capacity-low affinity thyroid binding globulin (TBG), transthyretin (TTR) and thyroid binding per-albumin (TBPA) and albumin with 75– 80% THs binding to TBG [17, 18]. These binding proteins provide a large

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capacity reservoir for release of free TH to meet the day-to-day energy demands of the body as well as to meet the sporadic iodine deficiency situation.

18.6

Iodine metabolism and their mechanism of action

18.6.1 Thyroid stimulating hormone (TSH) Thyroid stimulating hormone, a major regulator of the morphologic and functional status of the thyroid gland circulation of α-subunit of 14 kD (92 amino acids) is common to leutanizing hormone (LH), folliclestimulating hormone (FSH) and chrionic gonadotrophin (CG) and a specific β-subunit (112 amino acid) that is a glycoprotein produced in the pituitary gland by thyrotrophs under the influence of thyrotrophin-releasing hormone (TRH) secreted by hypothalamus. It displays both pulsatile and circadian variations. The linear inverse relationship between serum-free T4 concentration and TSH makes it a sensitive indicator of thyroid status of patients with intact hypothalamic-pituitary axis. All steps in the formation of and release of thyroid hormones are stimulated by Thyroid Stimulating Hormone (Thyrotrophin; TSH) [19].

18.6.2 Thyroid peroxidase (TPO) The synthesis of T4 and T3 from DITs and MITs requires the TPO-catalysed coupling of two iodotyrosine moieties. TPO is a microsomal antigen whose recombinant form is used for detection of anti-thyroid microsomal antibodies commonly present in the serum of patients with Hashimoto’s disease. Some of such abnormalities have been reported to be present in subjects with history of iodine deficiency and administered excess iodine. Though such cases are rare, the advent of the same has been used as an argument against universal salt iodization programs [13, 14, 20, 21]. Sideeffects of excess iodine in general include: (1) Iodine-induced hyperthyroidism. An increase in toxic nodular goitre is probably transient and eventually its incidence is expected to decrease. However, an increased incidence of autoimmune Graves’ disease is probably permanent. (2) Iodine-induced hypothyroidism. (3) Iodine-induced autoimmunity, both of the Hashimoto and of the Graves types. (4) An increase in the incidence of papillary cancers, probably with a decrease in the more aggressive types. In any case, the benefits of iodisation programs far outweigh the risks, provided they are implemented and monitored carefully.

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18.6.3 Response of thyroid-pituitary-hypothalamic axis to iodine deficiency Iodine, being a limited resource, thyroid-pituitary-hypothalamic axis is designed to conserve this scarce micronutrient and improve the efficacy of its proper utilization. The severe decrease in dietary iodine supply over a prolong period of time results in fall of T 4 and simultaneous increase in circulating TSH. Human body tries to meet the moderate to mild iodine shortfall in several ways that involves adjustments occurring at hypothalamic-pituitary-thyroid axis and peripheral tissue levels. Surprisingly, majority of goitreous population in iodine deficiency areas are euthyroid (normal thyroid function). This condition is maintained through the adaptive response that involves TSH-mediated increase in thyroid gland size, Tg synthesis, etc. [22– 23]. The adaptive response is also the result of economical use of iodine by the thyroid gland by enhancement of DIT–MIT coupling to produce T3 (a more active thyroid hormone). The TSH-mediated increase in thyroid-gland size in populations is indicated by goitre prevalence rate that constitutes the primary impact assessment of iodine deficiency and its correction. Although thyroid size changes inversely in response to alterations in iodine intake, there is a lag before the goitre rate normalizes after iodine repletion. The duration of this lag period is unclear, with experts suggesting it may last from months to years [2]. During this period, the GR is a poor indicator of effect because it reflects a population’s history of iodine nutrition but not its present iodine status. Cross-sectional studies have reported a discrepancy between the UI and the GR in the immediate post–USI introduction period [3–4]. The lower excretion of iodine through urine is the most apparent indicator of such an adaptive response and constitutes the most important impact assessment indicator of iodine deficiency. The severe iodine deficiency however produces hypothyroidism (less than normal Thyroid function), with abnormally high circulating TSH, that results in majority of symptoms of poor-mental development and cretinism including stunted physical and mental growth, sluggishness, deaf-mutism and defective gait. The extent of symptomology and their manifestation depends on the time of insult of iodine deficiency that is encountered by an individual [24–28]. The in-utero deficiency occurring to fetus in early period (up to second trimester) leads to more neurological damage and the late deficiency results in myxedematous manifestations. It is interesting to note that it is not uncommon to find a full grown neurological cretin with normal physical growth and a normal size functioning thyroid gland and also a myxedematous cretin

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with signs of neurological deficits; however, it is more common to find cretins with mixed variety of symptoms [26, 29]. The elevated TSH among many functions primarily serves to stimulate the cell division and enlargement of thyroid cells and thyroid gland leading to goitre. Secondly, undetectable decrease in circulating T3 in iodinedeficient subjects indicates that reduced intra-pituitary conversion of T 4 to T3 acts as a signal of increased TSH synthesis/secretion from pituitary gland. TSH also helps to maintain the increased T 3 residence time in CNS. Thus the multifactor highly sensitive response of TSH to iodine deficiency makes it an ideal biomarker for impact assessment of correction of iodine deficiency [29].

18.7

Role of iodine in biological functions

Severe degree of iodine deficiency disorders (IDD) includes goitre, spastic dilplegia, squint, deaf-mutism and physical (myxedematous) and mental (neurological) retardation termed as endemic cretinism. Most abnormalities with iodine metabolism in patients with endemic goitre are consistent with iodine deficiency [30, 31]. Thyroid iodine clearance and radio iodine uptake (RAIU) are increased in proportion with decrease in urinary iodine excretion of stable iodine. The absolute iodine uptake is normal or low. In areas of moderate iodine deficiency, the serum T 4 concentration is generally in the lower range of the normal. However, areas of severe iodine deficiency the T 4 values are decreased. Nevertheless, most subjects in these areas do not appear to be in hypothyroid state because of an increase in the synthesis of T 3 at the expense of T 4 and because of the increase in activity of thyroidal deiodinases. In such situations, TSH levels are typically in the upper range of normal. However, persistent severe iodine deficiency in sub-set of population leads to hypothyroidism or myxedema with significant increase in TSH levels which is the most important clinical consequence of iodine deficiency [30, 31]. The reduced production of thyroid hormone is the central feature of the clinical state termed hypothyroidism. The symptoms include coarse or dry skin, periorbital puffiness, cold skin and delayed ankle reflex relaxation, reduced pulse rate, weight gain and general lethargy to perform routine tasks. The basal metabolic rate shows a significant decrease in hypothyroid state. The low circulating T4, T 3 and high TSH provide characteristic biochemical profile of hypothyroid state [31]. The immune manifestations do not come into play in the absence of hypothyroidism and the effects of goitre are only cosmetic. Chronic changes with reference to inadequate iodine intake as well as continuous; the changing thyroid hormonal status eventually leads to alternating enlargement and size reduction of the thyroid follicles. This

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results in an enlarged thyroid gland with nodules (classic multinodular goitre). However, a haemorrhage in one of the nodules can cause pain and a swelling, mimicking sub-acute thyroiditis. Susceptibility to excess iodine in a miniscule of iodine deficient individuals is also known to lead to immune response.

18.8

Importance of iodine nutrition for human populations

The populations at large require proper iodine nutrition for their development and achievement of their full potential. The vulnerability of human subjects to iodine deficiency depends not only on the extent but also on the timing of iodine deficiency. The iodine requirement also varies according to age as well as the physiological state of human being. Iodine requirement is highest during growth period and pregnancy, stabilizes during adulthood, and declines with advancement of age. This is borne out by the fact that neurological deficits constitute the most serious consequence of iodine deficiency resulting in socioeconomic burden of bringing up a cretin and compromised human potential of large number of school children due to learning disabilities, impaired memory, and inability to perform abstract mathematical and other skills. Combination of factors like road connectivity, measures to reduce floods, better land and water management with or without salt iodization program in place is known to introduce incremental iodine correction [25]. This is exemplified in insufficient penetration of adequate iodine supply in far flung rural areas reported from countries like India [32–33]. Unfortunately, dramatic disappearance of cretinism and reduced goitre rate with incremental iodine correction though to desirable strategy of universal iodised salt consumption, masks the subtle and clinically not visible ill effects of persisting iodine deficiency of moderate to mild grade leading to complacency among health planners. Persistence of subtle deficits on much wider scale than perceived at present can lead to great mass of populations in developing economies remaining away from achieving their full human potential [1]. Monitoring of impact assessment of intervention or corrective programs and appropriate choice of indicators is therefore of great importance for achieving the goal of Universal Salt Iodization (USI) and sustaining measures to ensure access to iodised salt by the entire population. WHO estimates that 54 countries out of 126 still have inadequate iodine nutrition (i.e., median UI <100 μg/l), and 16 countries globally need to rapidly accelerate and sustain USI programme (Table 18.2).

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Table 18.2 2006 UNICEF/Network high-priority countries for IDD control Country

Total Annual Households Infants unprotected population births using adequately from IDD (thousands) (thousands) (thousands) iodized salt (%)

Russia Ukraine Indonesia China Philippines Ethiopia Angola Sudan Egypt India Pakistan Bangladesh Afghanistan Niger Ghana Senegal

143,899 46,989 220,077 1,307,989 81,617 75,600 15,490 35,523 72,642 1,087,124 154,794 139,215 28,574 13,499 21,664 11,386

1,511 391 4,513 17,372 2,026 3,064 749 1,163 1,890 26,000 4,729 3,738 1,395 734 679 419

35 32 73 93 56 28 35 1 56 50 17 70 28 15 28 16

982 266 1,219 1,216 891 2,206 487 1,151 832 13,000 3,925 1,121 1,004 624 489 352

Source: Adapted from Zimmerman MB (2007) – www.a2zproject.org

18.9

Iodine requirement

Iodine turnover, thyroidal radioiodine uptake, and balance studies suggest that the average daily requirement for iodine in non-pregnant women is 91–96 μg/d [41]. The US Estimated Average Requirement (EAR) for iodine for non-pregnant, non-lactating women aged 14 years is 95 μg/d, and the Recommended Dietary Allowance – defined as the EAR plus twice the coefficient of variation (CV) in the population—is 150 μg/d [41–42]. This agrees with the WHO/ICCIDD/UNICEF recommended nutrient intake for iodine 150 μg/d for non-pregnant women [2].

18.9.1 Iodine requirements in pregnancy and lactation The iodine requirement during pregnancy [31, 34–36] is sharply elevated because of (1) an increase by 50% in maternal thyroxine (T 4) production to maintain maternal euthyroidism and to transfer thyroid hormone to the fetus; (2) need for iodine to be transferred to the fetus for fetal thyroid hormone production, particularly in later gestation; and (3) probable increase in renal iodine clearance (RIC). The US EAR is 160 μg/d for pregnancy in women of age 14 years, and the Recommended Dietary Allowance, set at 140% of the EAR rounded to the nearest 10 μg, is 220 μg/d [31, 34–36]. Recently, an increase in the nutrient intake for iodine

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during pregnancy from 200 to 250 μg/d has been recommended [34–36]. This implies the need for more data on the level of iodine intake and the corresponding urinary iodine (UI) concentration that ensures maternal and newborn euthyroidism. Pregnancy is associated with profound changes in thyroid function and iodine metabolism to meet the increased demand of hormone production by the maternal thyroid gland (Tables 18.3 and 18.4). The events associated events constitute a transition from a preconception steady-state thyroid gland to a pregnancy steady-state thyroid gland. Once the new equilibrium has been reached, the increased demand for hormones during pregnancy is sustained until full term [36]. Calculation of estimated average requirement (EAR) of 115–120 μg/ day for pregnant women based on balance studies indicating retention 20–25 μg of iodine per day by full-term fetus have been flawed. The error has crept in due to not taking in to consideration the need for increased maternal T4 production and higher urinary iodine losses. Studies seeking correlation between thyroid volume and iodine supplementation in pregnant women have also suggested increased need of iodine in the range of 200–250 μg per day during pregnancy [56–57]. During lactation, the physiology of thyroid function and urinary iodine excretion returns to normal. Iodine during lactation is concentrated in mammary gland for excretion in breast milk. The mean breast milk concentration in iodine-sufficient women has been found to be 146 μg/l and average daily loss of iodine through breast milk has been estimated to be 115 μg/day [34]. Addition of EAR for non-pregnant women the EAR for lactating women works out to be 210 mg/day [34]. The WHO recommended daily intake of 250 μg of iodine is found to be sufficient to take care needs of both pregnant and lactating women [3]. When diet lacks iodine, adequate physiological adaptation is difficult to achieve and is progressively replaced by pathological alterations occurring in parallel with the degree and duration of iodine deprivation which leads to maternal hypothyroxinaemia. Pregnancy typically acts to reveal an underlying iodine deficiency even in conditions with only a marginally poor intake, a state that is observed in many countries [3]. The borderline supply of iodine in many areas of mild iodine deficiency is also exemplified of compensatory maternal and fetal goitre during pregnancy and adolescence girls due to the increased requirement of thyroid hormone during gestation and adolescence.

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Table 18.3 Pregnancy is associated with profound changes in thyroid function and iodine metabolism Parameters

Preconception steadystate iodine sufficient state ~150 μg per day

Pregnancy steadystate iodine sufficient state ~150 μg per day

Oestrogens Thyroxine binding globulin

Normal Normal

Renal blood flow Glomerular filtration Iodine clearance with obligatory loss of iodine Thyroid gland stimulation Free T4 Peripheral metabolism

Normal Normal Normal

Elevated Elevated in first trimester reaches plateau in second that is maintained in third trimester Elevated Elevated Enhanced

Iodine metabolism

Thyroid gland metabolism unaltered

Normal through TSH Normal Unaltered

Enhanced through elevated HCG (Chorionic gonadotrophins) Slight elevation Alters in second half of gestation under the placental type 3 iodothyronine deiodinase Thyroid gland requires 50% increase in TH production by maternal thyroid gland (physiological adaptation).

Table 18.4 Higher iodine requirement in pregnant women accentuates the deficiency [36] Preconception steady-state iodine sufficient state(a)

Pregnancy steady-state iodine sufficient state

Pregnancy in Iodine deficient state(b)

50% is used by thyroid gland for TH production by ~35% uptake of available iodine Of daily intake, onetenth is lost through faeces and one-third is distributed among thyroid and irreversible urinary loss. Metabolic balance remains positive and ample thyroid stores of iodine are maintained in range of 10–20 mg.

Metabolic balance is maintained in equilibrium mainly through; (a) 30–50% increase in renal iodine clearance; (b) sustained increase in TH production by 50%; (c) lowered circulating plasma inorganic iodine is accompanied by compensatory increase in thyroidal clearance. This is reflected in increased physiological state of thyroid gland. Thyroid stores of iodine are adequately maintained.

Body increases iodide trapping through pituitary-thyroid feedback to maintain necessary absolute iodine intake. A shortfall of 10–20 μg per day occurs. Thyroid gland is forced to use stored iodine that progressively falls to 2–5 μg in continuous deficient state. Metabolic balance becomes negative. In iodine-deficient healthy pregnant women physiological adaptation changes to pathological alterations.

(a) Iodine sufficient ~150–200 μg per day (b) Iodine deficient ~50–75 μg per day

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Epidemiological studies have shown that children born to women with mild to moderate hypothyroxinemia exhibit neurological alterations and reduced IQ scores, as well as an increased incidence of attention problems [25]. Although, a study of children with mild to moderate ID reported an association between first trimester ID and reduced IQ in as many as twothirds of the children [37] confirming the findings reviewed earlier [38], most studies were carried out in the context of maternal hypothyroidism or isolated hypothyroxinemia. A conclusive proof of deficient iodine status in each trimester causing subtle neuro-psychiatric and intellectual deficits in infants/children born to mothers residing in conditions with mild to moderate ID was lacking. The results of a very well-designed study indicate that a brief delay of just a few weeks during early gestation in initiating iodine fortification increases the risk of neuro-developmental delays in the offspring and to almost the same level as in those whose mothers were not iodine-supplemented until term [39]. The fascinating aspects of reported results and its clever study design, unique among all other studies published so far on the consequences of iodine deficiency (ID) during pregnancy have been brought about by equally absorbing editorial [40]. This work not only conveys the message that dietary iodine fortification is important throughout pregnancy, especially at the beginning, but also supports the recommendation of an urgent-daily supplement of iodine to all women when considering conception. The present study confirms that earlier recommendation, based on the randomized clinical trial carried out, was justified not only for maternal health, but also for the offspring [41]. The report gains in importance if one looks at the number of unprotected infants from IDD all over the world (Table 18.2).

18.10 Assessment of iodine status (Impact indicator) 18.10.1Goitre surveys Thyroid size enlargement has been one of the signs of glandular disease that accompanied stunted growth and occurrence of deaf-mutes in mountain ranges all over the world. Recognition that a visible enlargement indicates severity and decrease in thyroid swelling indicates effective correction of iodine deficiency made the size measurement an important tool for clinicians and epidemiologists to make a situation analysis of extent of problem before and after the intervention programs in place. Assessment of goitre size by palpation by trained observers as per criteria’s laid down by WHO–UNICEF from time to time has served the purpose of large scale surveys and national correction program implementation assessment [2– 3]. However, subjectivity in size assessment, lack of understanding of criteria’s and training, over-burdened health system compounded with

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compromise in designing and implementation of survey tools more often leads to erroneous data collection and interpretation. Thyroid-size assessment still remains an instrument of choice for majority of national surveys at least in developing nations due to economic and logistic constraints. In last decade the improvisation in thyroid size measurement by ultrasonography has been validated in most of the western countries especially of Europe [42–43]. Though the technique has the desirable component of accuracy, in terms of training and technical competence at primary health care system, it is still beyond the affordability of developing economies.

18.10.2 Urinary iodine concentration The approximate thyroid clearance rate (TCR) of 0.4 L/h and renal clearance rate (RCR) of 2.0 L/h of a euthyroid normal individual indicate that thyroid gland and kidneys are two major competing organs for the amount of iodine ingested daily. The low TCR of thyroid indirectly reflects daily synthetic output of TH and increased TCR reflects the thyroidal hunger for iodine in a deficient individual [6]. This hunger is directly reflected in lowering of urinary iodine excretion (UIE) making it an exceptionally good marker of very recent dietary-iodine intake. Many studies have convincingly shown that profile of iodine concentration in even a casual urine sample provides an adequate assessment of population’s iodine nutrition provided a sufficient number of samples are collected representing the population group to surmount the day to day and within a particular day variations. It should be borne in mind that UI test done in an individual’s casual sample and its expression in terms of creatinine can further lead to erroneous conclusions. Iodine/Creatinine ratio is of little clinical value due to ignorance of protein intake of the individuals and often leads a unreliable estimates especially in populations suffering from malnutrition Acceptance of urinary iodine (UI) indicator is very high due to ease of collection of a casual urine sample, minimum need of storage like refrigeration and preservatives and simple assay method based on iodine’s catalytic activity in reduction of ceric ammonium sulfate (yellow color) to cerous form (colorless). A digestion/purification step using ammonium persufate or chloric acid is necessary to get rid of interfering substances prior to catalytic reaction [44]. The method is amenable for automation and large-scale analysis and availability of quality control and reference material allows for inter-laboratory comparisons [45]. The median UI concentration is recommended by the WHO [2–3] for assessing iodine

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intake in populations with cut-off levels defined separately for pregnant women. More reference data on UI concentrations in chronically iodine-sufficient pregnant women, including trimester-specific values, would be valuable. The WHO[8] recommends that a median UI concentration in a population of pregnant women of 150–249 μg/l indicates adequate iodine intake (Table 18.5). Table 18.5 Epidemiologic criteria for assessing iodine nutrition in a population of pregnant women based on median urinary iodine concentrations [8] Median urinary iodine

Iodine intake

<150 µg/l 150–249 µg/l 250–499 µg/l

Insufficient Adequate Excessive

The median urinary iodine concentration (UI) in school-aged children is recommended for assessment of iodine nutrition in populations. If the median UI is adequate in school-aged children, it is usually assumed that iodine intakes are also adequate in the remaining population, including pregnant women. The data suggest the median UI in school-aged children should not be used as a surrogate for monitoring iodine status in pregnancy; pregnant women should be directly monitored [47]. The meta-analysis of samples of 6 study sites included 3529 children evenly divided between boys and girls at each year (Mean ± SD age: 9.3 ± 1.9 years) showed a range of median urinary iodine concentrations 118–288 μg/L [48].

18.10.3 Blood constituents as impact assessment indicators: TSH and Tg In spite of the fact that hypothyroidism in an iodine-deficient subject is accompanied by increase in TSH in the measurement of TSH is not recommended for monitoring iodine nutrition for school-based or adultbased surveys due to large amount of overlap. TSH estimations in neonates, however, are a valuable indicator of iodine sufficiency. The neonatal thyroid has a low-iodine content compared to that of an adult, and hence iodine turnover is much higher. This high turnover is exaggerated in iodine deficiency and requires increased stimulation by TSH. Hence, TSH levels are increased the neonates in the first week of life in iodine-deficient populations for first week of life. The prevalence of neonates with elevated TSH levels is therefore a valuable indicator of the severity of iodine deficiency in a given population. Recent data from a large-representative Swiss study suggest that newborn thyrotropin concentrations, obtained with the use

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of a sensitive assay from blood samples collected 3–4 days after birth, is a sensitive indicator of even mild iodine deficiency in pregnancy [50]. These findings support the WHO recommendation that a <3% frequency of thyrotropin values >5 μ/l indicates iodine sufficiency in a population. This finding should be confirmed in other iodine-sufficient countries with newborn-screening programs. For UI, the WHO states that a median 100 μg/l in infants is sufficient [3]. The median UI concentration during infancy that indicates optimal iodine nutrition is estimated to be = 100 μg/l. In iodine-sufficient countries, the medianUI concentration in infants ranges from 90–170 μg/l, suggesting adequate iodine intake in infancy. Nevertheless, TSH screening is inappropriate for developing countries where health budgets are low- and high-infant mortality due to nutritional deficiencies and infections makes the whole exercise costineffective. Thyroglobulin (Tg) In contrast T g, a thyroid protein that acts as a matrix for TH synthesis, is found to be increased in circulation as a result of thyroid hyperplasia and goiter a characteristic of iodine deficiency. In this setting serum Tg reflects iodine nutrition over a period of months or years. This contrasts to urinary iodine concentration which assesses more immediate iodine intake. A serum Tg assay has recently been adapted for use on dried blood spots and makes sampling practical even in remote areas [54]. Measurement of Dried blood spot (DBS) T g in school age children is a sensitive indicator of iodine status in a population and can be used to monitor improving thyroid function after iodine repletion. The international reference range of 4-14 μg /L for DBS Tg assays has been established for iodine sufficient five to fourteen year children. DBS Tg correlates well with urinary iodine and thyroid size and complements these tests and can be used in conjunction with UI to measure recent iodine intake and thyroid volume to assess longterm anatomic response [55].

18.10.4 Assessment of iodine status during pregnancy The median-UI concentration is recommendations by the WHO (2–3) for assessing iodine intake in populations with cut-off levels defined separately for pregnant women have been recently reviewed. Traditionally, the median UI in school-going children is recommended for assessment of iodine nutrition in population. If median UI is adequate in school children, it is usually assumed that iodine intake is also adequate in rest of the population, including pregnant women. A recent study carried out within family eating

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from the same food supply showed that while children had adequate median UI their pregnant mothers had significantly low-median UI [47]. Daily iodine intake can be extrapolated from the UI concentration assuming 24 hours urine volumes and iodine bioavailability of 92% using the formula: urinary iodine (μg/l) × 0.0235 × body weight (kg) daily iodine intake [6, 7, and 34]. Using this formula, a median UI of 100 μg/l corresponds roughly to daily iodine intake of 150 g per day. The pregnancy often occurs in adolescence in developing countries; in a 15 year girl weighing approximately 50 kg, daily iodine intake of 200 to 250 μg would correspond to median UI of 185–215 μ/l. The recommended daily iodine intake during pregnancy of 220–250 μg [31, 35] would correspond to a median UI concentration of 135–155 μg/l during pregnancy. However, during pregnancy this extrapolation of iodine intake from the UI concentration may be less valid because of an increase in RIC [31, 46]. If RIC increases in pregnancy, the daily-iodine intake extrapolated from the UI concentration in pregnancy would be lower than that in non-pregnancy. Table 18.6 Usefulness of impact-assessment indicators of iodine insufficiency are influenced by pregnancy

S. no.

Effects on indicators

Usefulness of indicator

1.

Hypothyroxinemia (low T4 )

2.

Preferential secretion of tri-iodothyronine (T 3)

Non-usable due to changes sometimes within normal range Non-usable due to changes sometimes within normal range

3.

High TSH

4.

Enhanced thyroid volume

5.

Low urinary iodine

6.

Increased serum thyroglobulin

Useful indicator (invasive) cost and feasibility makes its use difficult for populations Good indicator, physical grading is subjective, ultrasound measurement requires trained personal, costly equipment and validation (non-invasive) Useful indicator for short-term iodine deficiency in populations (non-invasive) Useful indicator for long-term iodine deficiency in populations (invasive), amenable to blood spot collection and analysis

18.11 Conclusion Iodine deficiency disorders have multiple adverse effects in humans, most serious being the compromised mental and physical development of progeny. The adequate iodine intake during pregnancy and infancy is essential for prevention of impairment of growth and development of the offspring. Assessment methods including urinary-iodine concentration, goitre, and blood thyroglobulin carried out in school-going children

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frequently overlook the prevailing iodine deficiency during pregnancy and lactation. The monitoring of universal salt iodization programs to assess the impact often does not take into account the need of additional iodine requirement of pregnant and lactating women due to incomplete understanding of iodine metabolism and difficulties in carrying out the metabolic balance studies during pregnancy and lactation. The median UI in school-aged children may not always be a good substitute for monitoring iodine status in pregnancy; it may be sensible to monitor pregnant women directly. The recommended iodine intake in pregnant women by WHO needs further proving by additional scientific evidence to clarify the issue.

References 1. 2. 3.

4.

5.

6. 7.

8. 9. 10. 11. 12.

13. 14.

HETZEL BS (1988). Iodine-deficiency disorders. Lancet 1, no. 8599, pp 1386– 1387. WHO , UNICEF , ICCIDD (2007). Assessment of iodine deficiency disorders and monitoring their elimination. Geneva, Switzerland: WHO. WHO (2007). Technical consultation for the prevention and control of iodine deficiency in pregnant and lactating women and in children less than two years old. 2nd ed. Geneva, Switzerland: WHO. RISTIC - MEDIC D , PISKACKOVA Z , HOOPER L , RUPRICH J , CASGRAIN A , ASHTON K , PAVLOVIC M , GLIBETIC M (2009). Methods of assessment of iodine status in humans: a systematic review. Am J Clin Nutr 89, no. 6, pp 2052S–2069S. YADAV S, GUPTA SK , GODBOLE MM , JAIN M , SINGH U , V PAVITHRAN P , BODDULA R , MISHRA A , SHRIVASTAVA A , TANDON A , ORA M , CHOWHAN A , SHUKLA M, YADAV N , BABU S, DUBEY M , AWASTHI PK (2009). Persistence of severe iodine-deficiency disorders despite universal salt iodization in an iodine-deficient area in northern India. Public Health Nutr 11, pp 1–6. DUNN JT , DUNN AD (2001). Update on intrathyroidal iodine metabolism. Thyroid 11, no. 5, pp 407–414. ALEXANDER WD , KOUTRAS DA , CROOKS J , BUCHANAN WW , MACDONALD EM , RICHMOND MH , WAYNE EJ (1962). Quantitative studies of iodine metabolism in thyroid disease. Q J Med 31, pp 281–305. WOLFF J (1998). Perchlorate and the thyroid gland. Pharmacol Rev 50, pp 89– 105. DAI G , LEVY O , CARRASCO N (1996). Cloning and characterization of the thyroid iodide transporter. Nature 379, pp 458–460. DOHAN O , DE LA VIEJA A , PARODER V (2003). The sodium iodide symporter (NIS): character, regulation and medical significance. Endocrine Rev 24, pp 48–77. SPITZWEG C, HEUFELDER AE , MORRIS JC (2000). Thyroid iodine transport. Thyroid 10, pp. 321–330. VAN SANDE J , MASSART C , BEAUWENS R , SCHOUTENS A , COSTAGLIOLA S, DUMONT JE , WOLFF J (2003). Anion selectivity by the sodium iodide symporter. Endocrinology 144, pp. 247–252. TAUROG A , DORRIS ML , DOERGE DR . Mechanism of simultaneous iodination and coupling catalysed by the thyroid peroxidase. GERARD AC , DAUMERIE C, MESTDAGH C , GOHY S , DE BURBURE C, COSTAGLIOLA S, MIOT F , NOLLEVAUX MC, DENEF JF , RAHIER J , FRANC B, DE VIJLDER JJ , COLIN IM , MANY MC

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19 Sustaining iodine deficiency disorders (IDD) control programme Chandrakant S. Pandav

Chandrakant S. Pandav is a physician, medical scientist, public health specialist, epidemiologist & health economist. Currently, he is Professor and Head at the Centre for Community Medicine at All India Institute of Medical Sciences, New Delhi. Dr. Pandav completed his MBBS and MD (Community Medicine) from AIIMS; M.Sc (Health Economics, Clinical Epidemiology and Biostatistics) from the McMaster University, Hamilton, Canada. He has worked as a consultant for WHO, UNICEF, ICCIDD, PAMM & MI at the global and regional level in over sixty countries, and also in India for more than twenty five years.

'.

Introduction

Only a few countries like the Scandinavian countries, Switzerland, Japan, Australia, the USA and Canada were completely iodine sufficient before 1990. Since then, globally, the number of households using iodized salt has risen from 20% to 68%, dramatically reducing iodine deficiency [1]. This effort has been spurred by UN agencies and International NGOs including WHO, UNICEF, MI and ICCIDD, working closely with national IDD control committees and the salt industry, and funded by Kiwanis International, the Gates Foundation and country aid programs. In 2007, WHO estimated that nearly two billion individuals have an insufficient iodine intake including 1/3 of all school-age children [2] (Table 19.1). Achieving the Universal Salt Iodisation (USI) and thus ensuring that adequate iodine intake is only the first step towards the goal of elimination of IDD. Sustaining USI efforts and tracking progress of IDD elimination is of utmost importance to prevent recurrence of IDD. IDD cannot be eradicated in one great global effort like smallpox and, hopefully, poliomyelitis. Smallpox and poliomyelitis are infectious diseases with only one host, i.e. man. Once eliminated, they cannot come back. In contrast,

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Table 19.1 Prevalence of iodine deficiency in WHO Regions (2007), total number (millions) and percentages, in general population (all age-groups,) in school-age children (6–12 years) in 2007 and the percentage of households with access to iodized salt.

WHO regions(a)

Population with urinary iodine 100 μg/L (b) General population

Africa 312.9 Americas 98.6 Eastern Mediterranean 259.3 Europe 459.7 Southeast Asia 503.6 Western Pacific 374.7 Total 2000.0 (a) (b)

(c)

(41.5%) (11.0%) (47.2%) (52.0%) (30.0%) (21.2%) (30.6%)

% of households with access to iodized salt (c)

School-age children 57.7 11.6 43.3 38.7 73.1 41.6 263.7

(40.8%) (10.6%) (48.8%) (52.4%) (30.3%) (22.7%) (31.5%)

66.6 86.8 47.3 49.2 61.0 89.5 70.0

193 WHO Member States. Based on population estimates for 2006 (United Nations, Population Division, World Population Prospects: the 2004 revision). These figures do not include data for non-UNICEF countries (e.g., the US and Western Europe).

IDD is a nutritional deficiency that is primarily the result of deficiency of iodine in soil and water. Although IDD can be eliminated with iodine supplementation, the iodine deficiency of soil and water would remain and persist with massive deforestation, flooding, and rivers changing its course. IDD can therefore return any time after elimination if there is slackening in iodine supplementation efforts. Thus regular monitoring of Iodine Deficiency Disorders Control Programmes is absolutely critical.

19.2

Controlling of IDD – a three prong strategy

The control of IDD is an essential “three-pronged” involving the following components: ● ● ●

Correcting iodine deficiency Sustaining IDD elimination Tracking progress of sustainable elimination of IDD

19.2.1 Correcting iodine deficiency Correcting iodine deficiency can be done through iodine supplementation or food fortification. (a) Iodine supplementation The first iodine supplements were in the form of an oral solution of iodine

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such as Lugol, which was given daily. In the original controlled trial in Ohio school children (1917–1922), Marine and Kimball used 200 mg sodium iodide in water daily for 10 days in the spring and repeated this in the autumn. Satisfactory regression of goiter was observed. After the Second World War, considerable progress was made in reducing IDD with iodized oil, initially using the intramuscular form and in the 1990s, using the oral form. For example, iodized oil was used with success in Papua New Guinea and thereafter in China, several countries in Africa and Latin America and in other severely endemic areas. The oral form of iodized oil has several advantages over the intramuscular form: it does not require special storage conditions or trained health personnel for the injection and it can be given once a year. Compared to iodized salt, however, it is more expensive and coverage can be limited since it requires direct contact with each person. With the introduction of iodized salt on a large scale, iodized oil is now only recommended for populations living in severely endemic areas with no access to iodized salt. (b) Food fortification with iodine Over the past century, many food vehicles have been fortified with iodine: bread, milk [3], water source [4] and salt. Salt is the most commonly used vehicle. It was first introduced in the 1920s in the United States [5] and in Switzerland [6]. However, this strategy was not widely replicated until the 1990s when the World Health Assembly adopted universal salt iodization (USI), for the iodization of salt meant for both human and livestock consumption, as the method of choice to eliminate IDD. As mentioned above, in 2002 at the Special Session on Children of the United Nations (UN) General Assembly, the goal to eliminate IDD by the year 2005 was set. USI was chosen as the best strategy based on the reasons presented below: In order to meet the iodine requirements of a population it is recommended to add 20–40 parts per million (ppm) of iodine to salt (assuming an average salt intake of 10 g/capita/day) [7]. There are two forms of iodine fortificants, potassium iodate and potassium iodide. Since iodate is more stable under extreme climatic conditions it is preferred to iodide, especially in hot and humid climates such as in India where potassium iodate is used as a fortificant. For historical reasons such as high solubility and lower cost, North America and some European countries use potassium iodide whereas due to greater stability leading to decreased losses especially at high moisture and high temperature, most tropical countries use potassium iodate [8]. (c) Safety in approaches to control iodine deficiency Iodine fortification and supplementation are safe if the amount of iodine

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administered is within the recommended range. Though the optimal requirement of iodine for adults is 150 μg many people are regularly exposed to huge amounts of iodine in the range of 10–200 mg/day without apparent adverse effects. The threshold upper limit of iodine intake (the intake beyond which thyroid function is inhibited) is not easy to define because it is affected by the level of iodine intake before exposure to iodine excess. The WHO stated in 1994 that, “Daily iodine intakes of up to 1 mg, i.e. 1000 μg, appear to be entirely safe” [9]. For more than 50 years, iodine has been added to salt and bread without noticeable toxic effects [10]. Iodine-induced hyperthyroidism (IIH) is the most common complication of iodine prophylaxis and it has been reported in almost all iodine supplementation programmes in their early phases [11]. IIH occurs in the early phase of the iodine intervention and primarily affects the elderly who have long-standing thyroid nodules. However, it is transient and its incidence reverts to normal after one to 10 years. The most well documented epidemic of IIH occurred in Tasmania in late 1960s following substitution of potassium iodate in place of potassium bromate as bread conditioner but increased cases were transient and lasted for only 5 years with only minor peaks following the 1960s epidemic [12]. Similar transient increases in thyrotoxicosis lasting for only a year were reported from Kivu, Zaire in 1990s [13]. Monitoring of salt quality and iodine status of populations and training of health staff in identification and treatment of IIH are the most effective means for preventing IIH and its health consequences [14].

19.2.2 Sustaining IDD elimination Elimination of IDD from a population should always be coupled with mechanism to ensure the sustainability of the program. As has been borne out by numerous case studies across the globe, one time elimination of IDD is not the answer. By virtue of iodine deficiency being the inherent nature of the soil, IDD do recur when the IDD elimination efforts slacken. In several countries where IDD had been eliminated by IS programs – including Colombia, Guatemala, Azerbaijan, and other countries of the former Soviet Union – control programs faltered, and IDD recurred [15, 16, 17]. In Guatemala, a previously effective iodized salt program deteriorated, currently, only 46% of households are receiving iodized salt, the median UI is 72 μg/L, and new cases of cretinism have appeared [15]. In addition, IDD may be reemerging in industrialized countries previously thought to be iodine sufficient, such as Australia and New Zealand [18, 19 ]. The task of sustaining iodine deficiency elimination requires constant

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vigilance. As borne out by experience from both developing and developed countries across the globe in the absence of sustainable efforts, iodine deficiency can reoccur (backsliding). One of the models proposed for sustaining IDD elimination efforts is the Social Process Model. There are three major components to consolidate and sustain the elimination of IDD: (a) Sustained political support (b) Effective administrative infrastructure (c) On-going assessment and monitoring (a) Sustained political support. Political support is essential for the passage of laws or regulations on salt iodization through the legislature. Since governments change, the mechanism to ensure continuity must be in place. The critical role of sustainable political support was highlighted by the removal of ban on sale of iodised salt in India in 2005 and subsequent set back to USI. The ban was reinstated after vigorous efforts by the various national and international agencies working for IDD elimination in the country and civil society at large. (b) Effective administrative infrastructure. The National Body responsible for the management of IDD control programme should operate with a process model. A useful example of such a process model is known as the social process model [20] or the “wheel” described by Hetzel et al (Figure 19.1).

19.1 The social process model

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The social process model for health care programmes may be represented by a six element circular model: Firstly, assess/reassess the situation epidemiologically. 1. Increase awareness of the situation through communication and dissemination of findings. 2. Develop and achieve political resolve and agreement at all levels (from national level to community level). 3. Create and update plans for infrastructure development and plan of action. 4. Vigorously implement the programme. 5. Assess/reassess the programme progress (viz. monitoring and evaluation) to track progress towards sustainable elimination of IDD. (c) On-going assessment and monitoring. The effectiveness of a national programme is providing an adequate amount of iodine to the target population. This is reflected in measurements of salt iodine (at factory, retail and household level) and urine iodine (measured in casual samples from school children or households). Additional measures that would help in the assessment are estimation of thyroid size and blood tests. All these procedures require internal and external quality control in order to ensure reliability of the data collected.

19.2.3 Tracking progress towards sustainable elimination of IDD Ensuring achievement of IDD elimination and sustaining the same thereafter requires tracking of progress made during both the phases. Tracking progress will broadly include indicators to monitor salt iodine content, iodine status of population and programme indicators. Salt iodine content needs to be monitored both at production and consumer level including the supply chain. The indicators short listed to monitor the iodine status of population are thyroid size by palpation and/or by ultrasonography, Urinary Iodine (UI), Thyroid Stimulating Hormone (TSH) and Thyroglobulin (TG). In Jan 2007 a joint WHO/UNICEF/ICCIDD Technical meeting (IDD Network Board Meeting, Atlanta, 22nd to 23rd February, 2007) looked at revising guidelines on IDD indicators. Changes agreed to include: 1. Introduction two new indicators: serum concentration of thyroglobulin and thyroid volume as measured by ultrasound. 2. Decision tree to facilitate choice of indicator (A decision tree would enable modeling of decisions taken to select a particular indicator and their possible consequences, including chance event outcomes, resource costs, and utility). 3. Inclusion of pregnant women among population to be surveyed.

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(a) Three phases of IDD elimination programmes – relationship between laboratory and clinical indicators Tracking progress towards sustainable elimination of IDD involves assessment of iodine status of the population. Iodine status can be done using a set of laboratory and clinical indicators which are closely related to each other. But the co-relation between these laboratory and clinical indicators is not a linear correlation and changes with the evolution of the IDD elimination programs. In general, the Iodine Deficiency Disorders Elimination Programmes in any region can be seen going through three phases. The three phases depict a gradual evolution from the .virgin state of iodine deficiency to the iodine replete state. The status of the indicators of assessment of Iodine Deficiency is variable from phase to phase (Figure 19.2). The three phases are given below: 1. Phase 1 – Community Diagnosis (Iodine deficiency) 2. Phase 2 – Community Intervention (Iodine deficiency to sufficiency) 3. Phase 3 – Sustainability (Ensuring optimum iodine intake) Phase 1: Community diagnosis. This is the phase where the problem has been newly detected. Iodine deficiency exists as a public health problem and efforts to recognize it and measures to control it are yet to be initiated. In this case there is a good association between the Total Goitre Rate (TGR) and Urinary Iodine Excretion (UIE). This is because the thyroid gland, which has been starved of iodine, will take up as much of the iodine as it possibly can and the rest is excreted in the urine. Phase 2: Community intervention. In this phase, the intervention has already begun and a mixed picture is often observed. The impact indicators are determined by environmental and community factors. Goitre is a historic marker of iodine deficiency. The inverse association between TGR and UIE is not seen. Even though the median urinary iodine values are on the increase, there is a time lag before the goiter prevalence also starts decreasing. Phase 3: Sustainability. Control of iodine deficiency is the initial success that an effective programme will achieve. Soon after, there comes into play the need for sustainability of the control programme already in place. This is with the aim to ensure optimum iodine intake on a regular and continuous basis for all time to come. In this phase, once again, there is a good association between TGR and UIE. The three indicators mentioned below in Fig. 19.2 assess different aspects of the IDD status in a community and thus help to track progress towards elimination of IDD. For example, iodine content of salt samples collected in a cross-sectional survey indicates the present level of iodine in salt, but gives no information about the variation occurring in the past.

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19.2 Relationship between laboratory and clinical indicators

Total goiter rates show long term effects of bioavailability of iodine and the urinary iodine excretion pattern reflects the existing levels of iodine intake and body iodine stores. To understand the status of IDD elimination programmes, the result of these indicators should be viewed in totality. In addition there are various environmental and community factors that play a role in Phase 2 of the IDD Elimination Programme (Figure 19.3).

19.3 Factors influencing duration of phase of transition

The following three environmental factors play a role in the Phase 2 of the IDD Elimination Programme: 1. Severity of iodine deficiency – The severity of iodine deficiency plays an important part in the efforts to eliminate IDD. It is known that more severe the iodine deficiency, more intense efforts that are needed to bring the iodine deficiency under control.

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2. Duration of iodine deficiency – To a part, it is also important how long the region/area has been under the effects of iodine deficiency. 3. Control measure – It is important that the monitoring of the control measure is in place. The persistence of goiter during Phase 2 can also be due to the consumption of non-iodized or inadequately iodized salt by part of the population. In case of iodized salt, one has to make sure that adequately iodized salt is consumed by the population on a regular basis. If it is not so, which is the case in most situations, a scenario emerges where there is no association between total goiter rate and urinary iodine excretion. The population factors that play a part in Phase 2 are age, gender and physiological status such as pregnancy and lactation. It is seen that the effects of iodine deficiency tends to show up more vividly in the younger age groups and in females whose physiological status such as pregnancy and lactation makes them vulnerable. (b) Tracking progress towards sustainable IDD elimination In order to achieve the failed global goal set for 2005, IDD control programmes and monitoring need to be constantly sustained due to the fact that IDD simply re-appears if salt iodization is interrupted. This may happen when the responsible public health authorities are demobilized or if the salt industry fails to effectively monitor iodine content. In order to assess the sustainability of control programmes and track their progress towards the IDD elimination WHO has established goals and indicators (Table 19.2). Table 19.2 Criteria for monitoring progress towards sustainable IDD elimination Indicators Salt iodization coverage (a) ● Proportion of households consuming adequately iodized salt Urinary iodine ● Proportion of population with urinary iodine levels below 100 μg/l ● Proportion of population with urinary iodine levels below 50 μg/l Programmatic indicators (i) National body responsible to the government for IDD elimination. It should be multidisciplinary, involving the relevant fields of nutrition, medicine, education, the salt industry, the media, and consumers, with a chairman appointed by the Minister of Health. (ii) Evidence of political commitment to USI and elimination of IDD;

Goals >90% <50% <20% At least 8 of the 10

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Indicators

Goals

(iii) Appointment of a responsible executive officer for the IDD elimination programme; (iv) Legislation or regulation of USI (v) Commitment to regular progress in IDD elimination, with access to laboratories able to provide accurate data on salt and urinary iodine (vi) A programme of public education and social mobilization on the importance of IDD and the consumption of iodized salt (vii) Regular data on iodized salt at the factory, retail and household levels; (viii) Regular laboratory data on urinary iodine in school-age children, with appropriate sampling for higher-risk areas; (ix) Co-operation from the salt industry in maintenance of quality control; and A database for recording results or regular-monitoring procedures particularly for salt iodine, urinary iodine and, if available, neonatal thyroid stimulating hormone (TSH), with mandatory public reporting. Source: WHO, UNICEF, ICCIDD. Assessment of iodine deficiency disorders and monitoring their elimination. Geneva, World Health Organization, 2001 (WHO/NHD/01.1) (a)

Adequately iodized salt refers to at least 15 ppm at household level

The problem of IDD is still largely perceived as equivalent to “Goiter”. People consider it a cosmetic problem and hence a low priority issue. Focus should be more on the implications that iodine deficiency has on the Intelligence Quotient (IQ) of the child and the contribution of elimination of IDD to at least six of the Millenium Development Goals. Iodized salt should be viewed as a vaccine to prevent brain damage. History teaches us that the sustained elimination of IDD requires constant vigilance of a range of professional and public interests. Achieving elimination of IDD and thereafter sustaining it more to put it more aptly, tracking progress towards sustainable elimination of IDD should be the priority goal for national policy makers. The experience from both developed and developing countries across the globe and over a long period of time has shown the recurrent nature of IDD and thus underline the importance of sustained efforts to combat IDD. The lessons learned from the more successful countries are ●

●

Hold regular “National Advocacy” events to assure that all actors in the field are informed, active and participating. Hold regular “National and Sub National Monitoring Activities” and report them widely to demonstrate not only progress but where problems are difficult

Sustaining iodine deficiency disorders (IDD) control programme ●

●

533

Maintain constant public information on the problems of iodine deficiency and the dangers of absence of iodine. Sustain high level national political commitment across the board.

There is a need for simple, operative, comparative and functional monitoring designs with a global oversight group not only to implement the 2005 World Health Assembly (WHA) Resolution of sustaining the elimination of IDD but to ensure that gains made are sustained thereafter. The control of IDD is essential a three pronged strategy involving correcting iodine deficiency, sustaining IDD elimination and tracking progress of sustainable elimination of IDD. Databases are moving toward urinary iodine (UI) as a key indicator (because it tracks improvements in iodine intake more rapidly than goiter). This trend needs to be accelerated. The global databases on iodine nutrition need to be strengthened. There is need to learn from countries like China, Bolivia, Brazil, Ecuador and Bhutan, which have a sustainable IDD elimination program in place. Sustainability requires national commitments. Sustained political support, effective administrative infrastructure and communication and on-going assessment and monitoring are essential components of proposed social process model of sustainable iodine deficiency disorders elimination. The country level policy maker need to short-list and arrive at a consensus on indicators to be used to track the progress of sustainable IDD elimination keeping in mind the relationship amongst the indicators changes with the phase of elimination and should be interpreted accordingly. Countries should redouble their commitment to sustained elimination of IDD as a part of their regular public health programs and anti-poverty efforts through USI. A critical component of this is to establish multidisciplinary national coalitions that include salt producers and the education and media sectors, to monitor the state of iodine nutrition every three years and report to the WHA on their progress.

References 1.

DELANGE F , BÜRGI H , CHEN ZP , DUNN JT ,

(2002). ‘World status of monitoring iodine deficiency disorders control programs’, Thyroid, 12(10), pp. 915–924. 2. BENOIST B DE, MCLEAN E, ANDERSSON M (2007). Iodine deficiency in 2007: Global progress since 2003’, Food Nutr Bull 2007 (in press). 3. PHILLIPS DIW (1997). ‘Iodine, milk, and the elimination of endemic goitre in Britain: the story of an accidental public health triumph’, Journal of Epidemiology and Community Health, 51, pp. 391–393. 4. Anonymous (1997). ‘Iodized water to eliminate iodine deficiency’, IDD Newsletter, 13, pp. 33–39.

534 5. 6.

7.

8. 9. 10. 11. 12. 13. 14.

15.

16.

17. 18. 19. 20.

Public health nutrition in developing countries MARINE D , KIMBALL OP

(1920). ‘Prevention of simple goiter in man’, Archives of Internal Medicine, 5, pp. 661–672. BÜRGI H , SUPERSAXO Z , SELZ B (1990). ‘Iodine deficiency diseases in Switzerland one hundred years after Theodor Kocher’s survey: a historical review with some new goitre prevalence data’, Acta Endocrinology (Copenhagen), 123, pp. 577– 590. WHO, UNICEF , ICCIDD (1996). ‘Recommended iodine levels in salt and guidelines for monitoring their adequacy and effectiveness’, World Health Organization, Geneva (WHO/NUT/96.13). Available at http://www.iccidd.org/pages/protecting-children/fortifying-salt/ how-salt-is-iodized/iodate-or-iodide-more-detail.php Iodine and health. Eliminating iodine deficiency disorders safely through salt iodization, Geneva, World Health Organization, 1994. BÜRGI H , SCHAFFNER T , SEILER JP. (2001). The toxicology of iodate: A review of the literature. Thyroid, 11, pp. 449–456. STANBURY JB et al. (1998). Iodine-induced hyperthyroidism: occurrence and epidemiology. Thyroid, 8, pp. 83–100. CONNOLLY RJ (1971). An increase in thyrotoxicosis in southern Tasmania after an increase in dietary iodine, Med J Austral i: 1268. BOURDOUX PP , ERMANS AM , MUKALAY WA MUKALAY A , FILETTI S , VIGNERI R (1996). Iodine-induced thyrotoxicosis in Kivu, Zaire. Lancet, 347(9000), pp. 552–553. TODD CH (1999). Hyperthyroidism and other thyroid disorders. A practical handbook for recognition and management. Geneva, World Health Organization, (WHO/AFRO/NUT/99.1, WHO/NUT/99.1). Current IDD Status Database. International Council for the Control of Iodine Deficiency Disorders Website. Internet: http:/www. iccidd.org (accessed 11 September 2009). MARKOU KB , et al. (2001). Iodine deficiency in Azerbaijan after the discontinuation of an iodine prophylaxis program: reassessment of iodine intake and goiter prevalence in schoolchildren. Thyroid,; 11, pp. 1141–1146. DUNN JT (2000). Complacency: the most dangerous enemy in the war against iodine deficiency. Thyroid, 10, pp. 681–683. LI M, MA G , BOYAGES SC and EASTMAN CJ (2001). Re-emergence of iodine deficiency in Australia. Asia Pac J. Clin. Nutr. 10, pp. 200–203. THOMSON CD, WOODRUFFE S , COLLS AJ, JOSEPH J and DOYLE TC (2001). Urinary iodine and thyroid status of New Zealand residents. Eur J. Clin. Nutr. 55, pp. 387–392. HETZEL BS (1987). An overview of the prevention and control of Iodine Deficiecncy Disorders. In: Prevention and Control of Iodine Deficiency Disorders (HETZEL BS, DUNN JT , STANBUIY JB, eds). Elseiver Science Publishers B.V. (biomedical Division), pp. 7–31.

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Iodine deficiency and iodine deficiency disorders (IDD) control program Sheila C. Vir

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

20.1

Epidemiology of iodine deficiency

Iodine, a micronutrient, is an essential element for normal growth and development in animals and men. Iodine is not synthesized by the body and is required to be provided through the daily diet in the recommended amounts. Iodine deficiency occurs when iodine intake falls below the recommended levels. Iodine requirements for various population groups range from 90 to 250 μg/day, the requirement being much higher during pregnancy and lactation (Table 20.1). During lactation, a higher level of iodine is required to meet the additional demands during the first six-month period of exclusive breastfeeding and for the maintenance of adequate level of iodine. Table 20.1 Recommended daily intake of iodine [1, 2, 3] Age/state

Micrograms per day

0–59 months 6–12 years >12 years (adolescents) to adults Pregnancy lactation

90 120 150 250 250

535

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Public health nutrition in developing countries

Iodine deficiency in food occurs when crops are grown in iodine-deficient soils. Reduction of iodine in soil is a natural ecological phenomenon that occurs in many parts of the world. Iodine occurs in the form of iodide in soil and sea water. Iodide is oxidized by sunlight to elemental volatile iodine. The concentration of iodide in sea water is about 50–60 μg per litre while the concentration of iodine in the atmospheric air is much lower at approximately 0.7 μg/m3. Iodine present in atmosphere is returned to the surface of earth by rain which has iodine concentration in the range of 1.8– 8.5 μg/l. Iodine in soil is further reduced due to leaching by rain, flooding, deforestation and glaciations. This cycle of iodine in nature between the ocean, the atmosphere, and rainfall into streams, river, and soil is not maintained resulting in loss of balance in the iodine cycle in nature and depletion of iodine in soil. Persistent lower level of iodine in soil occurs when return of iodine to soil by rain is slow and small in amount compared to original big loss of iodine by floods or glacial. In fact, large loss of iodine from soil surface has been occurring for years with continuous leaching of iodine from the surface soil by glacial, snow and rain which are carried by wind, rivers and floods into sea. Iodine content of soil can be assessed by estimation of iodine levels in local drinking water – iodine-deficient areas have water-iodine levels below 2 μg/l [4]. Crops and animals raised on iodinedeficient soil have low-iodine content (Table 20.2). Table 20.2 Iodine content of some common Indian foods [5] Food item

Iodine content (µg/1000 grams)* Goitrous region

Non-goitrous region

Cereals Rice Wheat Pulses / oils Lentil Soyabean Groundnut Vegetables / fruits Amaranth Ladies finger / cabbage / onion Fruits (apple, orange, banana, grapes, papaya)

10 15

40 32

4 4 14

13 49 47

8 Nil Nil

15 3–6 5–16

Iodine deficiency results from geological rather than social and economic conditions [6]. The richest dietary source of iodine is seafood and seaweeds. Iodine in drinking water is usually a small part of total iodine intake, providing less than 10% iodine in the most iodine rich areas [7]. Low-iodine content in foods grown in soil deficient in iodine fails to meet the daily recommended intake of this essential micronutrient and results in iodine deficiency in diets of human beings and animals. Iodine content is further reduced in foods during

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the cooking process – the average iodine loss is estimated to be about 20%. Depending upon the method of cooking used, the loss of iodine could range between 6 and 70 percent [3, 5, 7, 8]. Iodine deficiency cannot be eliminated either by changing dietary habits or by growing and consuming specific types of foods which is primarily produced in iodine-deficient regions. In the past, severe iodine-deficient environments were considered to commonly exist in only mountainous areas and in elevated regions with high rainfall as well as in regions with frequent flooding. The occurrence of iodinedeficiency disorders (IDD) was therefore primarily considered to be restricted to such specific geographic areas such as mountain ranges and alluvial plains. Goitre surveys, combined with increasing use of urinary iodine measurement and other methods for assessing iodine deficiency, have revealed that IDD has a much wider occurrence. Moreover, even those areas which are relatively free of IDD problem are at risk of becoming endemic because of intensive agricultural operations which can result in depletion of iodine in soil. Living on sea coast does not guarantee iodine sufficiency. In recognition of such wider occurrence of IDD than previously thought, the entire population of a region or a country is considered to be at risk of iodine deficiency. Iodine deficiency, when endemic, affects the entire population in various age groups and manifests different physiological and pathological consequences. In addition to lack of iodine from food consumed, environmental goitrogens found in food and water interferes with iodine metabolism at various levels, from absorption of iodine to synthesis and utilization of thyroxin and in such situations exacerbates iodine deficiency. Some of these goitrogens are thiocyanates, iso-thiocyantes, thio-oxazolidone, flavanoids, disulphides, phenols, phthalates, biphenyles, lithium, etc. Food items such as jowar, finger millets, tapioca ,cassava, kale, cabbage, cauliflower, mustard seeds, ground nuts contain goitrogens and regular consumption of these foods reduce production of thyroid hormone through a variety of mechanisms and play an important role in the aetiology of endemic goitre. Iodized salt can overcome the negative effects of environmental goitrogens. However, it may be necessary to discourage consumption of goitrogenic foods or increase the level of iodine during salt iodization [9].

20.2

Iodine deficiency disorders – a public health problem

In mid 1990s, it was estimated that more than 2 billion people from 130 countries were at risk of IDD (Table 20.3). In 2006, it was estimated that there were only 47 countries where IDD continues to be a public-health problem compared to 54 in 2004 and 126 in 1993 [3]. The human body contains about 15–20 mg of iodine, of which 70–80%

538

Public health nutrition in developing countries

is in thyroid gland. Iodine is an essential constituent of thyroid hormone thyroxine (T4) and triiodothyronine (T3). Thyroid hormones are involved in a wide range of biological functions and are also involved in the regulation of development and differentiation of nearly all organs and systems through their influence on gene expression. Iodine deficiency results in thyroid gland being not able to synthesize adequate amounts of thyroid hormone. In children, iodine deficiency is characteristically associated with goitre and the prevalence of goitre increases with age [9]. In adults, as in school children, the most common visible manifestation is a goitre – a mass in the neck that is consistent with an enlarged thyroid that is palpable. The enlargement may or may not be visible when neck is in a neutral position. Females from adolescence onwards have a higher prevalence of goitre than males and this is associated with difference in metabolism during the growth period. However, classical clinical hypothyroidism is characteristically absent in most adults suffering from endemic goitre, while sub-clinical hypothyroidism with reduced thyroxine (T4) levels accompanied by normal triiodothyronine (T3) levels is common. Adults do not reliably reflect the existing iodine status due to the fact that nodules and goitre could have occurred in childhood and iodine supplementation may only partially influence goitre size while thyroid stimulating hormones (TSH) levels would be normalized only in a fraction of population [9]. Table 20.3 Estimates of population at risk of IDD by WHO regions in 1997 (a) [10] WHO regions Africa America South-East Asia Eastern Mediterranean Europe Western Pacific TOTAL (a) (b)

(c)

Countries with IDD 44 19 9 17 32 9 130

Total population in IDD countries Millions 610 477 1, 435 468 670 1, 436 5, 096

At risk population (b) Millions 295 196 599 348 275 513 2, 226

% (c) 48 25 41 74 32 31 38

Based on UN population division (UN estimates 1997); The at risk population is the population living in iodine deficiency areas where total goiter rate (TGR) is more than 5%; Expressed as a percentage of the total population in the region (ICCIDD/WHO/UNICEF 1999).

The most important adverse effect of iodine deficiency is on foetal brain damage. Iodine deficiency is specially damaging during early pregnancy and childhood [15]. The most critical period is from the second trimester of pregnancy to the third year after birth since impaired synthesis of thyroid hormones by mother and foetus has serious implications on brain development [2]. A significant degree of neurological development

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occurs within weeks of conception and especially during the first month of foetal growth. An insufficient supply of thyroid hormones to the developing brain of foetus in early months of gestation adversely affects brain development and may result in mental retardation. In foetus, iodine deficiency affects neurological development and even mild deficiency of iodine in the mother has effects on rapidly growing foetal brain. The first three years of life is critical since 90 percent of human brain development occurs by the third year of life. Severe form of iodine deficiency causes cretinism [19, 20]. Cretinism is a syndrome of both neurological and physical parameters with mental and growth retardation resulting from the deficiency of thyroid hormones during foetal and early life. Endemic cretinism is usually found where the prevalence of endemic goitre is higher than 30% and median urinary iodine concentration is less than 25 μg/g of creatinine [7]. It is now well known that that cretin is the most extreme form of iodine deficiency while subtle degree of brain damage and reduced cognitive capacity affecting the population is often goes unnoticed and public-health significance of iodine deficiency is not well-appreciated. An association between iodine deficiency and brain damage was originally proposed after studies showed an association between goitre and endemic cretinism. A study with iodized oil in Papua New Guinea established the fact that cretinism could be prevented by correction of iodine deficiency before pregnancy [11]. This association was also reported from Europe where correction of iodine deficiency resulted in apparent spontaneous disappearance of cretinism in Europe [12]. Studies with animal models confirmed that iodine deficiency caused retardation of foetal brain development [13]. Studies of such animal models and controlled trials clearly established that prevention of brain damage could be achieved by correction of iodine deficiency before pregnancy [14]. The term iodine deficiency disorders (IDD) was proposed by Hetzel in 1983 [15]. “IDD refers to all the consequences of iodine deficiency in a population that can be prevented by ensuring that the population has an adequate intake of iodine” [3]. The adoption of the term emphasizes that the problem of iodine deficiency is extended far beyond simple goitre and cretinism (Table 20.4). These early effects are preventable but not reversible [4, 15]. Iodine deficiency is the world’s single greatest cause of preventable mental retardation [14, 15]. Effects on brain damage occur at all stages of life [14, 15] from foetal damage to the effects of hypothyroidism in the neonate, child or adult (Table 20.4). Incidence of neonatal hypothyrodism and median urinary iodine levels of general population have been observed to be correlated.

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Public health nutrition in developing countries

Table 20.4 The spectrum of iodine deficiency disorders (IDD) [3] All ages

Goitre Hypothyroidism Increased susceptibility to nuclear radiation Spontaneous abortions Still births Congenital anomalies Perinatal mortality Endemic cretinism including mental deficiency with a mixture of mutism, spastic diplegia, squint, hypothyroidism and short stature Infant mortality

Foetus

Neonate

Child and adolescent Adult

Impaired mental function Delayed physical development Iodine induced hypothyroidism (IIH) Impaired mental function Iodine induced hypothyroidism (IIH)

With acceleration of salt-iodization programme, the population at risk of iodine deficiency and risk of brain damage has been reduced. However, the magnitude of problem continues to remain a great concern to publichealth experts. Annually, as presented in Fig. 20.1, it is estimated that 38 million newborns in developing countries where the goal of Universal Salt Iodization (USI) has not been achieved are at risk of life-long consequences of brain damage associated with iodine deficiency [16]. Of the overall 38 million newborns, 18 million are in South Asia and of these 13 million are estimated to be in India.

20.1 Distribution of infants born in developing countries annually who are unprotected against IDD, by region, 2000–2006 [16]

Other effects of iodine deficiency include impaired psychomotor and cognitive development. Neonatal hypothyroidism due to iodine deficiency may cause impaired mental and physical development and has been

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recorded in IDD endemic regions [9]. Lower school performance and significant difference in IQ have been reported in various studies comparing children from iodine deficient and iodine-sufficient areas. A meta-analysis of 18 studies comparing the performance of iodine-deficient children with iodine sufficient peers on a standardized intelligence quotient (IQ) concluded that iodine deficiency alone lowered the mean IQ scores by 13.5 points in school-aged children [17]. Lowering of mental performance due to iodine deficiency has an immediate effect on child-learning capacity and school performance. In addition, deficiency of iodine has adverse impact on women’s health, the quality of life of communities and overall economic productivity with resulting adverse social and economic effects. The primary clinical manifestations of iodine deficiency in adults are goitre (Table 20.4). In a person affected by iodine deficiency, thyroid gland makes an effort to increase the level of thyroid hormones in the blood and enlarges to form goitre. Goitre, an enlargement of thyroid gland, usually represents thyroid hyperplasia in response to insufficient iodine intake. Goitre is defined as enlargement of thyroid such that lateral lobes are larger than the terminal phalanx of the thumb of the person who is being examined by palpation on physical examination. The severity of goitre is usually proportional to the severity of iodine deficiency and with persistent enlargement of thyroid; nodules can form [7]. The status of IDD in general population is reflected by the total goitre rate in school children. However, it may be noted that in fact significant iodine deficiency has been found even in regions where the prevalence of goitre, based on palpation, is normal [18]. Iodine deficiency in women is associated with infertility and impaired fetal development [21]. From areas of iodine deficiency, higher rates of spontaneous abortions and still births have been reported. Improvement in iodine status with regular use of iodized salt is associated with reduction in stillbirths and congenital anomalies [22]. Higher perinatal mortality has been associated with goitre during pregnancy. Various controlled clinical trials of iodine supplementation, in the form of iodized oil injections, oral iodized oil or iodinated water undertaken in countries such as Zaire, Papua New Guinea, Indonesia and China have demonstrated 30–50% reduction in perinatal, infant and child mortality with improvement in iodine status [7]. The impact of iodine deficiency on animals is not well-recognised. Epidemiological and experimental studies indicate that reproductive, neurological and other defects are important effects of iodine deficiency in animal population. Reproductive failure, abortions and still births as well reduced milk and meat yields from animals and lower wool production from sheep has been reported [6, 23]. Milk production is positively correlated with iodine intake for many animals. Long-term deficiencies

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Public health nutrition in developing countries

may result in decreased milk production that is important for the health of offspring as well as human consumption. Iodine supplementation has been reported to increase milk yield by 4–15%. Reproductive failure is the outstanding manifestation of iodine deficiency in farm animals. IDD in animals may also be more severe since animals are dependent on a relatively closed food chain compared to humans who have access to foods imported from non-deficient areas [24].

20.3

Elimination of iodine deficiency disorders (IDD) – international focus

At international level, a beginning was made in 1983 to address the problem of IDD [14]. In 1985, an international multidisciplinary network ICCIDD (International Council for Control of Iodine Deficiency Disorders) was formed to bridge the gap between research and its application in national programmes. The 1986 World Health Assembly (WHA), with representation of over 160 countries, passed a resolution which recognised the importance of iodine deficiency as a cause of brain damage and need for effective programmes of prevention and control [25]. This was followed by a WHA Resolution in 1990 [26] which adopted the goal of elimination of IDD as public-health problem by the year 2000. The goal for virtual elimination of IDD by the year 2000 was adopted by the World Summit for Children in September 1990 and was the part of action for child survival development and action – it was in fact one of the 27 goals accepted by the World Summit for Children [27]. In 1994, IDD prevention and control through universal salt iodization (USI) was endorsed as a safe, cost-effective and sustainable strategy to ensure adequate iodine consumption through achieving the USI goal. In 1996, there was an emphasis on significance of the sustainability of the programme through systematic monitoring [28]. The emphasis on sustainable elimination of IDD by 2005 was the goal adopted by the UN general Assembly in 2002. Table 20.5 presents the major milestones for elimination of IDD.

20.4

Fortification of salt with iodine

Unlike other nutrients such as iron, calcium or vitamins, the nutrient iodine does not occur naturally in specific foods but is in fact imbibed through foods grown on soil-containing iodine. Food grown in iodine-deficient regions can never provide enough iodine to the population or livestock living in the region. Daily dietary consumption of iodine through food fortification is essential. This led to efforts to experiment with fortification of selected food items as well as drinking water with iodine. Finally fortification of salt with iodine was considered the most suitable sustainable public health measure to ensure regular consumption of iodine.

Iodine deficiency and iodine deficiency disorders (IDD)...

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Table 20.5 Major United Nations milestones for elimination of iodine deficiency [3, 16] Year

Milestone

Programme progress

1990

Declaration of the World Summit for Children includes goal of virtual elimination of iodine deficiency disorders (IDD) 43rd World health Assembly accepts IDD elimination by 2000 as a major public health goal for all countries

Accelerated programme initiation and a shift from iodine supplementation to salt iodization

1993

WHO – UNICEF recommended universal salt iodization (USI) as the main strategy for elimination of IDD

1994

UNICEF – WHO Joint Committee on IDD prevention and control through Health Policy endorses universal expansion of salt-iodization salt iodization (USI) as a safe, cost- programmes effective and sustainable strategy to ensure sufficient intake of iodine by all individuals UN General Assembly Special Session Programme maturation with improveon Children adopts “A World Fit for ments in enforcement, public educChildren”, the declaration that set the ation and advocacy, monitoring and goal of sustainable elimination of IDD partnership with salt industry by 2005 World Health Assembly adopts resolution committing reporting on the global IDD situation every three years. “A World Fit for Children” commem- Enhancements in programme orative session reviews progress in sustainability achieving and sustaining IDD elimination through universal salt-iodization programmes

2002

2005 2007

Iodization of salt was first suggested by Boussingault of Colombia, South America in 1883 for prevention of goitre since it was observed that local people benefited from salt containing large quantities of iodine, obtained from an abandoned mine in Guaca, Antioquia [29]. The first large scale trials with iodine were carried out between 1916 and 1920 by Marine and Kimball in Akron, Ohio, USA and this was followed with the introduction of mass prophylaxis of goitre with iodized salt on community scale in Michigan in 1924. The impact of iodized salt in control of goitre in Switzerland is well-documented. In Asia, actions for supply of iodized salt was initiated in the 1950s and 1960s but the progress was minimal until the late seventies [6]. Salt has been accepted to be the most appropriate food vehicle for fortification with iodine for the following reasons: ●

Salt is universally consumed by almost all sections of a community irrespective of economic levels.

544 ●

●

●

●

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Public health nutrition in developing countries

Salt is consumed at approximately the same level through out the year in a region by all normal adults. Production of salt is limited to a few production centres and therefore processing on economic scale and under controlled conditions is feasible. The process of addition of iodine to salt is a simple technology and produces no adverse effect. The addition of iodine to salt does not impart any colour, taste or odour to the salt and iodized salt is indistinguishable from uniodized salt. The cost of iodization is low – on an average less than 5% of total cost at retail level.

The process of fortification with iodine or iodization consists of mixing salt with a determined quantity of a compound of iodine such as potassium iodide or potassium iodate. The iodine compound can be mixed with salt using the fortificant potassium iodide or potassium iodate in a dry form (dry method) or in solution form (wet method). Potassium iodate is more stable and therefore recommended for salt iodization in hot, humid environment where salt quality and packaging is less than ideal. Under proper iodization and packaging conditions (polyethylene bags of 75–80 micron thickness and containing 500 g salt), iodized salt has been found to retain at least 90% of iodine over 18-month period, irrespective of climatic conditions and textures [3]. Earlier it was estimated that iodized salt retained at least 75 percent of iodine after nine months of storage [5]. There is no universal global specifications for the level of iodine to be added to salt for iodization [30]. However, guidelines for estimating levels of iodine for salt at different salt consumption levels, environment and packaging conditions have been recommended [30, 31] as presented in Table 20.6. Every country therefore based on local conditions must have regulations defining a minimum and maximum level of iodine at the point of production and consumption levels. As presented in Table 20.6, for recommending level of iodine for a given population, numerous factors need to be taken into consideration such as per capita consumption of salt in the region, degree of iodine deficiency, type of packaging, transit losses due to heat and humidity, shelf-life required. Per capita consumption of salt in different countries is estimated to range between 5 and 15 grams per day. For example, in India, the average consumption of salt is estimated to be 10 g/ day and the cut-off level for minimum level of iodine in salt at production level is 30 ppm (50.6 mg potassium iodate) and at the consumption level 15 ppm. Most countries have fixed levels of 50 ppm (1 μg/g = 1 ppm) iodine at the time of production which corresponds to 85 mg potassium iodate. Global production and supply of iodine is derived from the nitrate deposits of Northern Chile, extraction of plants in Orient and North America and from brine wells in Japan as well as in North America.

Iodine deficiency and iodine deficiency disorders (IDD)...

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Table 20.6 WHO/UNICEF/ICCIDD guidelines for recommended levels of iodine in salt (a) [30, 31] Parts of iodine per million (ppm) of salt (i.e., µg/g, mg/kg, g/tonne) for bulk and retail pack Climate and Required at factory average per outside the country capita salt intake (g/head) Bulk Retail sacks pack (<2 kg) Warm moist 5g

Required at factory inside of country

Required at retail sale (shop/market)

Bulk sacks

Retail pack (<2 kg)

Bulk sacks

Retail pack (<2 kg)

Required at household

100

80

90

70

80

60

50

50

40

45

35

40

30

25

5g 10 g

90 45

70 35

80 40

60 30

70 35

50 25

45 22.5

Cool dry 5g 10 g

80 40

60 30

70 35

50 25

60 30

45 22.5

40 20

10 g Warm dry or cool moist

(a)

168.6 mg potassium iodate =100 mg iodine; 1 μg iodine/gram = 1 ppm

20.5

Universal salt iodization (USI)

Universal salt iodization (USI) has been recommended as a safe, costeffective and sustainable strategy to ensure sufficient intake of iodine by all individuals in a region [27]. The policy of USI for sustained elimination of IDD was adopted by the joint UNICEF/WHO Committee on Health Policy 1994 with the goal to ensure that all salt for human and animal consumption, both locally produced and imported, is properly iodized, according to the national legislative and regulatory environment [32]. USI requires that all food grade salt for human and animal consumption be iodized including salt used by food industry [33]. The international goal for USI is achieved when over 90% of a representative sample of households is found to be using adequately iodized salt, defined as >15 ppm iodine [1]. Following 1994 Health Policy, USI was globally adopted as the main strategy to eliminate IDD. USI efforts were accelerated between 1995 and 2000 and countries were mobilized to introduce the policy of iodization of all edible salt regardless of having reported IDD problem. The USI commitment was renewed at the UN General Assembly Special Session on Children (UNGASS) in 2002. In the declaration “World Fit for Children”, 190 countries reinforced the need to sustain elimination of IDD [34]. By 2005, about 120 countries were implementing salt iodization programme compared to 90 in 2000 [35]. For the long-term success of the programme, all salt needs to be iodized to correct levels [36]. Iodized salt

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is the first global experience in national fortification of a food item to eliminate a public health problem [37]. Also USI is a unique successful example of public–private partnership for addressing a public health problem. China and Nigeria were the first countries to achieve USI. In China, iodized salt intervention was first implemented in Chengde, Hebei Province and then expanded to the entire northern China after an important epidemiological survey, clinical investigation and intervention study was undertaken in 1960. The programme was later expanded to other IDD endemic areas in 1980s. In 1993, the Chinese Government made a political commitment for the elimination of IDD and achieved the goal of USI goal in the year 2000. Since 2000, the sustainability of USI has been maintained. China’s success demonstrates that political commitment by the government and a strong alliance between the Ministry of Health and the Salt industry is a key factor for the success of achieving the USI goal [38]. Nigeria was the first country in Africa to achieve the USI compliance certification by the Network for Sustained Elimination of Iodine Deficiency in 2005. Nigeria initiated the USI programme in 1993 and within a period of five years access to adequately iodized salt had grown from zero base in 1993 to 98% consumption of iodized salt at household level in 1998 [39]. The key factors contributing to the success were political commitment by government, commitment by salt industry and effective multi-sectoral partnership. The salt industry of Nigeria has taken iodization programme as their social responsibility and the National Agency for Food and Drug Administration and Control (NFDAC) also encourages salt industries to have efficient inhouse quality assurance (QA) and quality control (QC) systems which were and are continued to be duly certified by NFDAC. USI has been achieved and sustained through aggressive enforcement by government and compliance by salt industry. A ban on salt packaging in 25 kg sacs has been imposed by NFDAC and it is mandatory for all salt industries to pack salt for domestic use in small retail sizes (1 kg and less) to enhance retention of quality of iodine and content. With the introduction of iodized salt in Nigeria, the total goitre rate reduced to 6.2% in 2005 as compared to 20% in 1993. Median urinary iodine excretion has consistently been over 130 μg/dl since 1999. The USI programme in Nigeria operates with minimal domestic financing and donor investment and the incremental cost of potassium iodate is absorbed within the price of salt. NFDAC’s high profile image and reputation for protecting rights of consumers continues to mobilise industry commitment and strengthens the confidence of consumers and other stakeholders. According to UNICEF report [16], by 2006 more than 120 countries were reported to be implementing salt iodization programme. A total of 34 countries by this time had reached the USI goal and eliminated IDD as compared to 21 reported in 2001 (Figure 20.2). An additional 28 countries

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had greater than 70% household consuming iodized salt. WHO estimates that the number of countries where IDD is a public health problem has been reduced by half – from 110 countries in 1993 to 54 in 2003.

20.2 Countries (Numbers) by proportion of households consuming iodised salt in the last 5 years [35] (a) (b)

UNGASS (UN General Assembly Special Session on Children) SOWC (State of the World’s Children Report of UNICEF)

In 1990, less than one in five households in the world used iodized salt. In 2007, it was estimated 70% households have access to iodized salt [16, 35]. Table 20.7 presents the situation in six WHO regions with reference to proportion of population and estimated number of individuals in general population (all age groups) with inadequate iodine nutrition along with details on percentage of households consuming iodized salt. It is evident that there is a wide variation in the regions regarding percentage population having access to iodized salt – 47.3% in Eastern Mediterranean to 86.8% in Americas. In Europe, it was earlier estimated that only 27% salt was iodized while in 2007 it is reported to have increased to 49.2% [3, 16]. The significant progress in USI (Table 20.7) implies that every year 90 million newborn brains are protected against a significant loss of learning ability [40]. Table 20.7 Proportion of population and number of individuals in the general population (all age groups) with insufficient iodine intake by WHO regions during the period between 1994 and 2006, and proportion of households using iodized salt [3] WHO

Inadequate iodine nutrition

regions

Proportion (%)

Africa Americas South East Asia Europe Eastern Mediterranean Western Pacific Total

41.5 11.0 30.0 52.0 47.2 21.2 30.6

Total number (million) 312.9 98.6 503.6 459.7 259.3 374.7 1900.9

% households with access to iodized salt 66.6 86.8 61.0 49.2 47.3 89.5 70

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Public health nutrition in developing countries

Salt iodization has been recognised as the most successful public health effort in the past two decades. Salt iodization results in significantly decreasing risk of intellectual impairment caused by iodine deficiency [35]. World Bank 1994 [41] considers salt iodization as the most cost-effective intervention programme and estimates that each dollar dedicated to the prevention of iodine deficiency would yield a productivity gain of $28. A group of the World’s leading economists confirmed during the Copenhegan Consensus meeting that the benefit–cost ratio of for salt iodization could be as high as 520, the highest among all interventions related to hunger and malnutrition [42]. In 2006, UNICEF with its international partners identified 16 “make or break” countries with a view to accelerate the USI programme [16]. The selection criteria were based on the following: high number of unprotected newborns, low level of salt iodization, large salt export activities as well as the need for special advocacy and professional support to renew strategies for the IDD-elimination programme. The countries identified were Afghanistan, Angola, Bangladesh, China, Egypt, Ethopia, Ghana, India, Indonesia, Niger, Pakistan, Philippines, Russian Federation, Senegal, Sudan and Ukraine. Efforts are being made to accelerate the USI programme in these countries. It is estimated that if these 16 critical countries achieve USI, the global coverage of iodized salt will increase from 70 percent in 2007 to about 85 percent. An analysis of two decades of USI programme highlights the following lessons learned which are crucial for the success of USI: ●

●

●

Ensuring political commitment. Political and government commitment along with continued motivation of industry is essential. The demand for iodized salt should be seen as a right of every person and access to iodized salt should be ensured by the state [40]. Periodic advocacy events are critical for renewed focus and political commitment. USI programme efforts not require one-time elimination of IDD but focus on sustainability. To sustain USI programme, it is of utmost importance to have political will and commitment to eliminate IDD. Ensuring salt supply with adequate level of iodine. Capacity for sustained production, availability and access to salt with adequate level of iodine. There is a need to focus on production of quality product and mechanisms for market penetration to reach each and every consumer. A high-level involvement and motivation of multiple players of the entire salt chain who produce, procure and sell iodized salt, i.e. producers of salt and iodized salt, packers, truckers and rail transporters, wholesalers, retailers and enforcement officers. Consistent regulations which are effectively enforced. A framework,

Iodine deficiency and iodine deficiency disorders (IDD)...

●

●

●

●

549

in the form of legislation and supportive regulations for mandatory iodization is critical with specific details on iodine content in salt at the production site for both human and animal consumption along with an outline of monitoring mechanisms and enforcement of agreed on actions. Effective education and communication. Sustained communication through mass media and in coordination with other ongoing health and education systems is important. Continued specific effort to reach and motivate salt producers and sellers network, including both wholesalers and retailers, is crucial. Additionally, health professionals need to work as a team with salt industry for IDD elimination since each has a very different professional orientation. The public needs to be made aware of the dangers associated with accepting and consuming non-iodized or inadequately iodized salt. The messages should focus on the impact of IDD on brain damage and the potential loss of IQ. It is also critical to keep in mind the cut-off level for usage of maximum recommended level of salt for cardiovascular health and ensuring communication on promotion of iodized salt is correctly positioned and does not create confusion regarding daily recommended amount of salt consumption. Establishment of an effective system for monitoring. Regular and effective monitoring system to check salt from production to household level. It is important that the reporting process is rapid, regular, well-supported, transparent and benefits people, process and policy makers. Establishment of a multi-sector coordination and monitoring mechanisms for regular review of progress. Review system to facilitate in planning and execution of roles identified for various sectors or professional groups. The multi-sector group ideally should involve representatives of all stakeholders – health, salt industry and food manufacturers/industry, veterinary sciences and agriculture, education, legislation and justice, communication, finance, consumer groups, scientists and professional groups. Implementing USI as an integrated programme. Salt-iodization programme efforts linked with broader health and nutrition programme and not as a vertical programme. Such integration is critical for effective sustained implementation of USI.

20.6

Monitoring IDD control programme

Indicators for monitoring IDD control programme need to be considered in the following three major groups – monitoring process, impact and sustainability [3].

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Public health nutrition in developing countries

(a) Monitoring process – This involves monitoring the salt-iodization programme and deals with the entire salt-trade chain from production, procurement to distribution and sale to consumers. Monitoring of saltiodization programme process is critical to ensure that implementation is being undertaken as planned and information is available routinely to take corrective actions at the various points in the iodized salt trade chain. A monitoring mechanism involves setting up a system in a country to periodically check iodine levels in salt at production, distribution and consumption centres to ensure all edible salt is iodized to correct defined levels and to ensure that salt iodization is sustained. Such monitoring involves both governments and salt industry – a close collaboration between public and private sectors. Salt testing should be done using valid and reliable methods. Testing of salt for iodine levels is done by both quantitative and semi-qualitative tests – the former refers to use of the titration method (Box 20.1) and the latter to the use of spot testing kits (Box 20.2) or commonly referred as Rapid Test Kits or Salt Testing Kits (STKs). These kits provide results of iodine levels in a few seconds. However, since the sensitivity and specificity of STKs can be low, samples of salt should be tested by titration method which is a reliable quantitative test [30]. In the recent past, quantitative testing using potentiometer or spectrophotometer has also been developed. Figure 20.3 presents an overview of the monitoring and evaluation system for salt iodization as recommended by WHO/UNICEF/ICCIDD [3]. The most critical step in monitoring is “internal monitoring” by iodized salt producer at the site of iodization. Salt samples from the production line should be regularly analysed – checking each batch at least once – using the titration method. At production site, facilities and skills for titration should be ensured. Additionally, an “external monitoring” or quality-control mechanisms needs to be in place for monitoring iodine when importers, distributors or wholesalers receive salt. It is critical that iodine levels are checked prior to distributing edible salt further to retailers or consumers in order to take timely action when salt is found to be non-iodized or not meeting the prescribed standards. External monitoring is facilitated when a country has a legal framework and establishes a law which makes it mandatory for all edible salt to have specific level of iodine with iodine levels being defined in terms of amount and the specific form of the fortificant, i.e. potassium iodate or potassium iodide. In addition, for effective monitoring, regulations with details of approved packaging and labelling norms are critical. The packaging details must include specifications of polythene packaging that should be used. Additionally, for institutionalizing external monitoring, appropriate institutions with laboratory facilities for undertaking titration and external monitoring need to be designated.

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Box 20.1 Titration method for estimating iodine content in salt [3, 30] The iodometric titration method, as described by DeMaeyer, Lowenstein and Thilly (1979) has the following two major steps of reaction mechanism. At the level of iodized salt production, titration method is recommended. Use of the iodometric titration method by the quality control persons and food inspectors is recommended. Step 1: Liberation of free iodine from salt. The method of liberating iodine from salt varies depending on whether salt is iodized with iodide or iodate. ● ●

Addition of H2 SO 4 liberates free iodine from the iodate in the salt sample. Excess KI is added to help solubilise the free iodine, which is quite insoluble in pure water under normal conditions.

Step 2: Titration of free iodine with thiosulfate ●

●

●

Sodium thiosulfate is used for titration. The amount of thiosulfate used is proportional to the amount of free iodine liberated from salt. Starch is added as an external (indirect) indicator in the titration and reacts with free iodine to produce a blue colour. Starch drops when added towards the end of the titration (that is, when only trace amount of free iodine is left) results in loss of blue colour, or endpoint, with further titration. The end point indicates that all remaining free iodine has been consumed by thiosulphate. The concentration of iodine in salt is calculated based on the titration volume of sodium thiosulphate using a standard formula [3]. Reaction steps for iodometric titration of iodate 1. IO 3-

+

(from salt) 2. 2Na2 SO 3 Sodium Thiosulfate

→

5I – +

6H+

(from KI) +

(from H2 SO 4) I2 → Iodine

3I 2

+

3H2 O

2NaI + Na 2S 4O 6 Sodium Sodium Iodide Terathionate

Solutions can be kept for testing salt samples for 2–3 days, and the volume is sufficient for testing approximately 500 samples.

Box 20.2 Rapid-Testing Kits (RTK) / Salt-Testing Kits (STK) Salt-testing kits – salt testing kits, manufactured by MBI (India) are used in India and many other countries. These kits are simple, handy, in-expensive, an ideal tool for monitoring at the field level and an excellent advocacy material for the USI programme. These STKs can be used by health and social workers, nongovernmental organisations and even by school children. These are manufactured under strict quality control and all the raw materials and chemicals are thoroughly checked before use. These kits provide good semi-quantitative estimation of iodine in salt as they have sensitivity of 89.98%, specificity of 81.1%, positive predictive value of 80.9% and negative predictive value of 79.9%. STKs are specific for iodate and not iodide. These kits come ready to use and provide all the necessary materials needed for the test, including the test solutions (2–3 ampoules of 10 ml each), 1 red ampoule containing recheck solution for alkaline salt samples (containing sodium carbonate), a detailed instruction sheet in local language and a colour chart with circular colour spots with defined iodine levels against each spot. All contents are packed in a small kit box that can fit into a shirt pocket. The cost of a kit, tests about 100 samples, is about one-third of one US dollar. These kits have a shelf-life of 12–18 months when not opened and a reduced shelf–life of generally 3–6 months once opened. Kits which have outlasted their shelf-life should not be used.

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552

Procedure ● ●

●

●

●

A spoon of salt is spread flat. The test solution ampoule is opened and the test solution is dropped on the surface of salt. The spot of salt surface where the test is dropped will turn from light to dark violet depending on the iodine content. The colour formed should be instantly compared with the colour chart. If the colour is not interpreted straight away, colour fading may occur over time. In the absence of any colour formation, a few drops of the recheck solution are to be spread on the salt surface before using the test solution.

Reaction mechanism of the test kit is as follows: IO 3 -

+

5I –

+

(from salt)

(from KI)

I2

Starch

+

6H+

→

3I 2

+

3H2 O

(from H 2SO 4 ) →

Blue colour

The reaction liberates the iodine and depending on the iodine content starch turns the salt blue. The intensity of colour varies with the amount of iodine in the salt sample.

Monitoring iodine levels in salt at household level is the critical indicator for measuring the success of the USI programme. Household-level monitoring, through national surveys or community-based methods, is recommended. It is recommended that the use of STK for checking iodine levels is complemented with the simultaneous use of titration method for checking iodine levels in sub-samples of salt. Testing of salt samples at household level can be rapidly and easily undertaken by working with school network and school children bringing salt samples from their homes for testing iodine adequacy in salt. Instant feed back to community, using school child to community approach, has also proven to be effective [43]. School-level monitoring combined with the establishment of a monitoring mechanism to test iodine levels in salt at wholesalers’ levels has been demonstrated to be a useful strategy for positively influencing correct iodized salt-trade practices.

20.3 Monitoring and evaluation system for salt iodization [3]

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553

20.6.1 Assessing iodine nutritional status – impact of IDD control programme The following two methods are used for assessing impact of IDD control programme on iodine nutrition of the population: (a) assessment of thyroid size by palpation; and (b) urinary iodine excretion. The recommended sensitive methods are urinary iodine and the two recently added methods – measurement of thyroid stimulating hormone (TSH) levels in neonates and thyroglobulin (T g) levels. Use of TSH and Tg have been proposed as indicators of iodine nutrition but their usefulness in assessing iodine status from cross-sectional surveys has variable results. However, the principal indicator of impact monitoring is urinary-iodine levels since the measurement of TSH and Tg is not feasible in public health programme situations of developing countries while measurement of thyroid size lacks sensitivity to acute changes in iodine intake resulting from introduction of salt-iodization programme. Measurement of thyroid size, however, is considered useful for baseline assessment of severity of IDD in a region and is also considered useful for the assessment of long-term impact of IDD control programme [3]. (a) Assessment of thyroid size. The term goitre refers to a thyroid gland that is enlarged. The grading classification adopted by WHO (Table 20.8) for the total goitre rate (TGR) is used for the assessment of iodine status in a population [3]. The goitre rate includes both visible and palpable goitre. Table 20.8 Simplified classification of goitre (a) by palpation [3]

(a)

Grade 0

No palpable or visible goitre

Grade 1

A goitre that is palpable but not visible when the neck is in the normal position (i.e. the thyroid is not visibly enlarged). Thyroid nodules in a thyroid which are otherwise not enlarged fall into this category.

Grade 2

A swelling in the neck that is clearly visible when the neck is in a normal position and is consistent with an enlarged thyroid when the neck is palpated.

Thyroid gland will be considered when each lateral lobe has volume greater than the terminal phalanx of the thumbs of the subject being examined.

Surveys assessing the prevalence of goitre are recommended to be performed in accessible population of school children around the ages of 6–12 years. However, with highest prevalence of goitre occurring during puberty and child bearing age, a lower age range of 8–10 years has been used in many studies [3]. School children group is easy to reach and investigators can easily palpate a large number of children. Ultrasonography of the thyroid gland provides a more precise measurement of thyroid size but the inter-observation are reported

554

Public health nutrition in developing countries

to be high and thyroid volume is slow to change in an evolving iodine-nutrition status [36]. Use of thyroid size or TGR for measuring impact is not recommended to assess impact once the salt-iodization programme has been introduced [3]. In fact, despite improvement in iodine-nutrition status of a population, it may take years for most palpable goitre to return to normal size. Goitre prevalence therefore has limitation to be used as a tool for assessment of iodine changes over a period of time [44]. Total goitre rate or TGR (number with goitres of grades 1 and 2 divided by total examined) of 5% or more in schoolchildren 6–12 years of age is recommended to indicate the presence of iodine deficiency as a public health problem [3]. This recommended cut-off on the TGR percentage is based on the observation that in normal, iodine-replete populations, the prevalence of goitre should be quite low. The cut-off point of 5% allows both for some margin of error of goitre assessment, and for goitre that may occur in iodine-replete populations due to other causes such as goitrogens and autoimmune thyroid diseases. Thyroid size is considered more useful in baseline assessments of the severity of IDD and is also useful for the assessment of the long-term impact of the programme. (b) Urinary iodine. With the limitation in usefulness of thyroid size and biological markers for thyroid function, urinary iodine levels are used as the primary indicator for assessing iodine-nutrition status in representative group of subjects (Table 20.9). Urinary iodine reflects the recent intake of iodine and tends to vary within a day or day to day. However, this variation tends to even out among populations. Urinary iodine excretion provides an excellent indication of iodine intake of population [3]. Urinary iodine is not recommended to be used for the purpose of individual diagnosis and treatment. The median urinary iodine value for sampled population is the most commonly assessed indicator and can be easily assessed using the median level from only 40 subjects from each local community [3]. Taking into consideration the fact that developing foetus suffers the greatest damage as a result of iodine deficiency, two other potential targets have been recently proposed for urinary iodine estimations – women in the reproductive age group 15–49 years and pregnant women [3, 36]. As indicated in Table 20.9, in children and non-pregnant women, lower median urinary iodine concentrations of between 100 and 199 μg/l defines a population which has adequate iodine nutrition. In addition, not more than 20% samples in this population group should be below 50 μg/l in nonpregnant and non-lactating women [3]. During pregnancy, median urinary concentration between 150 and 249 μg/l defines a population which has no iodine deficiency.

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Table 20.9 Epidemiological criteria for assessing iodine nutrition based on median urinary iodine concentrations of school age children (≥6 years) (a) and pregnant women [3] Median urinary iodine (μg/l)

Iodine intake

Iodine status

Children ≥ 6 years

(a) (b)

(c)

<20 20–49 50–99 100–199 200–299

Insufficient Insufficient Insufficient Adequate Above requirements

>300

Excessive

Pregnant women (b) <150 150–249 250–499 >500

Insufficient Adequate Above requirements Excessive (c)

Severe iodine deficiency Moderate iodine deficiency Mild iodine deficiency Adequate iodine nutrition Likely to provide adequate intake for pregnant/lactating women but may pose a slight risk of more than adequate intake in the overall population. Risk of adverse health consequences (iodine-induced hyperthyroidism, autoimmune thyroid diseases).

Applies to adults but not to pregnant and lactating women. For lactating women and children <2 years of age median urinary iodine concentration of 100 µg/l can be used to define adequate iodine intake, but no other categories of iodine are defined. Although lactating women have the same requirement as pregnant women, the median urinary iodine is lower because iodine is excreted in breast milk. The term “excessive” means in excess of the amount required to prevent and control iodine deficiency.

Box 20.3 Measuring urinary iodine [45] Urinary iodine assay require total avoidance of contamination. Small amount of urine (0.5–1.0 ml) is required. Urine samples are recommended to be collected in small cups which are tightly sealed. No refrigeration is required. These samples can be stored for months, preferably in a refrigerator to avoid odour. Criteria for assessing urinary iodine methods are reliability, speed, technical demands, complexity of instrumentation, and availability of high quality reagents, safety and cost. Two methods are recommended – ammonium persulphate method and chloric acid methods [3]. These methods depend on iodine acting as a catalyst in the reduction of ceric ammonium sulphate (yellow colour) to the cerous form (colourless) in the presence of arsenious acid (the sandell-kolthoff reaction). Due to potential hazards of chloric acid method, ammonium persulphate is recommended [3]. Modification of these methods is commonly used for measuring urinary iodine [45]. Choice of methods depends on local resources and need. External quality control is essential since unrecognized iodine contamination is a common occurrence. To overcome this problem, an international network of resource laboratories has been established which collaborates with the Centers for Disease Control of USA.

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Public health nutrition in developing countries

Based on these facts, there is a proposal to examine urinary iodine levels not only in school children but also in pregnant women (sample pregnant women from prenatal clinics) for assessment of iodine nutrition status in a cross-sectional surveys, since information of school children alone is not adequate to reflect the urinary iodine status of women of child bearing age, pregnant or non-pregnant [36]. It is important that laboratories use recommended procedures for measuring iodine in urine and set-up mechanisms for internal quality control and also link up with recognised institute for external quality control programme [45].

20.7

Monitoring progress towards sustainable elimination of IDD as a public health problem

IDD is a nutritional deficiency and efforts for elimination through USI need to be sustained. Indicators for programme sustainability therefore comprise of (i) indicators to measure achievement of salt iodization and iodine status in population and (ii) indicators for measuring ongoing political support and programme strength [3]. Information about salt iodization is recommended to include measures of quality assurance at iodized salt production facilities as well as monitoring compliance of the requirements set by the country programme guidelines for imported iodized salt. Indicators for monitoring of political support and programme strength includes various elements of programme which are critical to sustainability such as multisector coalition, budget allocation, legislation and regulating mechanisms for monitoring of iodine levels in edible salt and iodine status, system for regular reporting of programme and updating of the national database. The criteria for monitoring progress towards elimination of IDD as a public health problem were originally determined by a Joint WHO/ UNICEF/ICCIDD working group on assessment and Monitoring of IDD in 1994 [46, 47] and was endorsed at the subsequent meeting in 2001 [1]. The sustainability criterion was introduced in 2007 and is presented in Table 20.10. This involves a combination of median urinary iodine levels in the population, availability of adequately iodized salt at the household level. Additionally, a set of programmatic indicators are recommended to be assessed as evidence of sustainability. A network for sustained elimination of iodine deficiency has been launched by the Director General of WHO [47]. The network in a costeffective manner is expected to provide USI / IDD review through use of simplified guidelines. The process is proposed to be initiated by the government who requests for such an external USI assessment through the country office of UNICEF or WHO. Such a process is viewed to be very important for national ownership of the situation and commitment to the process of sustained IDD elimination. The main objective of the review

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Table 20.10 WHO / ICCIDD / UNICEF criteria for monitoring progress towards sustainable elimination of IDD as a public health problem [3, 48] Indicator (1)

(2)

(3)

Salt iodization Availability and use of adequately iodized salt (over 15 ppm iodine and <40 ppm at household level) Urinary iodine – median in the general population – median in the pregnant women Programmatic indicators

Goal >90% households

100–199 μg/l 150–249 μg/l

Attainment of 8 out of 10 following indicators – National body appointed – Evidence of political commitment – Appointment of executive officer – Regulation of USI – Commitment to regular progress in IDD elimination – –

– – –

Public education and social mobilisation Regular data on iodized salt at factory, retail and household level Regular laboratory data on urinary iodine Cooperation from salt industry Data base (salt and urinary iodine, mandatory public reporting)

Box 20.4 Upper limit of iodine intake and iodine-induced hyperthyroidism Excess of iodine ingestion can be harmful, which may inhibit the synthesis of thyroid hormones by the thyroid. This iodine-induced hypothyroidism is known as “Wolff-Chaikoff” effect, the manifestation of which depends on level of iodine intake before exposure to iodine excess. This is generally encountered among newborns as neonatal chemical hypothyroidism when women during pregnancy receive high doses of iodine, in the form of iodized oil injections. When iodine is supplemented to severely iodine-deficient communities, even at the total daily intake level of 100–200 μg, hyperthyroidism may occur, mainly amongst middle-aged people. It is related probably to (i) relative increase and (ii) rapidity in increase of iodine intake consequent to iodine supplementation in iodine-deficient communities. With intensive efforts to address IDD, examples of iodine excess are being recognised in situations

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Public health nutrition in developing countries

where iodine levels in salt are excessive due to poor monitoring. The major epidemiological consequence of iodine excess is iodine induced hyperthyroidism (IIH). IIH occurs in severe iodine deficiency of long duration and in situations of introduction of salt with high iodine content (100 ppm) in a short period of time. Increased incidence of IIH is transient, minimal and self-limiting [47]. It has been reported that IIH occurs more commonly in older subjects with pre-existing nodular goitres and commonly affects older age group of over 40 years [3].

by the network is to help governments and program managers to assess and verify the country achievement towards their goals to sustain elimination of iodine deficiency. The network proposes to facilitate progress comparisons across regions by means of standardized tools/ guidelines. Additionally, the review will also analyse and identify lessons learned and best practices of the country programs and identify ways to address bottlenecks to ensure USI and recommend steps to sustain USI.

20.8

Supplementation with iodised oil in special situations of insufficient access to iodized salt

As indicated in Table 20.11, a substantial increase in intake of iodine is recommended to meet the higher biological needs for iodine during pregnancy. It is crucial that women have adequate iodine stores during the first trimester of pregnancy and iodine nutriture of women of reproductive age is taken care of to meet the added needs of developing foetus. Efforts to improve salt iodization programme must continue and given the highest priority. However, for regions with poor household consumption of adequately iodized salt, special additional temporary measures such as administration of iodized oil supplement has been proposed to ensure optimal iodine nutrition in the vulnerable group comprising pregnant and lactating women and children below two years [2, 3]. It is important that countries assess the country situation of iodization programme at national and sub-national levels and consider introduction of temporary measures to address the risk of iodine deficiency to the vulnerable groups in specific identified regions. Such a situation is particularly applicable in countries which are often in conflict situations and have not succeeded to achieve salt-iodization coverage of over 20% due to a number of hindrances. In such conditions, additional temporary measures are recommended to be introduced to ensure that optimal critical nutrition at the highest risk period of life – pregnancy and under-2-year children – is addressed. It has been proposed that in situations of poor iodized salt programme, the most vulnerable groups, pregnant and lactating women, need to be considered for supplementation with iodine until salt-iodization programme improves (Table 20.11). For children of 7–24 months, either supplementation or use

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of fortified complementary food for 7–24 months has been proposed as a possible temporary public health measure [2, 3]. Table 20.11 Recommended dosages of daily and annual iodine supplementation [3]

(a)

(b)

Population group

Daily dose of iodine supplement (μg/d)

Single annual dose of iodized oil supplement (μg/y)

Pregnant women Lactating women

250 250

400 400

Women of reproductive age (15–49 years) Children < 2 years (a, b)

150

400

90

200

For children 0–6 months of age, iodine supplementation should be given through breast milk. This implies that the child is exclusively breast fed and the lactating mother receives iodine supplementation as indicated above. These figures for iodine supplements are given in situations where complementary food fortified with iodine is not available, in which case iodine supplementation is required for children of 7–24 months of age

References 1.

2.

3.

4.

5. 6.

7. 8.

9.

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Public health nutrition in developing countries ICCIDD/ WHO /UNICEF (1999). Progress towards elimination of iodine deficiency disorders. WHO/NHD/99.4. PHAROAH POD, BUTTERFIELD IH , HETZEL BS (1971). Neurological damage to the foetus resulting from severe iodine deficiency in pregnancy. Lancet 1, pp. 308–310. BURH H , SUPERSAXO Z , SELZ B (1990). Iodine deficiency disease in Switzerland: historical review and some new goitre prevalence data. Alta Endocrinologica 123, pp. 577–590. HETZEL BS and MANO M (1989). A review of experimental studies of iodine deficiency during foetal development. J Nutr 119, pp. 145–151. HETZEL BS (2007). Global progress in addressing iodine deficiency through USI: the making of a global health success story – the first decade (1985–1995). SCN#35, pp. 5–11. HETZEL BS (1983). Iodine deficiency disorders and their eradication. Lancet 2, pp. 1126–1129. UNICEF (2009). Sustainable Elimination of Iodine Deficiency. Progress since the 1990. World Summit for Children. BLEICHRODT N and BORN M (1994). A meta-analysis of research into iodine and its relationship to cognitive development. In: Stanbury JB (ed): The Damaged Brain of Iodine Deficiency. New York: Communication Corporation, pp. 195–200. ICCIDD / UNICEF / WHO (2001). Assessment of iodine deficiency disorders and monitoring their elimination. A guide for programme managers. 2nd edition. WHO/NHD/01.1, Geneva, WHO. DELANGE F (1994). The disorders induced by iodine deficiency. Thyroid 4, pp. 107–128. DELANGE F (1999). What do we call a goitre? Eur J. Endocrinol 140, pp. 486–488. PHARAOH POD , ELLIS SM , WILLIAMS ES (1976). Maternal thyroid function, iodine deficiency and foetal development. Clin Endocrinol 5, pp. 159–166. POTTER JD, MC MIACHAEL AJ , HETZEL BS (1979). Iodisation and thyroid status in relation to still births and congenital anomalies. Int J Epidemiol 8, pp. 137–144. HETZEL , BS (1996). The nature and magnitude of iodine deficiency disorders in SOS for a billion. In: HETZEL BS and PANDAV CS (eds): SOS for a Billion. International Council for the Control of Iodine Deficiency Disorders. PANDAV CS and MANNAR VMG (1996). IDD in livestock population. In: HETZEL BS and PANDAV CS (eds): SOS for a Billion. Oxford University Press. WHO (1986). Prevention and control of iodine deficiency disorders. Report to 39th World HEALTH ASSEMBLY, GENEVA, WHA 39.6. WHO (1990). Prevention and control of iodine deficiency disorders. Report of 43rd World HEALTH ASSEMBLY. GENEVA WHA 43.2. WORLD SUMMIT FOR CHILDREN (1990), United Nations, New York. WHO (1996). Prevention and control of iodine deficiency disorders. Report of 49th World HEALTH ASSEMBLY, GENEVA WHA 49.13. HETZEL BS (1989). History of goitre and cretinism. The Story of Iodine Deficiency. Oxford University Press. SULLIVAN KM , HOUSTON R , GORSTEIN J , CERVINSKAS J (1995). Monitoring Salt Iodization Programme UNICEF/ICCIDD/PAMM/WHO/MI. WHO (1994). Iodine and Health; eliminating iodine deficiency disorders solely through salt iodization. WHO/NUT/94.4, WHO, Geneva. NATHAN R (1999). Regulation of Fortified Foods to Address Micronutrient Malnutrition: Legislation, Regulations and Enforcement, Micronutrient Initiative: Ottawa.

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(1996). Recommended iodine levels in salt and guidelines for monitoring their adequacy and effectiveness. WHO / NUT 96.13. WHO. Geneva. UNICEF (2002). A world fit for children, UNICEF, New York (online). GAUTAM K (2007). Global progress in addressing iodine deficiency through universal salt iodization: the making of global public health success story – the second decade (1995–2007). SCN Newsletter # 35, p. 12. SULLIVAN KM , SACHDEV PS , GRUMMA - STRAUUS L (2007). Achieving and sustaining USI: doing it well through quality assurance, monitoring and impact evaluation. SCN News, pp. 48–52. UNICEF (2006). The state of the World’s children. 2007. UNICEF online. CHEN Z, DANG Z, LIN, J (2007). Effective programme development and management. Lessons learnt from USI in China. SCN News, pp. 33–36. AKUNYLLI DN (2007). Achieving and sustaining universal salt iodization. Doing it well through regulation and regulation enforcement, lessons learned from USI in Nigeria. SCN News, pp. 43–47. MANNAR V (2007). Guest editorial, SCN News, p 3. WORLD BANK (1994). Enriching lives, overcoming mineral and vitamin malnutrition in developing countries. World Bank, Washington DC. BEHRMAN JR , ALDERMAN H , HODDINOTT J (2004). Hunger and malnutrition. Copenhagen Consensus – Challenges and Opportunities, Copenhagen. VIR SC , DWIVEDI S , SINGH R, MUKHERJEE A (2007). Reaching the goal of Universal Salt Iodisation: Experience of Uttar Pradesh, India. Food and nutrition Bulletin 28, no. 4, p. 384. GORSTEIN J , SULLIVAN KM , HOSUTON R (2001). Goitre assessment: help or hindrance in tracking progress in iodine deficiency programme? Thyroid 11, pp. 1201– 1202. CALDWELL KL , MAKHMUDOVA JR , HOLLOWELL JG (2005). EQUIP: A world wide programme to ensure the quality of urinary iodine procedures. Accreditation and Quality Assurance 10, pp. 356–361. WHO /UNICEF /ICCIDD . Indicators for assessing iodine deficiency disorders and their control through salt iodization. Geneva, WHO, 1994. UNICEF (2006). Network for sustained elimination of iodine deficiency. Review guidelines New York, UNICEF, 2006. PANDAV CS , CHAKRABORTY A , SUNDARESHAN S , ANSARI MA , JAIN P, AGUAYO V , AG AYOYA M and KARMARKAR MG (2008). Salt for freedom and iodized salt for freedom from preventable brain damage. All India Institute of Medical Sciences.

Universal salt iodization (USI)

21 Universal salt iodization (USI) M. G. Venkatesh Mannar

M. G. Venkatesh Mannar is a leader in global health with thirty five years experience in pioneering effective international nutrition and development initiatives, focused on the world’s most vulnerable citizens. Currently, he is the President of the Ottawa-based Micronutrient Initiative (MI), and oversees the organization’s mission to develop, implement and monitor cost-effective and sustainable solutions for micronutrient deficiencies in more than 75 countries.

.

Introduction

Iodine is an essential nutrient for humans and animals. A deficiency of this mineral has a wide range of negative consequences such as still births, congenital abnormalities and decreased cognitive capacity. The food supply of more than 2 billion people is lacking in adequate levels of iodine, resulting in the widespread prevalence of a spectrum of iodine deficiency disorders (IDD) [1]. This public health problem can be corrected by the regular delivery of small doses of iodine to the population through commonly eaten foods or condiments. Salt is an excellent carrier for iodine and other nutrients as it is consumed at relatively constant, well-definable levels by all people within a society, independent of the economic status. Universal Salt Iodization (USI), which intends that all salt for human and animal consumption be iodized thus ensuring adequate iodine nutrition, was identified as the global strategy for the elimination of iodine deficiency. Salt is an excellent carrier for iodine and other nutrients as it is safe, consumed at relatively constant, well-definable levels by all people within a society, independently of economic status [2]. WHO provides guidelines as to the recommended prescribed levels of iodization as well as the recommended urinary iodine excretion levels for specific population groups. In 1990, seventy Heads of State gathered at the World Summit for Children in New York and pledged to eliminate iodine deficiency disorders (IDD) as one of the health and social development goals to

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reach by the year 2000. Salt iodization was identified as the main intervention to deliver iodine on a continuous and self-sustaining basis to populations around the world. Governments working with the salt industry and supported by international agencies and expert groups then set to plan and implement programmes that would enable this measure. Over the past two decades, as part of the Universal Salt Iodization (USI) initiative, a large number of developing countries have taken steps to ensure that all salt produced for human and livestock consumption is iodized. Once established in a country, salt iodization is a permanent and longterm solution to the problem. It eliminates iodine deficiency and continues to provide each individual with his/her daily iodine needs and prevents recurrence. Within one year of iodized salt containing the required iodine being widely available and consumed in a community, there will normally be a rapid decline in birth of cretins or children with subnormal mental and physical development attributable to iodine deficiency. Goitres in primary school children and adults will have started to shrink and even disappear altogether. Children will be more active and perform better at school.

.

Taking universal salt iodization to scale

The specific objective is to dovetail iodization into the prevailing salt production and distribution system in a country at minimum cost and disruption. The salt industry has obviously been a key player in enabling this major public health achievement. However, there is considerable variation in the production process and scale of this most ancient of industries. Salt manufacturing techniques and product quality vary over a wide range from cottage scale units producing a few hundred tons a year to very large fully automated plants producing several million tons. The production of salt (sodium chloride) is one of the most ancient and widely distributed industries in the world. It can be produced by mining of solid rock deposits and by the evaporation of sea water, lake and underground brines by solar digging. Rock and solar-evaporated salt account for roughly 50% of production each. The requirements of Europe and North America are met mostly by mining while in Asia, Africa, Australia and South America solar evaporation is the main source. In some countries both forms are used. The extraction of salt from sea water consists of progressive evaporation of brine in large open ponds using solar heat and wind. As the brine evaporates its concentration rises and the constituent salts crystallize in a set order. During this process the sodium chloride fraction is separated from the brine over a fixed concentration range in a series of flat rectangular ponds and deposits as

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a uniform crust. This salt is ‘harvested’ by a variety of processes ranging from simple hand labour to the use of mechanized equipment to scrape the salt and transfer it through a series of conveyors for storage and draining [3]. Iodine is added as potassium iodate to salt after refining and drying and before packing. Iodization can often be linked with existing production and/or refining lines. This is typically done by spraying a solution of potassium iodate on the salt at a uniform rate followed by thorough mixing of the salt with the sprayed solution (Table 21.1). Table 21.1 Methods of iodization and costs

Dry mix

Drip feed

Spray mix

Suitability of application

Key considerations

Operating cost ($/kg salt)

High quality dry refined salt with potassium iodide or iodate Low quality coarse crystal or powdered salt with potassium iodate

Suitable for large operations with continuous mixing

0.002–0.005

Typically installed on low-capacity salt grinders for continuous operation Applicable to continuous refineries ahead of drying Applicable to portable units for field operation

0.005–0.01

Medium to highquality powdered salt semi-dry with potassium iodate

0.01–0.03

For units with production >10,000 tons per year that are well organized with quality control systems, the integration of iodization has been relatively easy. Such large producers account for nearly 75% of all salt for edible consumption. However, a small but significant proportion of the salt is produced along coastlines or lake shores as a semi-agricultural operation by many small producers. The smaller units often operate with a minimum of organization and little or no quality control. They are scattered along the coast or lake shores and do not lend themselves to regulation by the government. Very often precise figures regarding even their location, extent of holdings and production statistics are not available. The producers may not be aware of IDD and of the potential of their product to be a carrier. Additionally they may be based in communities where consumer awareness is limited and, as business people, they are primarily interested in making a product that consumers will buy. The producers have limited financial means and lack of access to technical or financial assistance to institute quality iodization processes and to monitor quality. As a result the salt produced in these units is of poor quality. Additionally they have poor packaging practices or do not package the salt at all. Yet they are often the main salt supplies to the communities most at risk of IDD. This has complicated USI programmes.

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Box 21.1 Overview of global progress ● ● ● ● ●

More than 120 countries are implementing USI programmes. Globally, 70% of households are adequately consuming iodized salt. 34 countries have already achieved USI and another 28 are close to the goal. 84 million infants are protected annually from the risk of IDD. The number of countries where IDD remains a problem has dropped to 47.

Since the early 1990s, global efforts to introduce universal salt iodization world wide have resulted in impressive progress (Boxes 21.1 and 21.2). This progress has relied on effective multi-sectoral partnerships: Governments working with the salt industry, supported by international agencies and in functioning in coordination with the civic sector and expert groups. Each of these partners have gained experience from the past two decades, the lessons learned have been in turn, incorporated into the policy, programming and implementation frameworks that sustain USI (Box 21.2).

21.1 Households consuming iodized salt [4]

21.2 Progress in iodized salt coverage over the past decade [5, 6, 7]

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Box 21.2 Universal salt iodization – country experiences(a) A comparative review of the experience of 3 major countries in developing salt iodization programmes (India, Russia and China) indicates varying progress depending upon a number of factors but most importantly high-level government support.

Trends lines extrapolated from available data. As early as 1962, the Government of India (GoI) introduced iodization of edible salt. Under the National Goitre Control Programme, in effect from 1963 to 1982, however, salt iodization was permitted only in the domain of the public sector. In 1983, iodized salt production was opened to the private sector, thus marking the beginnings of a strategy towards universal salt iodization in India [8]. By 1996, India had issued state level bans in almost all states, including the major salt producing states forbidding sale of non-iodized salt for edible purposes. This was followed in 1998 with India instituting a national level legislation which banned the sale of non-iodized salt. This legislation was revoked in 2000 amidst political turmoil, and subsequently resulted in a drop of adequately iodized salt production from 70.3% in 1997 to 29.6% in the period 2000–2004. In 2006, Government of India reinstituted the ban on the sale of non-iodized salt for human consumption. Thus, India’s production of iodized salt went from 4.1 million tons in 1999 to 1.69 million during the course of the interruption in legislation and then increased to 5.1 million tons in 2007 [9]. The accelerated increase was achieved due to special attention to increasing production of iodized salt and at consumption level monitoring iodine levels in salt within the legal frame work of state level legal bans). In the former USSR, salt iodization was well established in an effort to eradicate endemic goitre which began in the 1950s. By the 1970s, goitre was declared virtually eradicated and with the problem “solved” prevalence not consistently tracked. With the dissolution of the USSR in 1991, the salt iodization programme also became fragmented as government infrastructures underwent major reorganization. In addition, during this period of decline, there was no investment into the salt production infrastructure further hampering the capacity to produce adequately iodized salt. Consequently, the USSR went from an era of iodized salt production of almost 1 million tons in the 1960s-1970s, of which Russia produced 318,000 tons and imported the remainder of their domestic demand from the Ukraine, through a period of decline. Such a trend had a negative impact and by 1997 Russia, as a country, produced less than 25,000 tons. Meanwhile, with the lack of iodized salt available, iodine deficiency re-emerged [10].

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Numerous subsequent attempts to get legislation passed have failed. Nevertheless, the production of iodized salt has improved somewhat but production remains low (at approximately 130,000 tons in 2008, compared to an estimated domestic demand of 500,000 tons) and the household consumption of iodized salt is approximately 29% [11]. In both examples, national coalitions of organizations responsible for the IDD elimination oversight (government, salt industry, health and civic) have been either non-active/functioning or not established at all. China, in contrast, is a study of dedicated government commitment at the highest level. Actual epidemiological evidence of the magnitude of IDD in China came to light in the 1960s which investigated the origins of endemic goitre and cretinism and showed that iodized salt was an effective intervention to address the problem. At that time an estimated 700 million people were at risk from iodine deficiency. In the 1970s, there were 35 million people with visible goitres and 25 million people with intellectual impairment due to iodine deficiency across the country [12]. Earlier efforts to deal with this public health problem were focused on highly endemic areas but were not entirely effective due to low government commitment, uneven salt iodization and, likewise, monitoring. Spurred by the UN Summit for Children in 1990, where the Premier signed the declaration which had the elimination of IDD as one of its goals, China launched into an era of dedicated strategy to eliminate IDD by the year of 2000. The defining moment, however, was a high-level advocacy meeting in September 1993 held in the Great Hall of the People involving national and state stakeholders as well as international agencies. The meeting resulted in a State Council Leading Group on IDD Elimination which reaffirmed the commitment to eliminate IDD by 2000; the establishment of a National IDD Control Programme; a roll out of USI, regulation on iodized salt, including the creation of a salt monopoly to ensure iodized salt production, and the establishment of a multi-sectoral mechanism for social mobilization and advocacy. These key developments have sustained China’s efforts. Universal salt iodization as the main strategy was adopted in the whole country in 1995 [13]. The result was an increase in iodized salt production from less than 3.3 million tons in 1993 to 8 million in 2005. Today nearly 96% of Chinese consume effectively iodized salt on a sustained basis. (a)

Achieving Universal Salt Iodisation: Lessions Learned and Emerging Issues. Mannar M.G. Venkatesh, Bohac Lucie M. Published Proceeding in Volume 2 of the 9th International Symposium on Salt, Gold Wall Press, 2009.

21.3

Components of effective USI programmes

While salt iodization is technically a simple process, its sustained large scale implementation calls for actions in the political, administrative, technical and socio-cultural spheres. Many countries have been moderately successful in this process, while others have struggled for several years to establish effective programmes. Available country experiences highlight certain key prerequisites:

21.3.1 Policy support Several health and nutrition programmes compete for priority action by policy makers. Raising high-level awareness among high-level political leaders and bureaucrats regarding the problem and effectiveness of its

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control within a short period of time through salt iodization has been an important factor in generating political will to support sustained control and monitoring efforts. Evidence of political commitment to USI and elimination of IDD usually comes in the form of legislation that mandates that all salt for human and animal consumption be iodized, a national coalition or oversight body responsible for the programme that reports to the Minister of Health, and the appointment of a responsible executive officer for the IDD elimination programme [14].

21.3.2 Legislation and enforcement For most developing countries an effective salt iodization programme needs to be supported by effective regulation, making iodization of all salt for human and animal consumption mandatory. The regulation must also require penalties for non-compliance.

21.3.3 Multisectoral approach Salt iodization probably represents the first large-scale experience in national fortification of a commodity to eliminate a public health problem. While the responsibility for initiating, coordinating and monitoring an IDD control programme rests with the health sector, its planning and implementation calls for active involvement of other sectors like industry, trade, planning, transport, legislators, communication and education.

21.3.4 Involvement of the salt sector Strengthening salt iodization and expanding it to cover all edible salt in the country is the key requirement to eliminate iodine deficiency in the country. The salt industry needs to be entrusted with the responsibility of dovetailing iodization into the prevailing salt production and distribution system, creating a standardized scheme for adequate iodization at minimum cost and disruption. Even where the extraction of the raw salt is done on a large scale its distribution and processing is often transferred to small processing plants at the consumer level. As stated earlier, in countries such as India, while large producers account for nearly 75% of all salt for edible consumption in salt producing countries, a small but significant proportion of the salt is produced by many small producers with inadequate quality control. As an industry the salt sector must embrace USI and also seek to find ways to resolve bottle neck i.e. the sector needs to reconcile the challenges posed by the informal segment of the sector, which nevertheless hold a market share, as well as

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the inputs which are vulnerable to market conditions such as availability (procurement) and cost. New strategies will be needed to systematically identify ways in which small processors can comply with universal iodization requirements through a combination of advocacy, technical support, monitoring and enforcement. Small processors also need sustained and secure markets as well as a sustainable and secure procurement chain for raw materials and consumables like KIO3 (in convenient size packages and prices), salt packaging material, equipment and supplies. Support is also needed for preventive maintenance assistance, training and orientation and management. Such initial support “opens the door” to gain their support and compliance in the long term [15].The period of support is situation and country specific and determined by merits and demands within each country. However, it should be managed so as to not affect the commitment of other (larger) producers who already purchase their supplies and iodize at their own cost.

21.3.5 Public education and social mobilization Goitre and cretinism provided the visual picture of iodine deficiency that gave it an easily identifiable reference. As IDD elimination progressed, these physical manifestations became far and fewer giving the impression that IDD problem had been solved. Yet iodine deficiency persists in its more common form – brain damage, to which the unborn foetus is especially vulnerable. In effect, IDD elimination programmes are threatened to be victims of their own success since a deficiency must be continuously addressed or it will re-emerge. Thus, on-going communication efforts are necessary. Ultimately, public education serves to solidify support for IDD elimination at all levels of the society and thereby creates a demand for iodized salt, a necessary component for the success of a USI strategy and for ensuring sustained demand and production of iodized salt.

21.3.6 Monitoring and evaluation Systematic testing of iodine levels in salt at point of iodization and periodically at intermediate points in the distribution network, retail outlets and household level is essential for effective monitoring. Additionally, involvement of other sectors like NGOs, voluntary organizations and schools in monitoring iodine levels in salt, using lowcost field testing kits (Salt testing kits or rapid testing kits to provide a qualitative indication of presence of iodine in the salt using a dropper solution) is useful in generating pressure for adhering to the recommended level of iodine.

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Box 21.3 Communicating the Message ●

●

●

●

● ●

Relating IDD to brain damage, thereby creating an understanding of the functional outcomes beyond goitre and cretinism that result from iodine deficiency. These include mental impairment, the loss of IQ points, the impact on educational achievement and ultimately productivity Tailoring messages to the audience with a specific call of action they can take. The audience to be influenced ranges from top levels of government to the public health community to salt industry to community to the household Education at all levels must add to the supply push by creating a demand pull for iodized salt. Educated and motivated consumers who insist on iodized salt can become a force that salt retailers and processors cannot ignore and to whom they must respond by ensuring a steady uninterrupted flow of iodized salt. Conversely, unaware consumers will resist change and become a major obstacle to the programme by encouraging the circulation of unfounded rumours against iodized salt. Understanding the “common wisdoms” that exist in a community and correcting misinformation. Religious leaders and community leaders have been engaged to address culturally entrenched practices (i.e. washing of salt before use) which are obstacles to USI [16]. Using multi-media to get IDD messages into popular culture [17]. Integrating updated information about IDD into technical and educational materials of food inspection and control bodies, health-care training and academic curricula. [18].

While quality assurance of iodized salt occurs at the factory or production level, the testing of salt samples at the household level, done by UNICEF Multiple Indicator Cluster Surveys (MICS) in the Demographic Health Surveys (DHS), are useful to assess whether that iodized salt is reaching consumers or to detect potential leakage of non-iodized salt into the household, the latter issue being especially important to countries with mandated salt iodization. The stability of iodine in salt and levels of iodization and packaging are also related to issues of quality assurance. Conditions of high humidity result in rapid loss of iodine from iodized salt, with iodine loss ranging anywhere from 30 to 98% of the original iodine content [19]. By refining and packaging salt in a good moisture barrier, such as low density polyethylene bags, iodine losses can be significantly reduced, during storage periods of over six months. Table 21.2 presents details on typical packaging methods of table salt. Table 21.2 Typical packaging methods for table salt Salt variety Low density polyethylene sachets Paper/paper board Woven high-density polyethylene/ polypropylene Polystyrene containers/paper board round cans

Refined dry or semi-dry salt Refined dry salt Unrefined crystal or coarse salt Refined dry or salt

Typical sizes 0.5/1 kg 0.5/1 kg 10/20/50 kg 0.5/1 kg

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The salt industry has also been at the vanguard of innovation in testing equipment to allow for field testing of iodine levels in salt thereby enabling salt producers to monitor the quality of their product at source. These include the electronic checker (a modified filter photometer that converts the absorbance of the blue starch-iodate complex directly into a numerical read-out of iodine concentration in the salt samples) developed by the Salt Research Institute of the China National Salt Industry Corporation and the salt test kits or rapid test kits for checking iodine levels manufactured made by MBI Kits International. Work continues to refine such tools. As a key component of any public health intervention, the monitoring of progress towards the goal and the evaluation of results, in this case the elimination of iodine deficiency is critical. Traditionally, testing for iodine deficiency relied on an assessment of goitre prevalence. However, a number of issues relating to the measurement of thyroid size (goitre) as well as the responsiveness to changes in iodine nutrition status have resulted in a move towards using urinary iodine excretion (UIE) as the standard mechanism of measurement [20]. In this regard, the key programmatic indicators [21] identified are as follows: ●

●

●

Commitment to assessment and reassessment of progress towards elimination with access to laboratories able to provide accurate data on salt and urinary iodine, Regular laboratory data on UIE in school age children with appropriate sampling for higher risk areas, A database for recording of results of regular monitoring procedures particularly for salt iodine, UIE and if available neonatal TSH monitoring with mandatory public reporting.

21.3.7 Programme administration and coordination While the responsibility for initiating, coordinating and monitoring the programme lies primarily with the Health sector, IDD control is a multisectoral activity that requires the motivation and active involvement of several sectors for specific functions: Function

Agency/Department

●

Planning

●

Administration and Coordination Salt iodization, packing Salt producers/processors/traders, Ministry of Industry and distribution Quality Control Medical Research Institutes, Ministry of Health, Food Standards Institute, Food and Drug Administration Agency

● ●

Ministries of Planning/Health/Industry/Information & Publicity Ministry of Health

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572 ●

●

●

Information, Education Ministry of Information and Publicity, Health Education and Communication Bureau, Ministry of Health, Medical and Nutrition Associations Legislation Ministry of Health/Law Monitoring and Ministry of Health Evaluation Technical and Ministry of Finance, Multilateral and Bilateral development Financial Support assistance agencies

21.4

USI – An example of successful fortification

Success with salt iodization will give the government, industry, consumer groups and other stakeholders a new confidence to address other more complex micronutrient problems using salt as well as other food carriers to deliver essential vitamins and minerals to the population. There is therefore much more at stake in the effort to achieve USI and eliminate iodine deficiency disorders in any country. Salt enjoys unique advantages as a carrier of nutrients in most parts of the world in terms of universal coverage, uniformity of consumption and low cost of fortification. Encouraged by the progress made in several countries in implementing successful salt iodization programmes, efforts have been directed at examining the feasibility of fortifying salt with iron and other nutrients such as fluorine along with iodine [22]. With production, surveillance and monitoring infrastructure for iodization programmes already in place, such an integration and coordination, would enable resource savings and maximum efficiency. The commercial application of large-scale multiple fortification programmes would be a major breakthrough in establishing a cost effective delivery system for these nutrients to cover large populations.

21.5

Conclusions

In as much as tremendous progress has been made in making salt iodization indeed universal and global, the fact still remains that 2 billion people world-wide are still at risk of iodine deficiency. Although universal iodization has been generally accepted as a major public health intervention, 30% of households are unfortunately still are not using iodized salt. It is clear that the foundation of a USI program requires mandatory iodization and this can be achieved only when there is strong government commitment. Recent reports by the Copenhagen consensus, which rate salt iodization as one of the top investments with a benefit cost ratio of 30:1, provide a strong argument to be directed at national policy makers in countries where national commitment has not been

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made [23]. In addition, in those countries which have existing USI programs, a reaffirmation in the form of commitment of both human and financial resources for salt iodization programs, would not only assure sustainability but also mark the national ownership of the program and the goal. Strengthening salt iodization and expanding it to cover all edible salt in the country is the key requirement to eliminate iodine deficiency in a country. There is no other activity that draws together the productive sector of the society, the government sector, the political party sector, civic society and the general public such as iodine deficiency elimination does. It has taught valuable lessons in collaboration between government, industry, international organizations, the community at large and other sectors. It has also offered insights into building and sustaining an intervention politically, technically, managerially, financially and culturally.

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23.

Public health nutrition in developing countries DIOSADY L , ALBERTI J , MANNAR M,

and FITZGERALD S (1998). ‘Stability of iodine in iodized salt used for correction of iodine-deficiency disorders’, Food and Nutrition Bulletin, 19 no. 3, pp. 240–250. SULLIVAN K , SUCHDEV P, and GRUMMER -STRAWN L (2007). Achieving and Sustaining USI: Doing It Well Through Quality Assurance, Monitoring and Impact Evaluation. SCN News, 35, pp. 48–53. WHO, UNICEF , ICCIDD . (2007, Third ed.). ibid HORTON S, ALDERMAN H , and RIVERA J (2008). ‘Challenge Paper 2008: Hunger and Malnutrition. Fredericksberg: Copenhagen Consensus’. SUNDARESAN S (2008, June 23). Sustained Elimination of Iodine Deficiency: Progress, Sattus, Challenges and Way Ahead. Presentation at the meeting of the Board of the Network For Sustained Elimination for Iodine Deficiency. Ottawa, On, Canada: Network for Sustained Elimination of Iodine Deficiency. VIR S (2009). ‘Advocacy and Demand Creation for adequately iodized Salt Lessons Learnt and Ways Forward’, Review of Salt Iodization in India, New Delhi: Network for Sustained Elimination of Iodine Deficiency. GERASIMOV G (2002). ‘Iodine Decificency Disorders in the Russian Federation: A Review of Policies towards IDD Prevention and Control and Trends in IDD Epidemiology (1950–2002). Moscow: web publication UNICEF. GERASIMOV G (2009, May 11). ‘Barriers to USI in Russia. Presentation at the Satellite Session on IDD at the Micronutrient Forum’, Beijing, China. QIAN M (2009, May 11). ‘Universal Salt Iodization and Sustained Elimination of IDD in China’, Presentation at Satellite Session on IDD at the Micronutrient Forum, Beijing, China. YIP R , CHEN Z , and LING J (2004). People’s Republic of China. In B .S . HETZEL , Towards the Global Emilimination of Brain Damage Due to Iodine Deficiency (pp. 364–395), New Delhi: Oxford University Press. BEHRMAN JR , ALDEIMAN H , HODDINOTT J (2004). Hunger and malnutrition. Copenhagen Consensus Challenges and Opportunities. Copenhengan.

22 National iodine deficiency disorders control programme of India Sheila C. Vir

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

22.1

History and current policy

The National Iodine Deficiency Disorders Control Programme (NIDDCP) of India, formerly known as National Goitre Control Programme (NGCP), is a central-assisted programme of the Government of India (GoI), which is being implemented in the country since 1962 [1]. The NGCP programme was launched following a prospective study undertaken in school children in the Kangra Valley of Himachal Pradesh which conclusively demonstrated (Figure 22.1) that iodized salt was effective in reducing goitre [3]. Iodization of edible salt was proposed to be the solution for prevention and control of goitre in the country. Potassium iodate was recommended to be the more suitable fortificant for iodization of salt than potassium iodide for Indian climatic conditions [2–6]. NGCP initially focused in addressing the problem of goitre primarily in the sub-Himalayan region, which was considered to be the only goitre endemic region. The three objectives of NGCP were (i) survey to identify goitre-endemic regions in the country; (ii) supply of iodized salt in place of ordinary salt in the identified endemic regions; and (iii) assessment of impact of goitre control measures in the form of resurveys over a period of time [2]. Evaluation of NGCP by the Nutrition Foundation of India in the year 1981 [2] presented a number of recommendations for strengthening the NGCP. In 1984, based on the evaluation findings and the surveys conducted by the Central Goitre Survey team of the Ministry of Health as well as the

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22.1 The Kangra Valley Study – iodized salt and goitre prevalence [3]

1984 recommendations of the Central Council of Health and Family Welfare, it was decided to implement the programme for compulsory iodization of salt for human consumption in the entire country. The participation of the private sector was recommended. The programme was launched in a phased manner in the entire country with effect from April 1, 1986 with a higher priority to the regions identified as goitre endemic. The nomenclature of the NGCP programme was changed to the National Iodine Deficiency Control Programme (NIDDCP) in August 1992 with a view to address not only goitre but a wide spectrum of iodine-deficiency disorders (IDD) like mental and physical retardation lowering of IQ in children, deaf-mutism, cretinism, still-births, abortions, etc. The goal of NIDDCP is “to reduce the prevalence of iodine-deficiency disorders below 10 percent in the entire country by 2012” [1]. Universal salt iodization (USI) was the strategy adopted under NIDDCP. Box 22.1 presents the major events resulting in launch of NGCP, NIDDCP and USI. The Central Government issued a notification banning the sale of noniodized salt for direct human consumption in the entire country with effect from 17th May, 2006 under the Prevention of Food Adulteration Act 1954. Box 22.1 presents the major milestones of the NIDDCP and Universal Salt Iodization in India. The NIDDCP strategy, as per the policy guidelines issued by the Ministry of Health and Family Welfare, Government of India, in 2006 [1], focuses on enhancing production, demand and supply of iodized salt for ensuring universal consumption by the population in the entire country. Following are the primary components stated to be part of the NIDDCP: ● ●

● ● ●

Surveys to assess the magnitude of the iodine-deficiency disorders. Supply of iodized salt (the government in the policy document uses the term “iodated” and not iodized) in place of common salt. Health education and publicity. Laboratory monitoring of iodized salt and urinary iodine excretion. Resurvey after every 5 years to asses the extent of iodine deficiency disorders and the impact of iodized salt.

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Box 22.1 Major milestones – NIDDCP and Universal Salt Iodization, India ● ● ● ● ● ●

●

●

●

●

●

●

1955 – Kangra valley experiments and iodization plants installed 1962 – Launch of the National Goitre Control Programme (NGCP) 1983 – Extended from public sector to private sector collaboration 1984 – Compulsory iodization entire country 1986 – Launch of national programme coverage – phased manner 1992 – NGCP renamed as National IDD Control Programme (NIDDCP) and a policy to cover entire country with iodized salt supply. 1994 – Acceleration of USI following endorsement of USI by UNICEF / WHO Joint Committee on Health Policy 1996 – GoI – Universal Salt Iodization: minimum iodine at production level – 30 ppm, consumption level – 15 ppm 1996 – State level ban notification (under the Prevention of Food Adulteration Act or PFA) on sale of non-iodized salt of edible purposes issued in majority of states, including the three primary salt producing states 1998 – National Legal Ban Notification under the PFA – banning sale of edible non-iodized salt 13th Sept 2000 – GoI lifted the national ban on sale of non-iodized salt for edible purposes 17th May 2006 – Notification re-issued the national ban on sale of noniodized salt for direct human consumption

Government of India [1] reports that 263 out of 324 districts of 28 states and 7 Union Territories (UTs) surveyed to be IDD endemic with a total goitre rate of over 10 percent. These surveys confirm that no state in the country is free from iodine deficiency. NIDDCP continues to be a cent percent centrally assisted program and is an integral part of the National Rural Health Mission (NRHM). The Ministry of Health & Family Welfare is the nodal ministry for policy decisions on NIDDCP. The Central Nutrition and Iodine Deficiency Disorders Cell at the Directorate General of Health Services (DGHS) is responsible for the implementation of NIDDCP in the country. For effective implementation of the NIDDCP, the government by 2006 has established a network of 31 IDD Cells at state level in all states and Union territories except for three (Table 22.1). In 21 of these 31 IDD Cells, laboratories have been established and following functions are proposed to be undertaken by the IDD Cells [1]. 1. Checking iodine levels of iodized salt with wholesalers and retailers within the state and coordinating with the Food and Civil Supplies Department. 2. The distribution of iodized salt within the State through open market and public distribution system. 3. Creating demand for iodized salt. 4. Monitoring consumption of iodized salt. 5. Conducting IDD surveys to identify the magnitude of IDD in various districts. 6. Conducting training. 7. Dissemination of information, education and communication.

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Table 22.1 An overview of results of state goitre surveys and state-level infrastructure of NIDDCP [1, 7]

(a) (b) (c)

State/UT

Total districts

Total districts surveyed

Total districts endemic (c)

Andhra Pradesh (a) Arunachal Pradesh (a, b) Assam(a) Bihar (a) Chattisgarh Goa (a) Gujrat(a, b) Haryana (a, b) Himachal Pradesh (a, b) Jammu & Kashmir (a) Jharkhand Karnataka ( a, b) Kerala (a)# Madhya Pradesh(a) Maharashtra ( a, b) Manipur ( a, b) Meghalaya ( a, b) Mizoram (a, b) Nagaland (a, b) Orissa ( a, b) Punjab (a) Rajasthan (a) Sikkim( a, b) Tripura ( a, b) Tamil Nadu ( a, b) Uttar Pradesh ( a, b Uttaranchal( a, b) West Bengal (a) Andaman and Nicobar Islands (a) Chandigarh ( a, b) Daman & Diu ( a, b) Dadra & Nagar Haveli ( a, b) NCT Delhi(a, b) Lakshadweep (b) Pondicherry Total

23 11 23 37 16 2 25 19 12 15 18 27 14 45 35 9 7 8 8 30 17 31 4 4 29 71 13 18 2

12 11 18 14 2 2 16 11 10 14 9 20 14 14 29 8 4 3 7 8 3 4 4 3 29 29 9 5 2

11 11 14 14 2 2 8 10 10 14 8 6 12 14 21 8 4 3 7 7 3 4 4 3 18 23 9 5 2

1 1 1

1 1 1

1 1 1

1 1 4 582

1 1 4 324

1 0 2 263

States with IDD cells established States with laboratory attached to IDD cells Endemic district – The district is declared as endemic district if the total goitre rate is above 5% in the children of the age group 6–12 years surveyed.

Supply of iodised salt is expected to be monitored by food inspectors under the Prevention of Food Adulteration (PFA) Act within the state. An evaluation undertaken by the National Institute of Health and Family Welfare recommends measures for satisfactory functioning of the state IDD cells [7]. The Salt Commissioner’s Office (SCO), commonly referred as the Salt Department, under the Ministry of Industry and Commerce, is responsible

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for adequate production and distribution of iodized salt to the entire country. “Salt” is a Central (federal) subject in the Constitution of India and the SCO is responsible for controlling various aspects of salt industry. Earlier one of the primary roles of the SCO was issue of licenses to salt manufacturers. With the discontinuation of policy of issue of licenses to iodized salt manufacturers in 1996, a major task of the SCO to issue licenses has ended. SCO provides technical inputs for setting up salt-iodization plants, refineries as well as laboratories for monitoring quality of iodized salt at production level. Additionally, the office of the Salt Commissioner is the nodal government department responsible for ensuring appropriate distribution of iodized salt to the entire country. SCO is headed by the Salt Commissioner with its head quarters at Jaipur (Rajasthan) and a team of deputy/assistant salt commissioners located at five regional offices based at Chennai, Mumbai, Ahmedabad, Jaipur, and Kolkata.

22.2

Universal salt iodization (USI) – an integral part of NIDDCP

In 1994, at global level, UNICEF–WHO Joint Committee on Health Policy (1994) endorsed universal salt iodization (USI) as a safe, cost-effective and sustainable strategy to ensure sufficient intake of iodine by all individuals [8]. Following this, effort for supplying iodized salt was accelerated in the entire country. In 1994, the Salt Commissioner’s Office, under the overall guidance of NIDDCP, directed efforts for accelerating universal salt iodization (USI) for elimination of IDD. The goal of USI programme in India, as per the international guidelines, initially was to ensure that over 90 percent population in the country consumes adequately iodized salt. In the 11th Five Year plan (2007–2012), the goal was revised to ensure 100 percent consumption of adequately iodized salt [9]. Following are the primary programme components of USI: ● Ensure accelerated production of iodized edible salt with minimum 30 ppm iodine at production level and minimum 15 ppm iodine at consumption level. ● Monitor iodine levels in salt (production to consumption) level, including implementation of the legal measures. ● Create demand for iodized salt. ● Assess impact on a continuous basis and organise required training for survey and laboratory activities.

22.3

Increasing production of iodized salt for edible purposes 22.3.1 Salt production in India

Salt is produced in India by solar evaporation from sea water in the east and

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Public health nutrition in developing countries

west coastal regions of Gujarat, Tamil Nadu, Andhra Pradesh, Orissa, Maharashtra, Karnataka and West Bengal and from the sub-soil brine inland sources of Rajasthan. The major of common salt or raw salt produced in the country is in Gujarat (72%), Rajasthan (14%) and Tamil Nadu (11%), while the remaining quantity is from several other states along the Southeast and Southwest coast [10]. The total quantity of raw salt produced in India is approximately 17.5 MMT and almost one-third or 6.0 MMT of the total salt produced is for edible consumption (including livestock), 9.5 MMT is used for industrial applications, and the balance is allocated for export [11]. Salt production takes places in salt fields and the ownership patterns of these fields vary enormously. Small units operate below 10 acres either in private land or land leased from the government. The medium-sized units operate between 10 and 100 acres of land. The large units operate above 100 acres. The rationale adopted by the Salt Department to classify salt production units as small, medium and large is not based on the quantity of salt production but the “salt cess” which is linked to the size of salt fields. Of the total estimated 11,500 salt production units, only 822 iodized salt production units are reported to be registered with the SCO by 2009.

22.3.2 Production of iodized salt – public and private sector partnership Production of iodized salt commenced in 1955 by the Government of India (GoI), and by 1981, a total of 15 iodization plants with a total production capacity of 225,000 tonnes per annum [12] were installed – nine plants in salt-producing states of Gujarat and Rajasthan and six plants in two nonsalt producing states of Assam and West Bengal. The fortificant instructed to be used is potassium iodate [3]. This is based on the experience of Kangra Valley study. The concentration of iodine in salt was standardized initially at 25 parts per million (ppm) which was increased to a minimum level of 30 ppm in the year 1988. Salt-iodization programme in early phases was confined to only the government-managed public-sector undertakings. In 1984, the programme was opened up for private sector collaboration since it was apparent that such a partnership with private salt industry was critical to meet the increased targets of iodized salt production – target was fixed at a low level of 0.7 MMT for 1986 since iodized salt was initially supplied to a very small identified goitre belt. Following ongoing-goitre surveys in the country, a larger number of districts were identified goitre endemic and these regions were included under the National Goitre Control Programme which resulted in higher requirement as well as a higher target for iodized salt – a target of 3.0 MMT. Between 1989 and 91, the NGCP shifted its focus from undertaking goitre surveys to accelerating and sustaining high level of production of iodized salt and

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simultaneously creating demand for iodized salt [12]. With the objective to supply iodized salt in the entire country, the target for production of iodized salt was increased to 5.2 MMT to meet the requirement of country’s population, including the live stock. The total requirement was calculated at the rate of 6 kg/per person/year which takes into consideration requirements for livestock. A number of measures, as presented in Box 22.2, were taken since the launch of NGCP, to accelerate production and access to iodized salt [12, 13, 14]. Box 22.2 Important programme measures taken for accelerating salt iodization in India ●

● ●

●

●

● ●

●

●

●

●

In 1984, permission extended to private sector to produce iodized salt. Launch of public–private partnership. Subsidy introduced for potassium iodate – 1st April 1986 to 1st April 1992. Higher priority was allocated for iodized salt transport by rail – ranked second to defence movement. Subsidy was given for using rail transport. Rail zonal scheme was introduced – relaxed in 2006. Since 1986, the Salt Commissioner’s Office was identified as the nodal agency for monitoring quality of iodized salt at production level and prior to rail loading. The latter was linked to payment of subsidy to iodized salt manufacturers using rail transport for distribution of iodized salt to the identified districts/states. Inclusion of goitre control in 1986 in the “20 Point Programme” of the Prime Minister under “Health for All by 2000 AD”. In 1986, customs duty on the import of iodine was reduced from 40% to 25%. In 1988, the Prevention of Food Adulteration Act (PFA) was amended to specify that iodized salt should contain not less than 30 ppm iodine at retail level. In 1989, the Ministry of Health approved the “Smiling Sun” logo for easy identification of iodized salt by the public. The logo is registered with the Salt Department. Use of logo, however, is not mandatory. Upto 1995, focus on state-level bans under on sale of iodized salt under the Prevention of Food Adulteration Act (PFA). In 1998, first time a national legal ban on sale of non-iodized salt for edible purpose issued. 2006, re-issue of the national legal ban which was lifted in 1999.

The second SAARC conference on children in South Asia held in Colombo, Sri Lanka, in September 1992 reiterated the earlier resolutions made at the 1990 World Summit for Children when “Universal access to Iodized Salt by 1995” was adopted as one of the goals. Between 1994 and 95, the Government of India’s efforts to universalize iodization of salt assumed new dimensions with the international focus on USI for elimination of IDD. There was intensive effort to mobilize private salt producers for accelerating production of iodized salt to meet the goal of USI. A significant increase in the establishment of iodized salt plants was the result of this effort—from only 15 plants producing 0.2 million tons of iodized salt established in 1983 to as high as 822 registered salt iodization plants by 2007-08. The number of unregistered iodization plants has also increased during this period. The total installed capacity of these plants for production of iodized salt is estimated to be about 13.83 million metric

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Public health nutrition in developing countries

tons (MMT) [10, 11]. The capacity to produce iodized salt in India is estimated to be almost twice the 2009 revised country target of production of 6.0 MMT iodized salt which includes 5.2 MMT for only human consumption. On the other hand, the earlier target was stated to be 5.2 MMT to meet both human and livestock requirement. The production of iodized salt in 2008–09 is reported to have increased to 5.37 MMT (Table 22.2) as compared to 4.9 MMT in 2007–08 [12]. The total iodized salt produced is not used entirely for edible purposes within the country but is diverted to some extent to industry and is also exported. Moreover, the estimated total production of iodized salt refers to the production of salt fortified with iodine, irrespective of levels of iodine. This implies the total production of iodized salt of 5.37 MMT includes both adequately and inadequately iodized salt. Gujarat produces almost 60 percent of the iodized salt in the country (Table 22.2). In the last decade, there has been a significant increase in the demand for powdered packaged salt, both refined and non-refined. The common perception that all the packaged powdered iodized salt is “refined” salt is not correct. The production of refined salt has been steadily increasing. By 2007, a total of 42 refineries, with the capacity to produce 3.76 MMT of refined iodized salt or 69.2% of the edible salt requirement of the country, were reported to be functioning. In 2009, the SCO reported an increase in the number of refineries to 65 with a much higher installed production capacity of 5.74 MMT of iodized salt [12]. These refineries are increasingly producing and selling good quality non-iodized common salt at a high price to the industries such as tannery, detergents etc . Table 22.2 Iodized salt produced (MMT) 2008–2009 [12] State

Iodized salt production (‘000 tonnes)

Non-refined iodized salt (‘000 tonnes)

Refined iodized salt (‘000 tonnes)

Total Gujarat Rajasthan Tamil Nadu

5368.04 3677.82 846.36 713.42

3165.98 1779.70 747.16 508.68

2202.06 1898.12 99.20 204.74

Figure 22.2 presents details on the target and production of iodized salt from 1970 to 2009. As indicated in Fig. 22.2, the target for iodized salt production in the initial phase of NGCP progressively increased since additional districts were continuously being identified to be goitre endemic and were gradually added to the programme. Following the 1984 policy to iodize all edible salt in the country, iodized salt supply targets were increased phase-wise up to 1990. Production of iodized salt accelerated in 1984 and there was a continuous increase in the production except for a drop in the production level in 2003–04 which has been attributed to the after effects of Tsunami (Figure 22.2). One of the major constraints of the USI programme is the regular production and supply of Bargara salt (big crystal salt produced in the

National iodine deficiency disorders control programme of India

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22.2 Target and production of iodized salt (Figures in million metric tonnes (MMT))

Rann of Kutch in Gujarat) which forms 22% of the total edible salt produced in the country. Due to unique chemical properties of Bargara salt, this variety of salt cannot be produced in small crystal size or crushed into powder and packaged. Bargara salt made into powder form becomes hard and lumpy within a few weeks of crushing. Bargara salt crystal is sold at a much lower cost and continues to capture the rural market of large states of Madhya Pradesh and Uttar Pradesh (UP). The study of salt trade in UP state in 2001 revealed that 49.3% of salt entering the state is bargara salt and very often this is the only type of salt available and sold in open market in remote rural areas or urban slums [15]. Such a supply situation is often misinterpreted to conclude that rural population prefers to purchase and consume bargara salt and not powdered salt. Moreover, conditions of storage, transport and marketing of bargara salt is invariably unhygienic and crystal salt, often covered with dust, is sold in non-packaged conditions at a low cost. The consumers traditionally wash and dry bargara salt prior to cooking. Such a process results in loss of iodine since the fortificant is primarily incorporated in the superficial layer of bargara salt and therefore gets washed off. Bargara salt with negligible or no iodine is at times the only salt available to consumers, especially for those below poverty lines.

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Public health nutrition in developing countries

22.3.3 Source of iodine and cost of iodization There is no indigenous source of iodine in India. All the iodine required for the salt iodization program is imported from Japan and Chile [13]. Iodine is converted to potassium iodate in India by 18 private manufacturers of potassium iodate who are registered with the Salt Commissioner’s office [16]. These manufacturers provide regular information to the Salt Commissioner’s office on the total import of iodine and supply of potassium iodate in the country. In the earliest stages of the salt iodization program in India, potassium iodate was provided free of charge to iodized salt producers since only the public sector, supported by the government, was involved in the production of iodized salt. Later with the inclusion of private sector in the programme for meeting the high requirement for iodized salt production, free provision of iodine supply was discontinued but iodine imported for fortification of salt was supplied at a subsidized rate and was exempted from import duty. It was observed that the subsidy policy created an environment of expectation among private salt producers that the government would continue to absorb the additional cost of fortification with iodine since it was a public health intervention. The subsidy policy was observed to result in lack of ownership of the USI programme by iodized salt producers. Such an attitude was considered to be a risk factor for sustained production of iodized salt. The policy of subsidy was withdrawn by the Government of India in 1992. The total potassium iodate requirement as fortificant for salt iodization in India is 250 MT (1 kg potassium iodate for 20 tons of salt) and is manufactured primarily by 14 of the 18 registered producers of the fortificant who are mostly located in the states of Gujarat and Mumbai. India, also, remains an exporter of potassium iodate. Fluctuating international price has adversely affected potassium iodate business. There has been an increase in the global prices for both elemental iodine and potassium iodate. Price of potassium iodate in India in 2009 is quoted as Rs 1050 per kg (about US$ 200/kg) compared to about Rs 600 per kg (US$ 14/kg) about 6 years back and $ 8.5 per kg in January 1995 [13, 16]. As presented in Fig. 22.3, the cost of iodization is estimated to be only about 2% of the total cost of production of iodized salt or about 25 paise (1– 2 US cents) per person per year. The issue of escalating cost of potassium iodate in the international market remains a concern since it can have an adverse effect on the sustainability of the USI programme [16].

22.3.4 Transport and supply of iodized salt Salt Commissioner’s office, in coordination with railways, follows the ‘zonal scheme’ system developed for distribution of iodized salt by rail to

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22.3 Cost of iodized salt – percentage distribution of various components

all parts of the country. This has been relaxed since 2006 resulting in removal of quota of iodized salt supply fixed for each state by the SCO and the Railway Department. The revised policy has resulted in flexibility in salt trade movement. Movement of iodized salt by railways is entitled to concession in tariff and is accorded priority for movement; non-refined iodized salt is given ‘B’ category which is only next to the priority given to the movement of defence items which moves under category A. No such preference is given to refined iodized salt moving by rail. SCO, in consultation with Ministry of Railways and State Governments, arranges for the priority rail movement of iodized salt from the production centre to the States and Union Territories. Salt Department, as per the policy, is expected to check iodine levels in salt prior to certifying and sanctioning rail rakes for subsidized transport of iodized salt. However, there is no such policy or authority with the Salt Department for checking iodine levels in salt that is being loaded at the production or distribution centre for road transport nor there is any system to check iodine levels in salt supply entering the state by road movement. This results in a gap in monitoring mechanisms for checking iodine levels in salt being transported by road and marketed for human consumption [13, 17]. In the past two decades, there is a consistent increase in the usage of road transport for moving iodized salt. In 2009, it is estimated that 55% salt moved by rail and 45% by road. Selection of transport by rail or road is based on factors such as distance and cost involved. It is not economical to use rail transport for distance below 500 km. Producers/traders are increasingly noted to be opting for road transport of iodized salt and not rail transport since the producers not only find it economically advantageous but also convenient since the road movement is not governed by any monitoring policy which adversely hinders their business interest. On the other hand, the salt traders

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Public health nutrition in developing countries

are increasingly moving away from opting for subsidized rail transport for the following two reasons: (i) the policy that loading of full rakes (carrying capacity 2500 MT) is essential prior to allowing the rail rake to move to destination resulting in time loss in transport which adversely affects business; and (ii) checking of iodine levels in salt by the SCO is mandatory for sanctioning of “allocation subsidized quota” for use of rail rakes. The increasing interest and preference for road transport as compared to rail is also attributed to the relaxation of the rail zonal scheme which allows salt traders and producers to a great extent to select the destinations of trade as well as the mode of transport. A special “nominee system” (appointed traders procure salt for the states), however, continues to operate in eight states comprising seven north-east states and the state of West Bengal. Salt moves to these states primarily by rail and is checked for iodine levels by the SCO. Within the state, salt trade is handled by the wholesalers and retailers. Figure 22.4 presents an overview of the salt trade chain. The wholesalers, private business persons, are a critical small group which control salt business within a state and are expected to follow the legal guidelines of procuring and selling salt as per the PFA. The number of wholesalers trading in salt business varies from state to state. A salt trade study undertaken in the largest state of Uttar Pradesh reveals that a total of about 344 salt wholesalers supply edible salt to over 180 million populations in the state [15, 18]. In an effort to ensure accessibility of iodized salt at a low cost to population below poverty line, as presented in Table 22.3, about 16 states have introduced the policy of subsidized iodized salt supply through the public distribution system or PDS [19]. The iodized salt supply policy through the PDS, subsidized on non-subsidized is continuously being reviewed and is often revised by the state governments. The advantages and limitations of subsidy system for ensuring the long-term interest in sustainability of the USI programme needs to be periodically examined by the state authorities since there is always a risk of leakage of subsidized iodized salt for marketing to neighbouring states as well as the problem of dependency on subsidy for procuring iodized salt.

22.3.5 Monitoring of iodine levels – production level Defining standards for iodine fortification and the legal framework for fortification In India, establishment of standards under the Prevention of Food Adulteration (PFA) Act of 1954 governs the quality of edible iodized salt in the country. The Act has been amended a number of times with reference to the provisions for labelling and packaging standards [1, 13]. Under the Prevention of Food Adulteration (PFA) Act, iodine levels for fortification is defined by taking into consideration the average iodine requirements of

National iodine deficiency disorders control programme of India

22.4 Iodized salt trade chain

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Public health nutrition in developing countries

Table 22.3 Iodized salt sold at subsidized rate through the Public Distribution System (PDS) system – situation mid-2009 [12] State

Cost (Rs/kg)

Comment

Andhra Pradesh

2.50 for non-refined alt 4.00–4.50 for refined salt – Arunachal Pradesh 0.75 / head State government provides transport subsidy from rail head to retail shops Assam 3.50 for unpacked salt 5.00 for poly pack – Chhattisgarh 0.25 to PDS card holders Procurement price Rs. 2.32 per kg Delhi 5.50 for refined salt Gujarat 0.50 for iodized salt Distributed to BPL / tribal areas of 11 districts. Procurement price = Rs. 1.29 per kg) Himachal Pradesh 5.50 for refined salt Transport subsidy to hard and inaccessible areas is Rs. 1.99 Haryana 3.50 Jharkhand 0.25 for iodized salt Two kg salt per month to 23.64 lakh BPL families Karnataka 3.00 for iodized salt – Orissa 1.80 for loose 3.80–5.40 for poly pack – Rajasthan 1.00 for iodized salt Distributed to 5.62 lakh card holders in 6 tribal dominated districts. Procurement price = 1.68 per kg Sikkim 2.90 for crushed – iodized salt in loose Tripura 3.50 in poly pack – Tamil Nadu 2.50 for iodized salt Distributed to BPL population Uttar Pradesh – Iodized salt in PDS shops by choice of shopkeeper

population, average estimated consumption of 10 gram salt per person per day as well as an estimated 50% loss due to weather conditions during transit, storage and distribution. The standards for iodized salt, prescribed under the provisions of the Preventions of Food Adulteration Act and the rules, are presented in Box 22.3. Since 1984, for ensuring availability of iodized salt with adequate level of iodine, state/UT were encouraged to issue state-level notification, under the Prevention of Food Adulteration Act, to ban the entry and sale of noniodized salt for edible purposes. Such state-level ban notification was considered critical and was accorded a very high priority in 1990s in order to monitor marketing of iodized salt within a state. Strategically, highest emphasis was placed for such ban notifications in the three primary saltproducing states, viz. Gujarat, Tamil Nadu and Rajasthan in order to prevent movement of non-iodized or inadequately iodized salt for edible purposes by road from the production sites to the various districts within the state or transport of inadequately iodized salt out of the salt-producing states to the neighbouring states. Intensive efforts were directed for issue of state-

National iodine deficiency disorders control programme of India

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Box 22.3 PFA standard prescribed for iodized/iodated salt [1] “Iodated salt means a crystalline solid, white, pale pink of light grey in colour, free from visible contamination such as clay, grit and other extraneous adulterants and impurities.” Salt Quality Sodium Chloride – not less than 96.0 % by weight on dry basis Matter insoluble in water – not more than 1.0% by weight on dry basis Matter soluble in water other than sodium chloride – not more than 3.0% by the weight on dry basis Iodine Content (a) At manufacturing level – not less than 30 parts per million (ppm) on dry weight basis. (b) At distribution – not less than 15 ppm on dry weight basis.

Anti-caking agent – It may contain aluminium silicate to an extent of 2.0% by weight. Total matter insoluble in water in such cases shall not exceed 2.2% and sodium chloride content on dry basis shall not be less than 97.0% by weight. Packing of iodated salt – The iodated salt (iodized salt) manufactures have been directed to pack iodated salt only in HDPE or polythene-lines jute bags of permitted capacity, i.e. 50 kg for bulk

level bans. In 1992, 22 of the 32 states and union territories had banned the entry of non-iodized salt for edible purposes while by 1996 all the three salt-producing states had also issued the ban notification. By 1997, all states and union territories, except part of Andhra Pradesh, Maharashtra, Kerala, Goa and Pondicherry, had issued the state-level ban on the sale of non-iodized salt for edible purposes [13, 20]. A national-level ban on the sale of non-iodized salt for human consumption was issued in 1998. On September 13, 2000, the Government of India lifted the central ban on the sale of non-iodized salt for edible purposes. This ban under the Prevention of Food Adulteration Act 1954 was subsequently reinstated with effect from 17th May, 2006 [21]. The legal ban specifies banning the sale of non-iodized salt for direct human consumption in the entire country. Box 22.4 presents the gazette notification. As per the GoI policy, food inspectors in each state are responsible to monitor the implementation of the PFA act including salt samples testing at the designated Central Food Laboratory based at Ghaziabad, Kolkata and Banglore. Salt samples are advised to be collected from producers and traders throughout the distribution channel. In case a salt sample is found not to be of the prescribed standard at the retail level, all responsible persons associated with iodized salt trade including the salt producer as well as retailers are considered offenders and are subject to non-bail warrants or imprisonment for not less than six months and fine up to 1,000 Indian Rupees. Monitoring at production level As presented in Figure 22.4, Salt Department or the Salt Commissioner’s

590

Public health nutrition in developing countries

Office is responsible for monitoring the quality of iodized salt produced by the registered salt iodization units. The Salt Department provides the monitoring support to the salt manufacturers and iodized salt producers through its five regional offices and over 100 field offices, including a network of 26 fixed laboratories and three mobile laboratories [22]. In addition, each iodized salt producer is responsible for checking iodine levels in salt during the production process. It is mandatory for each iodized salt producers to have a laboratory or titration facility attached to the iodized salt production unit. However, monitoring guidelines developed by the Salt Department for iodized salt producers regarding checking iodine levels in salt by the titration method are often not known or ignored or only partially adhered to by iodized salt producers [16] resulting in ad hoc method used for sampling salt for testing iodine levels. Very often, the salt iodization units depend on salt-testing kits and not the approved titration method for periodical checking of iodine levels in salt during the production process. In addition, external monitoring is undertaken by the SCO only with reference to issue of permits to salt traders for the sanctioning of the allocation quota for subsidized rail transport system. A major gap in monitoring mechanism is the total absence of a system to monitor iodine levels in salt produced by non-registered iodization units or transported by road. Such a gap in the monitoring system, to a great extent, results in incorrect trade practices and increase the procurement and marketing of non-iodized salt or inadequately iodized salt by wholesalers of salt based in various states.

22.4

Advocacy and demand creation for increased production, universal access and consumption of adequately iodized salt

Intensive efforts are being made by the Government of India since 1989 to increase demand for iodized salt along with increasing production of iodized salt [13]. During this period, following a systematic study by the Ministry of Health, in collaboration with UNICEF, the logo of “smiling sun” for iodized salt was developed for easy identification. This logo was approved by the Ministry of Health in 2004. The logo is registered with Salt Commissioner’s Office. Use of this logo (Figure 22.5) is not mandatory but the logo is being widely used by iodized salt producers on iodized packets for facilitating easy identification and promotion of use of iodized salt [23]. One of the major components of the NIDDCP is “health education and publicity” for iodized salt. Government of India uses print and mass media such as TV and radio to create public awareness. Since 1993, efforts are ongoing to sensitize politicians and policy makers to move away from the notion that iodine-deficiency results in merely a cosmetic problem of goitre

National iodine deficiency disorders control programme of India

591

Box 22.4 The Gazette of India

New Delhi, November 17, 2005 MINISTRY OF HEALTH AND FAMILY WELFARE NOTIFICATION

New Delhi, the 17th November, 2005 G.S.R. 670(E)–Whereas draft of certain rules further to amend the Prevention of Food Adulteration Rules 1955, was published, as required by the Proviso to sub-section(I) of section 23 of the Prevention of Food Adulteration Act, 1954 (37 of 1954), at pages 1 to 3 in the Gazette of India, Extraordinary Part II, section 3, sub-section (i), dated the 27th May, 2005 under the notification of the Government of India in the Ministry of Health and Family Welfare (Department of Health) number of GSR 340(E), dated the 27th May, 2005, inviting objections and suggestions from the persons likely to be affected thereby before the expiry of a period of sixty days from the date on which copies of the Official Gazette containing the said notification, were made available to the public; And whereas the copies of the said Gazette notification were made available to the public on the 27th May, 2005; And whereas objections or suggestions received from the public within the specified period on the said draft rules have been considered by the Central Government; Now, therefore, in exercise of the powers conferred by section 23 of the said Act, the Central Government after consultation with the Central Committee for Food Adulteration Rules, 1955, namely: 1. (1) These rules may be called the Prevention of Food Adulteration (8 th Amendment) Rules, 2005. (2) They shall come into force after 6 months from the date of publication in the Official Gazette. 2. In the Prevention of Food Adulteration Rules, 1955,– (i) in rule 42,– (a) for sub-rule (v), the following shall be substituted, namely:– “(v) Every container or package of table iodised salt or iron fortified common salt containing permitted anticaking agent shall bear the following label, namely:– IODISED SALT/IRON FORTIFIED COMMON SALT* CONTAINS PERMITTED ANTICAKING AGENT

*Strike out whichever is not applicable. (b) in sub-rule(zzz), after clause (21), the following clause shall be inserted, namely,– “(22) Every container or package of common salt shall bear the following label, namely:– COMMON SALT FOR IODISATION / IRON FORTIFICATION/ ANIMAL USE/PRESERVATION/MEDICINE/INDUSTRIAL USE* *Strike out whichever is not applicable

(ii) after rule 44H, the following rule shall be inserted namely:– “44L Restriction on sale of common salt No person shall sell or offer or expose for sale or have in his premises for the purpose of sale, the common salt, for direct human consumption unless the same is iodised: Provided that common salt may be sold or exposed for sale or stored for sale for iodisation, iron fortification, animal use, preservation, manufacturing medicines, and industrial use, under proper label declarations, as specified under clause(22) of sub-rule (zzz) of rule 42”; (iii)in rule 49, in sub-rule(10), for the words “Edible common salt or iodised salt or iron fortified common salt”, the words “Table iodised salt or table iron fortified common salt” shall be substituted. [F.No.P. 15014/4/2005-PH(Food)] Rita Teaotia, Jt. Secy.

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Public health nutrition in developing countries

22.5 “Smiling Sun” logo for iodized salt, India

but to appreciate the serious adverse implications of iodine deficiency on brain development of unborn child, IQ levels of children (a decrease of average 10–13 IQ points is attributed to iodine deficiency), school performance as well as national productivity. Active support is sought from the politicians for the USI programme implementation and a number of events are organized every year on 21st October, the Global IDD Day. Since 1993, communication efforts are being directed to reach iodized salt producers and sensitize them of their social responsibilities regarding protecting brain and young minds of children and mobilizing them to procure and sell salt only with the recommended minimum levels of iodine [13]. In 2003, such communication efforts were extended to include iodized salt wholesalers. Promotion of powdered or fine crystal packed iodized salt, both refined and non-refined, was emphasized. It is evident from experiences documented in mid-2000 (Box 22.5) that it is critical that communication strategy sensitizes the state-based wholesalers and mobilises them to appreciate their social responsibility and follow the correct trade practices of procuring only adequately iodized salt. Salt-testing kits have proven to be very effective communication and semi-quantitative testing tools.

22.5

Innovative efforts to accelerate USI

Intensive innovative efforts were made in 1993–96 in selected 13 states including all north-east states to establish an effective monitoring and management information system linked to the primary health care network [7, 23, 24]. As per the system, salt samples were tested using the salttesting kits at health sub-centre levels by the auxiliary nurse mid-wife (ANM) and information obtained by ANMs was put together at block primary health care centre level and finally at the district health unit. The evaluation findings [7, 23] reported that such a monitoring mechanism created pressure on salt traders and was effective. The system is reported to have been discontinued in all the states except for the states of Gujarat and Sikkim.

National iodine deficiency disorders control programme of India

593

Between 2003 and 2008, successful experiences from two states of India – Uttar Pradesh and Tamil Nadu – have been reported. In the state of Uttar Pradesh, the strategy focused on monitoring of iodine levels in salt at the wholesalers as well as at the household level through a network of the middle and high school children. Figure 22.6 presents an overview of the strategy. These two primary actions complemented each other and proved effective not only in monitoring iodine levels in salt procured and consumed but also in alerting the entire salt trade chain of their social responsibilities and the legal guidelines. The impact was positive in influencing sale, procurement and in turn production of adequately iodized salt [18].

22.6 Overview of the strategy

Moreover, as presented in Box 22.5, monitoring of iodine at school level (over 20,000 salt samples per quarter) acted as a catalyst in the creation of demand for adequately iodized salt and also equipped the public to “discard” salt brands, locally packaged or otherwise, with inadequate level of iodine. The impact was evident in a few months. Figure 22.7 presents the impact at the wholesalers’ level while Fig. 22.8 presents the impact at the consumption level [18]. In the state of Tamil Nadu, a state-based consumer organization was involved in the task of monitoring presence or absence of iodine in salt at retailer and household level. Over 0.1 m salt samples were tested in a period of three years resulting in a significant impact on increasing iodized salt supply and consumption [16].

594

Public health nutrition in developing countries

22.7 Trends in procurement (30 months) of iodized salt at wholesaler level in the state of Uttar Pradesh [18]

22.8 Trends in consumption (30 months) of iodized salt at wholesaler level in the state of Uttar Pradesh [18]

It is evident from these innovative activities that monitoring of iodine levels in salt, using salt testing kits, resulted in creating demand as well as in improving supply. Intensive ongoing monitoring of iodine levels in salt at community or at school level positively influences trade practices and results in an accelerated shift in reducing supply of salt with nil iodine, improving availability of iodized salt as well as increasing awareness and consumption of iodized salt.

National iodine deficiency disorders control programme of India

595

Box 22.5 Uttar Pradesh innovative strategy – recognizing the strategic role of wholesalers Pressure on iodized salt producers to produce and supply only powdered packed iodized salt can be achieved and sustained by working with the network of wholesalers who procure salt from salt-producing regions. This implies mapping and sensitizing wholesalers of their roles in mental and physical health of the population, including the optimum brain development of newborns. Further, a system simultaneously needs to be put in place to keep a sustained pressure on the wholesalers to adhere to the legal ban under the PFA Act. Three to six monthly testing of iodine levels in salt samples, brought from homes by school children of middle and high school grades, generate such a pressure. Retailers become cautious and market only those salt brands which are tested at school level to have an adequate level of iodine. Involving school children of higher grades is more useful as compared to working with primary schools in situations such as in rural India where middle and high schools are smaller in number but cater to population coming from a larger geographical area. Such a strategy therefore increases the chances of influencing a larger number of retailers. This project design was based on the principle that buying and selling iodized salt must be perceived not only as a basic responsibility of salt manufacturers and salt industry but of wholesalers and retailers who procure and sell salt [14, 18, 25]. The programme strategy has been demonstrated to be successful in the state of Uttar Pradesh (UP). As a first step for the implementation of the above strategy in the state of UP, a study on mapping of salt wholesalers and understanding the salt trading system as well as understanding the knowledge, attitude and practices of salt traders was undertaken. This was done with a view to accelerate efforts to influence availability, marketing and accessibility of iodized salt. The study revealed that a total of only 344 primary wholesalers supplied salt to the entire state of 180 million populations. Of these, only one-third of these wholesalers – about 126 – marketed 80% of the total salt in the state. These primary traders were located in only 15 of the total 70 districts of the state. Effort was made to sensitize this core group of salt traders of their roles in the optimum mental development of young children and in school performance of young children. The informed salt wholesalers were also equipped with salt-testing kits (STKs) for facilitating routine checking and for ensuring that the salt purchased by them from salt producers had adequate iodine content. School-level activities of testing iodine levels in salt samples brought by school children and disseminating information on salt samples with inadequate level of iodine was also undertaken simultaneously. The activity of testing salt samples brought by school children was complemented with another action of six monthly testing of open and all available packaged branded salt purchased from local markets. Each and every brand of packed salt and 2–3 samples of open salt available in the markets of the administrative block headquarters of the district was collected. This was followed by testing of these samples of salt using the salt-testing kits (STKs) in the presence of school children during the school assembly time. In a block with 100,000 populations, on an average a total of 12–15 brands of packaged salt were available in a particular block head quarter market. Children were informed of the specific iodized salt brands with nil or low levels of iodine and were informed of the importance of discontinuing its usage. These children were encouraged to disseminate the information of salt-testing results in their neighbourhood and community. Over 217,000 salt samples, about 26,000 salt samples per quarter, were brought to school by school children and these were tested for iodine content using the salt-testing kits. Community was reached through the launch of “school child-tocommunity” approach. The households with salt samples not having adequate levels of iodine were visited by a group of students to sensitize them about the importance of iodine. Such a comprehensive programme strategy also resulted in protecting the business interest of wholesalers since demand was generated in the community for powdered packaged salt with adequate level of iodine.

596

Public health nutrition in developing countries

The school activities resulted not only in influencing consumption of iodized salt, but also in galvanizing the entire chain linking consumers, retailers and wholesalers. Pressure resulting from school-based activities had an immediate impact on reduction in procurement of salt with nil iodine (Fig. 22.7). The school efforts were complemented by equipping the wholesalers to test iodized salt using STKs and technical support to get selected salt samples tested by titration method in a laboratory especially set up in a medical college for providing salt testing service to wholesalers. The impact was noted in the shift in pattern of sale of iodized salt. In less than 2 years, salt procured with nil iodine decreased from 38% to 15.3% and salt marketed with adequate iodine level increased from 28.6% to 64.9% (Figures 22.7 and 22.8).

It is evident from the innovative efforts of the two states, Tamil Nadu (TN) and Uttar Pradesh (UP), that even if public is made aware of the significance of iodized salt and convinced to consume only adequately iodized salt, the consumers are not in a position to distinguish adequately iodized salt from non-iodized or inadequately iodized salt due to the misleading practice of incorrect labelling regarding iodine content. A communication strategy, promoting consumption of powdered packed adequately iodized salt, needs to be complemented with actions for introduction of a mechanism to check iodine levels in salt. Such a combined effort is essential to guide consumers to purchase the right product at an affordable cost and not to be misled by false labelling which is a malpractice followed commonly by non-refined iodized salt manufacturers or re-packers [18, 25]. Measures are required to be introduced for equipping consumers with information for “rejecting” those salt brand packages which are found to have inadequate level of iodine. Use of low-cost salt-testing kit (costing about US $ 0.20 for testing 100 samples) produced by MBI Chemicals of Chennai, India [26] has proved to be not only a semi-quantitative monitoring tool but a very effective communication tool (Box 22.5). Box 22.6—Testing Kit

National iodine deficiency disorders control programme of India

22.6

597

Elimination of IDD – impact and progress

(i) Monitoring system at consumption level As per the NIDDCP policy, the task of monitoring iodine level in salt and impact on iodine nutrition status at consumption level is the responsibility of the state governments. The procedures adopted for sample collection and testing are clearly laid out in the existing protocols and guidelines of the government [1] but implementation of these guidelines is a low priority and has a number of weaknesses [7]. According to the NIDDCP Policy, each state under the Government of India centrally sponsored scheme, is encouraged to establish an IDD Cell (Table 22.1) along with laboratory facility for routinely monitoring iodine content of salt and assessing urinary iodine excretion. The network of state-based IDD cells are linked to the National Reference Laboratories established at the Bio-Chemistry and Biotechnology division of the National Centre for Disease Control or NCDC (earlier referred as the National Institute of Communicable Diseases) at Delhi, for training medical and paramedical personnel for undertaking monitoring iodine content of salt and urine. In addition to this, four regional IDD monitoring laboratories have been set up at Hyderabad (National Institute of Nutrition) for southern India, Kolkata (All India Institute of Public Health and Hygiene) for East, New Delhi (AIl India Institutes of Medical Sciences) for the western regions and NCDC for the northern states. These four regional centres have been assigned the responsibility for undertaking regional training and providing support in monitoring iodine contents of salt, measurement of urinary iodine levels as well as for conducting Thyroid Function Test (TFT). Recent evaluation by the National Institute of Health and Family Welfare (NIHFW) recommends measures for improving the challenging task of strengthening the monitoring system through the network of IDD cell [7]. In addition to IDD cells, the food inspectors at states/provinces are assigned the responsibility to collect samples, under the PFA, and to organise testing of iodine levels at the designated laboratories for testing. Testing of salt is considered a low priority task by food inspectors. In 2009, under the NIDDCP, salt-testing kits are being supplied to voluntary health worker, referred as ASHA (Accredited Social health Activists) built-in for monitoring iodine levels in salt at household levels as well as at ICDS centres and schools.

(ii) Progress in access and consumption of iodized salt An analysis of the progress of USI programme presented in Figure 22.9 indicates that iodized salt consumption with adequate level of iodine (over 15 ppm) has remained stagnant in the past decade. A sharp increase in iodized salt consumption to 70 per cent was reported in 1996 by the

598

Public health nutrition in developing countries

evaluation study conducted in 1996 in eight states (three salt-producing states Gujarat, Rajasthan, Tamil Nadu and non-salt-producing states Manipur, Karnataka, Bihar, Himachal Pradesh, Madhya Pradesh), by the Ministry of Industry [23,25]. Consumption of salt with nil iodine was reported from only 11% households. The substantial increase trend in iodized salt consumption, observed in 1996, is attributed to monitoring system which was introduced at consumption level using the primary health care network [23, 26]. In 1998–99, there was a decrease in percentage households consuming iodized salt. This decrease is attributed to lifting of the national ban notification during this period resulting in weakening of the monitoring system at the production level. Additionally, discontinuation of the primary health care system linked monitoring system of mid-1990s also is considered responsible for the decrease observed. As presented in Fig. 22.9, since 1999 there is no increase in the pattern of consumption of adequately iodized salt in the last decade [27, 28]. According to the National Family Health Survey NFHS-3 [27], conducted during 2005– 06, (report published in 2007), 76% of people consume iodized salt while only 51.1% households consume iodized salt that is adequately iodized (containing a minimum of 15 parts per million of iodine) while 25 percent households consume salt with inadequate iodine. About 24% population consume salt with nil iodine. As per the two large national surveys (Table 22.6) consumption of adequately iodized salt has remained stagnant at 50% [27]. This implies 50% of the estimated 26 million children born each year, i.e. as many as 13 million are unprotected against iodine-deficiency disorders and are at risk of brain damage.

22.9 Iodized salt consumption trend 1997–2007

National iodine deficiency disorders control programme of India

599

The situation regarding consumption of iodized salt varies widely among states (Table 22.4). In 14 out of 29 states, over 90% population are reported to consume salt with some iodine. States consuming salt with adequate level or at least 15 ppm of iodine varies between 31.0 per cent (Andhra Pradesh) and 93.8% (Manipur) and only the state of Manipur meets the criteria of USI goal with over 90% population being reported to be consuming salt with recommended minimum level of iodine. The situation Table 22.4 Consumption of iodized salt-state-wise data from two national surveys [27, 28] State None (0 ppm) NFHS 2 NFHS3 (1998–99) (2005–06) Andhra NFHS 3 Arunachal Pradesh Assam Bihar Chhattisgarh Delhi Goa Gujarat Haryana Himachal Pradesh Jammu and Kashmir Jharkhand Karnataka Kerala Madhya Pradesh Maharashtra Manipur Meghalaya Mizoram Nagaland Orissa Punjab Rajasthan Sikkim Tamil Nadu Tripura Uttaranchal Uttar Pradesh West Bengal India

Iodine content of salt Inadequate (<15 ppm) NFHS 2 (1998–99)

NFHS 3 (2005–06)

Adequate (≥15 ppm) NFHS 2 (1998–99)

NFHS 3 (2005–06)

36.8

40.0

35.7

29.0

27.4

31.0

0.8

1.2

15.0

15.2

84.1

83.6

1.8 22.9 –

2.8 5.3 21.0

18.2 30.1 –

25.4 28.6 24.1

76.9 47.0 –

71.8 66.1 54.9

6.1 37.3 29.5 19.5 3.2

8.1 22.7 27.9 28.2 5.9

4.5 20.2 14.2 9.2 6.2

5.9 12.5 16.4 16.5 11.6

82.9 77.9 56.1 71.0 90.5

86.0 64.8 55.7 55.3 82.5

24.8

9.5

22.3

14.7

52.9

75.8

– 24.1 47.6 25.0

7.3 34.0 17.4 41.2

– 32.4 13.2 16.3

39.1 22.7 8.7 22.4

– 43.4 39.3 56.7

53.6 43.3 73.9 36.3

32.0

25.8

6.9

13.3

60.1

61.0

2.3 6.7 0.7 10.9 29.6 16.7 37.1 3.1 62.7

1.2 2.9 1.2 2.2 23.9 14.2 36.7 2.9 34.5

9.7 30.0 8.0 21.2 35.1 7.8 15.3 17.5 15.8

5.0 15.2 12.9 14.5 36.5 11.2 22.5 18.8 24.2

87.9 63.0 91.2 67.2 35.0 75.3 46.3 79.1 21.2

93.8 81.9 85.9 83.3 39.6 74.6 40.8 78.3 41.3

– – 22.7

2.9 29.0 23.4

– – 26.9

21.7 25.1 40.2

– – 48.8

75.5 45.9 36.4

11.3

6.7

26.5

24.2

61.8

69.1

28.4

23.9

21.6

25.0

49.4

51.1

600

Public health nutrition in developing countries

regarding consumption of salt with adequate levels of iodine of over 15 ppm is remarkably better than the national average in eight northern states as well as in the eastern states of West Bengal, Bihar and Jharkhand. It is evident from Fig. 22.10 that the mode of transport of salt to a state seems to influence the availability of adequately iodized salt. Availability of salt adequately iodized is much higher in states where iodized salt is transported from salt-producing centres primarily by railways since a policy to monitor iodine levels in salt for the allocation of rail wagon quota exists. On the other hand, the adverse impact on the availability of adequately iodized salt in the absence of such a monitoring mechanism for salt moving by road transport is also evident. This is well-reflected in the poor consumption of iodized salt pattern in most of the salt-producing states

≥65% adequately iodised salt

≥50–65% adequately iodised salt

<50% adequately iodised salt

22.10 State-wise profile of availability of adequately iodized salt and mode of transport used for iodized salt supply

National iodine deficiency disorders control programme of India

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(Andhra Pradesh, Orissa, Tamil Nadu, Karnataka and Rajasthan) as well as in other states (Uttar Pradesh, Haryana, Madhya Pradesh, Maharashtra, Andhra Pradesh, and Karnataka) where road transport is the primary mode of transport for procuring iodized salt. Analysis of nation-wide data with reference to socio-economic situation [27] indicates that a disproportionately large percentage of the rural poor continue to be deprived of adequately iodized salt. Iodized salt consumption shows a wide variation – higher in upper socio-economic group and much lower in the poorer socio-economic group. This is possibly due to the fact that in the absence of an appropriate system for monitoring of salt moving by road, iodized salt (often non-refined packaged or open salt or bargara salt) which contains inadequate iodine is procured and sold at a lower cost resulting in the poorer section of the population purchasing such lowcost salt. In contrast, in the north-eastern states, a very high percentage of households (varying from 71.8% to 93.8%) consume adequately iodized salt, irrespective of the socio-economic status. It is therefore evident that in situations where only adequately iodized salt is procured and sold for edible purposes, economic situations of households has negligible impact on iodine levels in salt purchased and consumed.

(iii) Status of iodine nutrition Since 1999, besides goitre survey, iodine nutrition is assessed by measuring urinary iodine excretion. As per the Policy [1], IDD survey at district level is recommended to be conducted by using the method of population proportional to size (PPS) sampling in the age group of 6–12 years children. The indicators recommended under NIDDCP are presented in Table 22.5. The cut-off presented By NIDDCP corresponds to the epidemiological criteria recommended by WHO/UNICEF/ICCIDD for assessing the severity of IDD based on the prevalence of goitre in school-age children and for assessing iodine nutrition based on urinary iodine concentration of school-age children [30]. Table 22.5 IDD prevalence indicators and criteria for classifying IDD as a significant public health problem [1] Indicator

Severity of public health problem Mild Moderate Severe

Goitre grade >0 Median UIE (Microgram/I)

5.0–19.9% 50–99

20.0–29.9% 20–49

≥30% <20

Iodine nutrition surveys have been carried out and reported by the National Institute of Nutrition (NIN), and International Council for Control of IDD (ICCIDD) and the Human Nutrition unit of the All India Institute of Medical Sciences (AIIMS). In 2003, NIN carried out a survey in forty selected districts

Public health nutrition in developing countries

602

of various states located in five different regions (Southern, Northern, Eastern, North Eastern and Central) of India to assess the impact of NIDDCP on the prevalence of IDD [29]. Districts with a higher percentage of goitre prevalence, prior to the launch salt iodization programme, were selected for the study. The findings revealed that the overall prevalence of total goitre declined significantly from 14–69% during 1984–94 to 2–40% in 2003, especially in the north-eastern regions. The prevalence of total goitre was ≥10% in half of the districts and ≥5% in 37 out of 40 districts surveyed. The median urinary iodine excretion levels among 6–11 year children was observed to be <100 μg/L only in 9 out of 40 districts (Table 22.6). IDD survey undertaken by ICCIDD during 1999–2006 in seven states (Kerala, Tamil Nadu, Goa, Rajasthan, Bihar, Orissa, Jharkhand), presented in Table 22.6, indicates that the situation is much better in Kerala and Jharkhand with median urinary iodine being over 100 μg/l and only about 8-10 percentage of subjects having urinary iodine <50 μg/l. Table 22.6 Status of iodine deficiency – regional surveys [3] Strata

Year

Coverage

Urinary iodine Median (μg/L)

(% <50 μg/L)

Kerala Tamil Nadu Goa Rajasthan Bihar Orissa Jharkhand

1999–2001 2001–2002 2001–2002 2002–2003 2003–2004 2003–2004 2006

State State State State State State State

123.3 89.5 76 138.7 85.6 85.4 173.2

8.2 22 36.2 16.9 31.5 32.2 10

22.7

Elimination of IDD – challenges ahead

India has been recognised as one of the sixteen “make or break” countries which require intensive efforts to accelerate the USI programme for achieving the global goal of USI. It is evident from Figure 22.11, that the consumption of adequately iodized salt in India is much lower than other Asian countries [31]. For addressing the goal of USI, and for sustained elimination of IDD, the following programme issues are critical. ●

●

Ensuring higher political commitment and urgent enforcement of legal ban that was re-instated on 17th May, 2006. Advocacy to increase attention to the implications of iodine deficiency on increasing risk of brain damage to unborn children. Shifting the focus from merely iodized salt to “adequately iodized salt”. Strengthening of the monitoring system at consumption level to ensure universal consumption of iodized salt with minimum 15 ppm iodine at household level.

National iodine deficiency disorders control programme of India

603

22.11 Progress in households consuming adequately iodized salt in South Asia [31] ●

●

●

Integrating IDD programme activities in broader health-nutrition programmes. Active promotion of powdered packed or fine crystal (includes both refined and non-refined) iodized salt through traders network, school system, Integrated Child Development Services (ICDS), Maternal and Child Health (MCH) programme. Complementing quality iodized salt production efforts with actions to reach wholesalers of salt by urgently mapping, reaching and sensitizing wholesalers in each salt producing and non-salt producing states – it is estimated that not more than 300–350 salt wholesalers operate in each state and need to be recognized as critical partners in the NIDDCP. Institutionalizing mechanisms at state/district levels not only for creating demand for iodized salt but for exerting and maintaining pressure on salt trade chain – from consumption level to levels of retailers, wholesalers and producers by establishing a system of monitoring and regularly disseminating information at every level. Equipping consumers with information on iodine levels in salt that is available in local market so that they are in a position to “reject” and not purchase inadequately iodized salt.

References 1. Revised Policy Guidelines on National Iodine Deficiencies Disorders Control Programme (2006). IDD and Nutrition Cell, Directorate General of Health services, Ministry of health and Family Welfare, Government of India, New Delhi. 2. Nutrition Foundation of India (1998). The National Goitre Control Programme. A blue print for its intensification. 3. AIIMS / Salt Department, GoI / ICCIDD / MI/ UNICEF (2008). Salt for freedom and iodized salt for freedom from preventable brain damage.

604 4.

5. 6.

7.

8.

9.

10.

11. 12. 13. 14. 15. 16. 17. 18.

19. 20. 21. 22. 23. 24. 25.

Public health nutrition in developing countries SOOCH SS , DEO MG , KARMARKAR MG , KOCHUPILLAI N , RAMACHANDRAN V

(1973). Prevention of endemic goitre with iodized salt. Bull World health Organisation 49, pp. 307–312. HETZEL BS (1989). The story of iodine deficiency. An international challenge in nutrition. PANDAV CS , CHAKRABORTY A , SUNDRESHAN A , ANSARI MA , JAIN P, AGUAYO V , AYOYA M (2008). Salt for freedom and iodized salt for freedom from preventable brain damage. National Institute of Health and Family Welfare (NIHFW) (2006). Evaluation and implementation status of NIDDCP in India. Brief findings and recommendation. UNICEF and WHO, “World Summit for Children: Mid decade goal – iodine deficiency disorders”. Report from UNICEF and WHO Joint Committee on Health Policy, Special Session, Geneva 27th January 1994. Government of India, Ministry of Women and Child Development (2006). 11th Five Year Plan. Report of Working Group on Integrating Nutrition with Health (2007-2012). Directory of iodized salt manufacturers, salt refineries, potassium iodate manufacturers and iodization plant fabricators, Government of India, Office of Salt Commissioner, ministry of Industry, Department of I.P.P. (2006). Salt Department (2009). Personal Communication on “Particulars of iodization plants commissioned upto 30th September 2009. Salt Department (2009). Personal Communication, October 2009. USI: Universal Iodization India – Progress and Current Status (August 1996), salt Department, Ministry of Industry. VIR SC (1995). Editorial: iodine deficiency Disorders in India. Ind J. Public Health 32, pp. 132-134. Salt Trade in Uttar Pradesh – mapping of wholesalers and major traders and KAP study. Government of UP and UNICEF 2001. VIR S (2007). Universal salt Iodization (USI) in India – Current Situation and Proposed Actions. Consultancy report presented to UNICEF, December 2007. Salt Department and Ministry of Industry and UNICEF (1993). Universal Salt Iodization – We must act now. VIR S, DWIVEDI S , SINGH R, MUKHERJEE A (2007). Reaching the goal of Universal Salt Iodization (USI): Experience of Uttar Pradesh. Food and nutrition Bulletin 28(4), pp 384–390. Salt Commissioner Office (May 2009). Personal Communication. Salt department and UNICEF (February 1995). Banning Sale of Edible non – iodized salt – An urgent measure. The Gazette of India, Ministry of Health and Family welfare Notification, New Delhi, 17th November 2005. Monitoring system at production level, USI (India). Salt department, Ministry of Industry (August 1996) Evaluation of Universal Salt Iodization in India—A mid term Evaluation , Indian Institute of Health Management Research for the Ministry of Industry, March 1998, Iodine deficiency Disorders control programme, UNICEF-Department of Health Project Document, Ministry of Health and Family welfare, July 1993. VIR SC (2008). How to increase consumption of iodized salt in India: a situation analysis. ICCIDD Newsletter, 30(4): 7–10.

National iodine deficiency disorders control programme of India 26. 27. 28. 29. 30.

31.

CHANDRASHEKHAR , MBI CHENNAI .

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International Workshop on Micronutrient and Child Health , Human Nutrition Unit, AIIMS, 20-23rd October 2009, New Delhi. National Family Health Survey (NFHS 3), 2005-06, Volume I, International Institute for Population Sciences 2007. National Family Health Survey (NFHS 2), 1998-99, Volume I, International Institute for Population Sciences. VIJAYARAGHAVAN et al. Current status of IDD in select districts of different regions of India, National Institute of Nutrition 2003. WHO, UNICEF, ICCIDD (2007). Assessment of iodine deficiency disorders and monitoring their elimination. A guide for programme managers Geneva, World Health Organization, 2007. UNICEF (2009). Sustainable Elimination of Iodine Deficiency. Progress since the 1990. World Summit for Children.

23 Metabolism of iron, folic acid and vitamin B12 K. Madhavan Nair

K. Madhavan Nair, PhD in Biochemistry from Osmania University, Hyderabad, is a Scientist (E) and Head of the Micronutrient Research Division at the National Institute of Nutrition. He has received the Public Health Service International Research Fellow Award in1988 and ICMR’s prestigious B.G.R.C. Silver Jubilee Oration Award for the year 1996 for his contributions in the field of Nutritional Hematology. His expertise includes basic, applied and population-based intervention programs in micronutrients. Dr. Nair has made significant contributions in understanding iron-induced free radical damage and its prevention by antioxidant supplementation and micronutrient food fortification.

!.1

Introduction

Iron along with folate and vitamin B12 are by far the most important nutrients for cell proliferation. Major advances have been made in understanding the physiology of human iron metabolism. In addition to its role in cellular proliferation, it plays vital role in oxygen transport, oxidative metabolism and other physiological processes. Folic acid deficiency reduces the proliferative capability of rapidly dividing tissues of the body and a primary deficiency of vitamin B12 can lead to a secondary deficiency of folic acid. There is a great deal of biochemical interdependence of iron, vitamin B 12 and folic acid in maintaining purine and pyrimidine supply to synthesize genetic material and maintain cell division. The scope of this chapter is to review the latest developments in the area of metabolism of these nutrients, highlighting their interactions in various metabolic pathways in order to provide a holistic understanding to improve public health nutrition.

!.

Iron

Iron (Fe, atomic number 26, atomic weight 55.65) is the fourth most abundant element (O, Si, Al, Fe) and second most abundant metal in the earth’s crust. In aqueous solution iron can exist as ferrous (Fe2+) or ferric

607

608 Public health nutrition in developing countries (Fe3+) ions and is associated with a large variety of biological molecules. Iron is the most versatile of all biologically active metals owing to its ability to switch between the ferrous and ferric forms. It acts as a catalyst in redox reactions by donating or accepting electrons and participates in free radical chemistry by donating electrons to oxygen. It is the major hemopoietic factor [1]. Iron in the environment is almost exclusively in the Fe3+ state. In spite of its abundance, iron deficiency anemia is the most common nutrient deficiency in the world today. It affects all age groups and both sexes. The prevalence of anemia is significantly higher especially in women of child-bearing age and infants. To a large extent the physiology of iron and the factors leading to iron deficiency are well defined. Healthy, non-anemic individuals have an optimum balance between iron intake and excretion [1, 2].

23.3

Distribution

Total iron content in an average adult man (60 kg) is estimated to be about 3.8 g, that in a woman (50 kg) is 2.3 g and in a new born it is about 70 mg per kg body weight or a total of 250 mg iron. The distribution of iron in the human body is conceptualized to exist in three main biological compartments; functional, transport and storage (Fig. 23.1). The functional compartment accounts for about 75% of total body iron and consists of hemoglobin (65–70%), myoglobin (3–4%) and enzymes (3%). The transport compartment corresponds to iron in circulation bound to plasma transport protein transferrin, contributing to less than 1% of body iron. The storage compartment contributes to the remaining 25%, and comprises iron stored in a nontoxic form as ferritin and hemosiderin proteins in liver, spleen and marrow. The storage compartment corresponds to iron absorbed in excess of that required for the functional compartment [1, 2].

23.1 Distribution of iron in man.

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The three components are interlinked and coordinated to maintain systemic iron homeostasis. The transport compartment, estimated to turnover about 25 mg iron per day, links the storage and functional compartments by transporting iron to the functional compartment from the body stores [3].

23.4

Functional compartment

Iron containing proteins are conveniently grouped into two categories – heme and, non-heme proteins. The first category, heme-proteins, includes hemoglobin, myoglobin and certain enzymes involved in oxidative metabolism. The second category of non-heme iron proteins includes ferritin (iron storage), transferrin (transport) and certain enzymes containing the iron–sulphur cluster.

23.5

Heme proteins

Heme refers to a molecule that has a protoporphyrin IX ring with a ferrous ion coordinated to it (Figure 23.2). It thus consists of an organic component and an iron atom. Protoporphyrin IX is made of four pyrrole rings (tetrapyrrole).

23.2 Chemical structure of the Fe2+ protophorphyrin IX - heme group in hemoglobin and myoglobin.

610 Public health nutrition in developing countries The iron atom in heme binds to four nitrogens in the center of protoporphyrin ring. The ferrous ion can form two additional bonds, one above and one below the plane of the heme molecule. These bonding sites are termed fifth and sixth coordination positions respectively. There are a number of heme-containing proteins, most abundant are hemoglobin (Hb) and myoglobin (Mb). Hb is the oxygen carrier and plays a vital role in the transport of carbon dioxide and hydrogen ions. Normal hemoglobin concentration in humans ranges from 11 to 14 g/dl and is age and sex specific. Myoglobin, located in muscle, serves as a store of oxygen and facilitates the movement of oxygen within skeletal and cardiac muscles. The concentration of myoglobin is about 3–5 mg/g of muscle tissue. The globin or protein component of Hb is made up of four separate chains and is hence called a tetrameric protein. In humans, four different types of globin chains are found, namely, α (alpha), β (beta), γ (gamma) and δ (delta). Human adult hemoglobin has a α2, γ2 configuration and the chains are held together by non-covalent interactions. Each chain binds a heme molecule. The α and β chains of hemoglobin closely resemble those of myoglobin, which is a monomeric heme protein. Hb can also have a α2, δ2 configuration called HbA2 and fetal Hb has a α2, γ2 configuration. Myoglobin is a monomeric protein, meaning it has only one globin chain with a heme attached to it. The capacity of hemoglobin and myoglobin to bind oxygen depends on the presence of the heme group, which also gives them the distinctive colour. The iron atom can be in the Fe2+ or Fe 3+ oxidation state and the respective forms of hemoglobins are called ferrohemoglobin and ferrihemoglobin (methemoglobin). Only Fe2+ oxidation state can bind oxygen. The, globin chain, in these molecules confers a distinctive microenvironment to the heme, enabling it to carry oxygen and this phenomenon is termed co-operative binding. When fully saturated, each gram of hemoglobin is capable of carrying about 1.34 ml of oxygen [4, 5].

23.6

Heme enzymes

Heme enzymes, as the name suggests, are enzymes containing a heme group and are functionally different from the heme proteins discussed in the previous section. Examples include cytochromes a, b and c which are present within the cristae of mitochondria in all aerobic cells. The highest concentration of cytochrome c is present in heart muscle. The iron atom present in the heme moiety of the cytochrome oscillates between Fe3+ and Fe 2+ during the process of oxidative phosphorylation. Oxidative phosphorylation is redox process that results in cellular energy production in the form of adenosine tri phosphate (ATP). Given below is a nonexhaustive list of important heme-containing enzymes and their functions.

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These examples illustrate the myriad functions of these enzymes in physiology and metabolism and thus underscore the importance of iron in systemic homeostasis [4]. Cytochrome b5 is a component of liver microsomal membranes where it probably provides energy for protein synthesis. It is also present within the cytoplasm of the red blood cells, where it functions as an intermediate in the reduction of methemoglobin. Cytochrome P-450 family of enzymes is involved in xenobiotic or drug metabolism and are located predominantly within the microsomal membranes of liver cells and also in the intestinal mucosa. Other heme enzymes, catalase, peroxidase, myeloperoxidase are part of the cellular antioxidant defense mechanism(s) and tryptophan pyrrolase is involved in tryptophan metabolism. The other important heme enzymes are nitric oxide synthase (NOS) and prostaglandin synthase or cyclooxygenase (COX). Both these enzymes are important for initiating and propagating immune responses. The enzyme NOS catalyzes the formation of nitric oxide (NO) from oxygen, arginine, requires several cofactors and contains a heme group which is part of the catalytic site. NO is an important signaling molecule with major roles in neurotransmission, blood pressure control and blood clotting. (COX) converts arachidonic acid to prostaglandin H2 (PGH2), the precursor of eicosanoids. The enzyme contains two active sites, with the heme moiety having peroxidase activity. The eicosanoids, prostaglandins, prostacyclins and thromboxanes are known to be involved in reproductive functions, in inflammation, fever, and pain, associated with injury or disease; in the formation of blood clots and the regulation of blood pressure; in gastric acid secretion; and in a variety of other processes important in human health or disease [4, 5].

23.7

Non-heme iron proteins

In these proteins, the iron is present not as a heme moiety but in other forms such as iron-sulfur clusters, such as proteins of oxidative phosphorylation. The iron transport protein transferrin and storage proteins ferritin are the other forms of non-heme iron proteins and will be discussed in detail subsequently. Aconitase, ribonucleotide reductase, lipoxygenases, tyrosine hydroxylase, inositol oxygenase, proline and lysine hydroxylase, dehydrogenases, and xanthine oxidase are some of the important enzymes of this class. Aconitase is an enzyme that catalyses the stereo-specific isomerization of citrate to isocitrate via cis-aconitate in the tricarboxylic acid cycle (TCA) that occurs within the mitochondria. Aconitase contains four iron atoms that are complexed to four inorganic sulfides as [4Fe-4S]2+ cluster (iron– sulphur cluster) in its active site. These sulphide groups are provided by cysteine residues in the protein. The fourth iron atom of the [4Fe-4S] 2+

612 Public health nutrition in developing countries cluster, called the labile iron, is not coordinated by a sulphide but by water molecules. Thus the Fe–S cluster binds citrate (substrate) and participates in sequentially dehydrating and rehydrating the bound substrate. The aconitase protein is bifunctional in that it can function either as an active aconitase (enzyme), or as a RNA-binding protein which controls the expression of proteins involved in cellular iron metabolism. The cellular iron status enables the protein to switch between the enzyme form and the RNA-binding protein form. This phenomenon is called the ‘aconitase switch’ and is discussed in detail later in the chapter. This protein illustrates the possible role of iron in energy homeostasis. Ribonucleotide reductase is essential for DNA synthesis and therefore cell proliferation. This enzyme catalyzes the de novo synthesis of deoxyribonucleotide diphsophates (dNDPs) from ribonucleotide diphosphates (NDPs). The dNDPs are in turn subsequently used for DNA synthesis. The active site of the enzyme contains an iron centre consisting of two ferric ions (Fe3+), a tyrosyl free radical and two sulfhydryl groups. The free radical at the active site is stabilized by the two Fe3+ ions connected to each other by an oxygen atom. The mechanism of catalysis is as follows. The hydroxyl group bonded to C-2 of the ribose ring is steriospecifically replaced by a H. This reduction is initiated by the free radical at the active site [6]. Actively dividing tissue such as the bone marrow requires a constant supply of dNDPs. This supply can be met only if ribonuclotides are not limiting, implying that NDPs also have to be continuously synthesized. However, NDP synthesis involves one-carbon transfer reactions carried out by methyl transferases. Most methyl transferases require methylated forms of tetrahydrofolate (e.g., N10-formyl-tetrahydrofolate for thymidylate synthase) as the carrier of the transferable carbon. Deficiency of folate severely hampers NDP synthesis, thus inhibiting DNA synthesis and finally cell division. This pathway is a good example of why anemia, caused by iron deficiency or folate deficiency, has similar clinical manifestations. This example also highlights the importance of accurately identifying the etiology of anemia, as iron supplementation alone will not correct an underlying folate deficiency. It is for this reason that folic acid is given along with iron supplements for correcting anemia. Lipoxygenases are iron-containing enzymes that catalyze the dioxygenation of polyunsaturated fatty acids. Products of lipoxygenases are leukotrienes which are involved in inflammatory pathways. Tyrosine hydroxylase or tyrosine 3-monooxygenase catalyzes the conversion of the amino acid L-tyrosine to dihydroxyphenylalanine (DOPA). DOPA is a precursor for dopamine which in turn is a precursor for norepinephrine (noradrenalin) and epinephrine (adrenaline) all of which are important neurotransmitters.

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Myo-inositol oxygenase catalyzes conversion of myo-inositol to Dglucuronate, initiating the only known pathway in humans for catabolism of the carbon skeleton of cell-signaling inositol (poly) phosphates and phosphoinositides. Proline and lysine hydroxylase enzymes. Collagen contains 2 posttranslationally modified amino acids hydroxyproline and hydroxylysine. The hydroxylase enzymes responsible for these modifications require Fe 2+ for activity. Ascorbic acid, acting as a reducing agent keeps the iron in the reduced Fe2+ state. This is the reason why ascorbic acid deficiency causes scurvy [1–5, 11, 16]. Thus, from the above examples it is evident that depletion of iron in the functional compartment can adversely affect energy production, DNA synthesis, response to inflammation, neurophysiology and collagen integrity. The effects of iron deficiency are therefore manifested as anemia, impaired psychomotor development, impaired effort tolerance and adverse pregnancy outcome. The cited examples also provide a biochemical explanation to the observed multi-systemic manifestations of iron deficiency [5].

23.8

Storage compartment

The storage compartment is composed of intracellular iron storage proteins, ferritin and hemosiderin. In normal tissues, ferritin contains about 20% of iron. Stored iron serves as a reservoir of iron, primarily for the production of hemoglobin. Ferritin is a high molecular weight (450kDa) protein produced intracellularly in response to iron. It is a polymer of heavy (H, acidic) and light (L, basic) chains arranged so as to form a hollow sphere or core. The core can accumulate about 4500 atoms of iron. Iron is stored in the Fe 3+ state as ferrihydrite, [FeO(OH)] 8[FeO(H2PO4)]. Cells release ferritin into the systemic circulation in a glycosylated, iron-depleted form. The circulating ferritin is directly proportional to cellular ferritin content and ranges between 12–200 ng/ml. Quantitatively it has been established that 1 ng/ml serum ferritin is equivalent to 10 mg storage iron and therefore serum ferritin is used as a measure of iron stores [7, 10]. The second iron-storage protein, hemosiderin is formed mainly in the spleen, marrow and the Kupffer cells of the liver and is found only in abnormal conditions such as repeated transfusions or iron overload. Hemosiderin may contain up to 35% iron by weight and is believed to be a partially denatured form of ferritin. Hemosiderin iron is available for heme synthesis but is mobilized at a rate slower than that of ferritin.

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!.9

Transport compartment

The transport compartment represents the smallest pool of iron (<1%). Iron is transported in blood mainly bound to transferrin, the transport protein. Transferrin is a glycoprotein and each molecule can bind two ferric ions very tightly (affinity 1023 M-1 at pH 7.4) but reversibly. Although iron bound to transferrin is less than 0.1% (34 mg) of the total body iron, dynamically it is the most important iron pool, with the highest rate of turnover at 25 mg per 24 h.

!.10 Recycling of iron in the body Iron is derived from two major sources, viz. diet and destruction of RBC hemoglobin. As mentioned earlier, most of the iron in the body is located in the hemoglobin. When red blood cells reach a certain age (120 days, ageing RBCs), they are engulfed by macrophages in the spleen and bone marrow. In these cells, the internalized iron-containing hemoglobin is degraded; iron released and transferred onto circulating transferrin molecules in the blood. Most of the iron used for hemoglobin production comes from such iron recycling and is utilized for the synthesis of new RBCs in the bone marrow. Thus, iron is effectively recycled continuously for hemoglobin formation. It is because of this recycling phenomenon that it takes longer for iron deficiency anemia to develop in adult males when dietary iron alone is restricted. Further as presented in Figure 23.3, most of the iron is recycled efficiently within the body, the major factor affecting iron requirement is the amount of iron lost from the body [4, 8].

!.11 Iron losses 23.11.1 Obligatory (basal) iron losses In an adult, basal iron loss from the gastrointestinal tract, skin and urinary tract is about 1 mg/day or 14 μg/kg/day. This is also the quantity of iron lost by an adult male. In women of child bearing age, the losses due to menstruation are about 16 μg/kg/day (15 mg totally or 0.5–0.6 mg/d). This must be added to the basal iron losses for estimating loss / day. The iron loss for normal menstruating women is therefore 30 mg/kg/day or about 1.5 mg iron daily for a 50 kg woman.

23.11.2 Iron loss during pregnancy and lactation Although pregnancy is associated with a temporary cessation of menstruation, the overall cost to the mother in terms of iron balance is greater than in the non-pregnant stage. Total iron requirements include

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23.3 Recycling and utilization of iron in man [1].

those necessary to replace basal losses, to allow for expansion of the maternal red cell mass and to provide for the needs of the growing fetus and placenta. The obligatory iron loss, in terms of actual quantity of iron used, calculated throughout pregnancy in a well-nourished woman of 55 kg, is approximately 230 mg. Increase in red cell mass requires about 450 mg of iron. The fetus at term contains 270–300 mg and the products of conception account for a further 50–90 mg. Thus, the total cost of pregnancy just about exceeds 1000 mg or approximately 20 mg/kg body weight. Therefore, pregnancy and parturition result in severe depletion of stored iron, necessitating mandatory iron supplementation [8, 10].

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!.1

Dietary iron bioavailability

Bioavailability of dietary iron is defined as the proportion of iron that is actually available for absorption and utilization by the body. In the case of iron alone, absorption is synonymous with bioavailability, as there is no regulated excretion of iron. Variations in food iron bioavailability are determined by the dietary source of iron rather than the absolute amount of iron ingested. While the absorption of heme iron is unaffected by dietary promoters and inhibitors, non-heme iron is subjected to the interplay of dietary factors as shown in Fig. 23.4 [11].

23.4 Gastrointestinal digestion of dietary non-heme iron.

It is very well known that the food matrix can influence the solubility of iron in the gastric milieu before it reaches the absorptive surface of the intestinal mucosa. The majority of dietary non-heme iron enters the GI tract in the ferric form, which is soluble in the gastric milieu (pH 1–2) and reduced to the ferrous form. There are numerous dietary components that can render ferric iron to exist in its insoluble form (phytates, tannic acid, fiber) or to reduce it (ascorbic acid, organic acids) to the soluble ferrous form.

23.12.1 Promoters of non-heme iron absorption The most powerful promoter of non-heme iron absorption is ascorbic acid. In the acid environment of the stomach, ascorbic acid forms a chelate with ferric salts which remains soluble even at alkaline pH of the duodenum. It also converts ferric iron to the ferrous state, which maintains its solubility in the alkaline environment of the upper gut. Meat has a two-pronged beneficial effect on iron nutrition. Not only is it an excellent source of bioavailable heme iron but it also promotes absorption of non-heme iron. The mechanism whereby meat facilitates

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non-heme iron absorption is not clear but may be related to the release of the amino acid cysteine and cysteine containing peptides during digestion.

23.12.2 Inhibitors of non-heme iron absorption A number of factors have been identified, which limit non-heme iron absorption. These include polyphenols, phytates, the dietary fiber complex, calcium and phosphorus, and the dietary protein complex. High molecular weight polyphenols (tannins) present in beverages such as tea and the polyphenol content of individual vegetables are major inhibitors of food-iron absorption. Phytate is present in many cereals, nuts and legumes to about 1–2% by weight. A number of plant foods which have high complex-protein content, including soya beans, significantly inhibit iron absorption.

23.13 Other factors influencing iron absorption The most important known stimuli to iron absorption are the rate of erythropoiesis and tissue iron stores. Accelerated red blood cell production, as in the case of bleeding, hemolysis or hypoxia, results in enhanced iron absorption. Conversely, diminished erythropoiesis due to starvation, blood transfusion or return to sea level from high altitudes decreases the absorption of iron. It has been postulated that an erythrocyte stimulating factor acts as a messenger to the gut to increase iron absorption. However, enhanced iron absorption continues in iron-deficient subjects long after the hemoglobin mass is restored to normal levels and persists until the body stores become normally replete with iron. Inflammation and inflammatory stimuli also determine iron absorption with iron absorption decreasing during inflammatory conditions. It has also been postulated that quantity of gastric acid secreted may play a significant role in iron absorption as patients with decreased gastric acid output have sub-optimal iron status [12, 13].

23.14 Recommended daily allowance (RDA) The RDA for iron has been determined using the factorial approach. Obligatory losses of 1 mg for men and 1.5 mg for women, requirement for growth in children and losses during pregnancy are taken into account for calculating the requirement (Table 23.1). The above losses have to be made up by absorption of an amount equal to the loss. The percent of iron absorbed from typical meals was estimated from studies carried out during the 1980s to be 3% for men, children and adolescent boys; 5% for adolescent girls and non-pregnant women; and 8% for pregnant

618 Public health nutrition in developing countries women [14]. These absorption figures have been employed by the expert group of Indian Council of Medical Research (ICMR) in 1989 to calculate iron RDA for Indians. Based on a more recent iron absorption values, the RDA for India has been recently revised [10].

23.15 Iron homeostasis At the systemic level, iron homeostasis is maintained by three key organs: the intestine, the liver and the macrophages of the reticuloendothelial system (RES). The absorptive epithelial cells of the intestine (enterocytes) are responsible for absorption, the hepatocytes sense iron requirements and store excess iron, and the macrophages efficiently recycle hemoglobin iron from senescent RBC. In the absence of regulated iron excretion, homeostatic control occurs by limiting iron absorption to requisite levels at the intestine. The rate of absorption appears to respond to a variety of interdependent factors such as total iron stores, the extent to which the Table 23.1 Iron requirement during various physiological stages Group Adult

Infants Children Adolescents 10-12 years 13-15 years 16-18 years

Body weight (kg)

Iron requirement μg/kg Total daily mg/day

Man Woman Pregnant woman Lactating woman 0-6 months 1-3 years 4.6 years 7-9 years Boys

60 50 50 50 4.5 12.2 19.0 26.9 35.4

14 30 60 30 70 29 29 29 29

0.840 1.500 3.000 1.500 0.315 0.354 0.551 0.780 1.027

Girls Boys Girls Boys Girls

31.5 47.8 46.7 57.1 49.1

30 26 30 26 30

0.945 1.243 1.401 1.485 1.497

Source: Nutrient Requirements and Recommended Dietary Allowances for Indian, A report of the Expert Group of the Indian Council of Medical Research, National Institute of Nutrition, Hyderabad 1990.

marrow is producing new red blood cells (erythropoiesis), the concentration of hemoglobin in the blood, oxygen content of the blood and inflammatory status of the individual. Iron absorption increases during hypoxia or enhanced “erythropoietic need” and in the presence of decreased stores; but decreases during chronic inflammation or in the presence of sufficient stores [4]. Therefore, the quantity of iron absorbed is determined by the net result of the above-mentioned stimuli. The molecular aspects of systemic iron homeostasis are discussed below.

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Mechanism of intestinal absorption of iron at the enterocyte

23.16.1 Heme iron absorption Most of the heme iron seems to enter the intestinal absorptive cell (enterocyte) as intact metalloporphyrin. Recent research suggests that a heme carrier protein (HCP), present on the apical surface of the enterocyte facilitates the uptake of the intact heme molecule. Subsequently iron is released from the porphyrin ring by the enzyme heme oxygenase, which then enters the circulation as transferrin-bound iron.

23.16.2 Non-heme iron absorption Non-heme iron absorption occurs throughout the small intestine but mainly in the duodenum (proximal small intestine). The enterocytes are known to adapt to the current body requirements of iron, which in turn are the resultant of all the above-mentioned interdependent stimuli. Although the exact mechanisms regulating iron transport across the intestinal mucosa are still being worked out, many factors affecting iron absorption have been studied. Unlike heme iron, only a small percentage of total non-heme iron from digested food or supplements is absorbed. To be absorbed, dietary iron must be in the ferrous (Fe2+) form. A ferric reductase enzyme on the enterocyte brush border, duodenal cytochrome-b (Dcytb), reduces dietary soluble iron from Fe3+ to Fe2+. A protein called divalent metal transporter-1(DMT-1), which transports a spectrum of divalent metal ions into the body, then transports the iron across the enterocyte apical membrane into the cell (Fig. 23.5) [4, 9].

23.5 Proposed mechanism of intestinal absorption of iron.

620 Public health nutrition in developing countries The enterocyte then transports acquired iron into circulation via the serosa through a protein called ferroportin-1 (FPN-1) located on the basolateral membrane. FPN-1 can transport only ferrous iron and not ferric iron, but transferrin can take up only ferric iron (Fig 23.6). This necessitates a ferroxidase. The exact mechanism by which iron in the cytosol of enterocytes is transferred to the blood is unknown and it is thought that circulating ceruloplasmin may be the ferroxidase. Recently, a basolateral membrane-associated ferroxidase, hephaestin protein, has been identified, which may also facilitate this process. Iron not transported to circulation is stored in the cell as ferritin, in which case the iron will leave the body when the cell exfoliates and is sloughed off into feces.

23.6 Interplay of key proteins in iron homeostasis [9].

The body regulates iron levels by regulating each of these steps, viz. apical uptake and transfer to circulation. Hepcidin or LEAP-1 (liver expressed antimicrobial peptide), is a relatively recently discovered peptide produced by the liver (hepatocytes), that appears to be the master regulator of iron homeostasis in humans and other mammals. Independently, the antimicrobial properties associated with the same peptide were discovered, and hence named “hepcidin” (produced in liver “hep-“, “-cidin” for “killing”). Now also called the iron hormone, this 25 amino acid residue peptide has been shown to regulate absorption of iron. The first evidence for the role of hepcidin in anemia and iron metabolism came from studies in patients with liver tumors who had severe anemia which did not respond to iron supplementation. The tumor tissue appeared to be overproducing hepcidin, and contained large quantities of hepcidin mRNA. Removing the tumors surgically cured the anemia. Taken together, these discoveries

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suggested that hepcidin regulated the release of iron in the body. The current scientific evidence suggests that hepcidin is a central regulatory hormone and its main action is to regulate systemic iron homeostasis. Circulating hepcidin levels vary with iron status, hypoxia, and inflammatory stimuli such as IL-6 (cytokine) levels. While Dcytb and DMT1 are unique to iron transport across the duodenum, FPN-1, which is the basolateral iron export protein, is present on all cells which store iron, viz. enterocytes, hepatocytes and macrophages. More recent discoveries have shown that hepcidin directly binds with FPN-1, causing it to be internalized into the cell. The internalized protein is subsequently degraded thus preventing iron transport into systemic circulation (Fig. 23.5). Regulation of FPN-1 activity is the main pathway of regulating the amount of iron in circulation [9, 15, 16].

23.17 Mechanism of iron uptake in cells other than enterocytes Each transferrin molecule has the ability to carry two iron ions in the Fe 3+ form. All cells need iron and obtain the same from diferric transferrin circulating in blood. As iron is tightly bound to transferrin, cells throughout the body have receptors for transferrin-iron complexes on their surfaces called transferrin receptor (TfR). These receptors bind diferric transferrin, the complex is engulfed (endocytosis) into vesicles called lysosomes. The lysosome is acidic (pH~4), causing transferrin to release its iron ions. The released iron is transported out of the lysosome and can be utilized in the functional compartment or be stored as ferritin. The receptor is then transported through the endocytic cycle back to the cell surface, ready for another round of iron uptake [3].

23.18 Molecular regulation of cellular iron Cells have advanced mechanisms for sensing their own need for iron (Figure 23.7). In human cells, the best characterized iron-sensing mechanism involves translational regulation of mRNA. The mRNA sequence (also called transcript) of proteins involved in cellular iron metabolism such as transferrin receptor, ferritin contain a special sequence called the Iron Responsive Element (IRE). The IRE is actually a short self-complimentary sequence of about 5–7 nucleotides. This sequence enables the mRNA to acquire a looplike structure at that point, called a ‘stem-loop’ structure. Certain proteins called IRE-binding proteins (IRE-BPs) bind specifically to these stem-loop structures to regulate the translation of the proteins in iron metabolism. The ends of any mRNA transcript are designated as the 5’ and 3’ end. The 5’ end is the beginning of the transcript while the 3’end is the end of the transcript. The IRE structures can be present either in the 5’ or 3’ end.

622 Public health nutrition in developing countries

23.7 Molecular regulation of iron metabolism. The synthesis of either ferritin or transferrin receptor depends on the iron status of the cell.

The type of translational regulation of the proteins depends on whether the IRE is present on the 5’ or 3’ end [17]. To understand the mechanism of such translational control, consider the following example. The ferritin mRNA has an IRE in the 5’ end while the transferrin receptor mRNA has the IRE in the 3’ end. The IRE–BPs can sense the level of iron in the cell. If the cells are iron depleted, the IRE–BPs bind to the IRE; but cannot bind to IRE if the cells are iron replete. Therefore, when the cells are depleted of iron, the IRE–BP binds to the 5’ end of the ferritin transcript. This binding prevents the translation of the protein and prevents iron incorporation into ferritin, making iron available for cellular functions. However, when the IRE–BP binds to the 3’ IRE of the transferrin receptor transcript, it actually prevents the transcript from being degraded. These results in increased protein synthesis for a longer time, enabling the cell to acquire more iron to fulfill its needs as there are more number of TfR molecules on the surface of the cell. Essentially, the reverse occurs when the cells are iron replete. IRE–BP cannot bind IRE under iron-replete conditions. Without IRE–BP binding, the ferritin mRNA is translated and the excess iron is incorporated into the newly synthesized ferritin. In the absence of IRE–BP binding, the TfR transcript is degraded and no more TfR is synthesized. Thus the cells cannot acquire anymore iron as there are less number of TfR molecules on the cell surface [17]. This phenomenon is called reciprocal regulation and is vital to maintain cellular concentrations of iron (Fig. 23.6). Cellular iron is tightly regulated as excess iron is toxic, capable of free-radical generation through Fenton chemistry. Central to this reciprocal regulation is the fact that the IRE–BPs can

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sense cellular iron status. The mechanism by which they sense cellular iron is as follows. Recall that aconitase is an enzyme that assembles a 4[Fe-S] cluster and one iron atom is called a labile iron. When the cell is iron-deplete, aconitase loses the labile iron atom and subsequently loses the cluster too. Upon such cluster disassembly, the aconitase is converted to IRE–BP and is capable of binding to IRE. When the cells are iron replete, the iron–sulfur cluster is reassembled, cannot bind to IRE and the protein functions as aconitase. Thus the IRE–BP sense cellular iron levels and co-ordinate cellular iron acquisition and storage. This mechanism of reciprocal regulation is operational in all cells in the body. We now consider the same in enterocytes and macrophages. Enterocytes acquire iron only through DMT-1 and the DMT-1 transcript has a 3’ IRE, similar to that of TfR. Ferroportin on the other hand has a 5’ IRE, thus enabling efflux of excess iron from enterocytes and macrophages. The significance of this exquisite molecular control of cellular iron is evident when considered in the light of systemic iron homeostasis. Hepatocytes sense body iron concentrations through the transferrin-TfR system and produce ferritin in response to excess iron. Depending on various stimuli such as iron status, erythropoietic need, inflammatory status and Hb, hepatocytes synthesize and secrete hepcidin. Hepcidin in turn controls iron transfer from enterocytes and macrophages, thus controlling systemic iron homeostasis [3, 15, 16].

23.19 Assessment of iron status Nutritional iron deficiency is commonly regarded as a state of insufficient iron supply to meet the need for functional iron after iron stores have been depleted. At the cellular level, iron deficiency can also result from insufficient release of storage iron despite sufficient iron stores, e.g. anemia of chronic disease. Physiologically, in iron deficiency there is a reduction in all iron-dependent functions, most importantly, the reduction in oxygen carrying capacity of hemoglobin and myoglobin resulting in lowered physical work capacity. Therefore, it is very important to understand the sequence of events leading to frank iron deficiency anemia. Various iron biomarkers are currently in use to define iron status [18–22].

23.20 Stages in the development of iron deficiency and iron status parameters Three overlapping stages in the development of iron deficiency are defined, each of which is associated with certain abnormalities in the indicators of iron status (Table 23.2). The first stage, referred to as

624 Public health nutrition in developing countries deficient iron stores, iron reserves are depleted although there is sufficient iron for erythropoiesis. This stage is recognized either by the absence of stainable iron on bone marrow examination or by a serum ferritin level below 12 μg/L. Serum ferritin is particularly valuable in nutritional surveys because of its high specificity. Quantitative phlebotomy studies have demonstrated that in normal adults, 1 μg/L serum ferritin is roughly equivalent to 10mg stored iron [18]. Expressed on a body weight basis, for a 50 kg adult, this is equivalent to 2.4 mg/ kg body weight. In the second stage of iron deficiency, referred to as iron deficient erythropoiesis, there is a curtailment in iron supply for erythropoiesis. As serum iron decreases and total iron binding capacity increases with iron deficiency, the most useful index is transferrin saturation, which is the ratio of serum iron to total iron binding capacity. Although transferrin saturation has been employed extensively in prevalence surveys, there are several limitations like susceptibility to iron contamination, diurnal variation and variations due to inflammation. Table 23.2 Diagnostic criteria for iron deficiency* Stages/ Parameter

Iron overload

Normal

Iron Iron deficient Iron deficiency depletion Erythropoiesis anemia

RE marrow Fe Serum ferritin (μg/L)

4+ >300

2-3+ 100 ± 60

0-1+ 20

0 10

0 <10

Transferrin Saturation (%)

>60

35 ± 15

30

<15

<15

RBC protoporphyrin 30 (μg/dL)

30

30

100

200

TIBC (μg/dL) Serum iron (μg/dL) Serum transferrin Receptor (mg/dL)

<300 >175 Less than normal

300 ± 30 360 390 115 ± 50 115 <60 5.36± 0.82 More than normal 13.9±4.6

410 <40

Erythrocyte Morphology

Normal

Normal

Normal

Normal

Microcytic/ hypochromic

Hematocrit cut-off value 0.35 (female) 0.40 (male)

Above cut-off

Above cut-off

Above cut-off

Above cut-off

Below cut-off

Hemoglobin (g/L) cut-off value 120 (female) 130 (male)

Above cut-off

Above cut-off

Above cut-off

Above cut-off

Below cut-off

*A report of the INACG 1985, Nair et al 2004

Higher than iron deficient erythropoiesis

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Another laboratory measurement that can be used to detect iron deficient erythropoiesis is erythrocyte protoporphyrin. In contrast to the transferrin saturation, the erythrocyte protoporphyrin is a more stable index of marrow iron supply because elevation occurs only after several weeks of iron deprivation and the return to normal level is similarly slow following the start of iron therapy. One disadvantage of erythrocyte protoporphyrin, particularly in children, is that the level increases with lead poisoning. Serum transferrin receptor (sTfR) is released from the cells into blood depending on the iron requirements after the stores have been exhausted. The concentration of sTfR is therefore increased in the second stage of iron deficiency. It is however less sensitive indicator than ferritin but more sensitive than Hb [22]. The third and final stage is iron deficiency anemia. This stage is characterized by a reduction in circulating hemoglobin high enough to be recognized as anemia. A decline in circulating hemoglobin equivalent to several hundred milligrams of iron is usually required before anemia can be identified clinically. The optimal measurement or combination of measurements to detect iron deficiency anemia in a given situation depends on several factors. WHO/CDC have recommended that a combination of hemoglobin, serum ferritin, sTfR and indicator of infection such as c–reactive protein (CRP), be used as the best indicators to measure iron status [20].

23.21 Iron toxicity A peculiar aspect of iron metabolism is the lack of a specific mechanism to eliminate excess iron. Excess iron, especially free iron, is toxic as it participates in free radical generation and the possible harmful consequences at the cellular level, have also been reported in numerous studies. It has been suggested that it is the difference in levels of stored excess iron that accounts for the gender difference observed in the mortality statistics of ischemic heart disease in developed countries. An epidemiologic study carried out in Finnish men showed a 2.2-fold increased incidence of acute myocardial infarction during the 3-year follow-up in men whose serum ferritin levels were high (>200 μg/L) at the beginning of the study. The authors hypothesized that free radicals induced by free iron caused increased peroxidation of low density lipoprotein and thereby contributed to atherogenesis. It was also observed in experimental studies that men who had higher levels of transferrin saturation had a greater incidence of cancer mortality. However, this type of relation was not observed in females [23].

626 Public health nutrition in developing countries Iron deficiency is also equally potent in promoting carcinogenesis in animal models. The iron deficient intestine is also susceptible to ironmediated oxidative damage. Iron could also enhance oxidative stress by interfering with antioxidant system components of the intestine during repletion with high doses of iron. However, when preconditioned with a combination of antioxidant vitamins C and E or simultaneous administration of zinc, almost all the intestinal oxidative stress is reduced. Therefore, daily administration of therapeutic doses of iron should be accompanied by foods rich in these vitamins or minerals [24, 26].

23.22 Folic acid Folic acid is chemically, pteroyl glutamate, consisting of a pteridine ring attached to p-aminobenzoic acid and glutamic acid. Mammals cannot synthesize p-aminobenzoic acid or attach glutamic acid to aminobenzoic acid and therefore depend on folic acid derived from microbial and plant sources.

23.23 Chemistry Folate is the generic term for compounds that have vitamin activity similar to that of pteroylglutamic acid, are anti-anemic and growth factors. Folates may have one or more glutamic acid residues (polyglutamates, PteGlun) and exist in many chemical forms. Naturally occurring folates, called food folate and referred to as PteGlu n, are present both in animal and plant foods. The naturally occurring forms, namely dihydrofolates (H2) and tetrahydrofolates (H 4) are reduced forms of folate. Tetrahydrofolate is the biologically active molecule and can carry various one-carbon units, which include 5-formyltetrahydrofolate, 10-formyl-tetrahydrofolate, 5-methyl-tetrahydrofolate, 5.10-methenyltetrahydrofolate, 5.10-methylene-tetrahydrofolate (MTHF) and formimino-tetrahydrofolate (Figure 23.8). Normally, only trace amounts are found in human tissues. Intracellular folates generally are PteGlu 7

23.8 Structure of tetrahydrofolate and conversion of one carbon units attached.

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or PteGlu 11. In contrast, extracellular folates are monoglutamates. The basic folate compound, PteGlu 1, is used therapeutically because of its stability [5, 6, 27].

23.24 Dietary sources and recommended intake Organ meats such as liver and egg yolk are good sources of folate and in the vegetarian context the major sources are whole grain cereals, legumes and green leafy vegetables. The recommended dietary allowance (RDA) of folic acid as folate equivalent for Indian adults is 200 μg/day. The intake of folate based on NNMB diet survey shows more than 60% of Indians obtain folate nutrition from cereals and pulses (Figure 23.9) [28].

23.9 Folic acid distribution from different Indian food stuffs ( g/CU) [19].

23.25 Availability of food folate All naturally occurring folates are unstable to varying degrees, due to the presence of an endogenous enzyme, pteroylpolyglutamyl hydrolase, which removes glutamic acid residues but leaves an active compound, PteGlu1. Heat, oxidation and ultraviolet light cleave the folate molecule, rendering it inactive. Reducing agents in food such as ascorbic acid provide greater stability to the vitamin. Germination, however, increases food folate availability. Information on the availability of food folate is fragmentary. Folate availability generally varies widely among foods with maximum availability found in egg yolk (72.2%) followed by cow’s liver (55.7%) and low availability from vegetables (3–6%). The absorption of folate from foods varies from 25% to 70%. Synthetic folic acid is considered to be more bioavailable than natural folate. The bioavailability of folic acid supplements under fasting conditions is close to 100% [28–30]. Currently, there are many accurate methods of estimating the food folate level and their bioavailability. Folate content is expressed in terms of dietary

628 Public health nutrition in developing countries folate equivalent (DFE) and is the amount derived after complete hydrolysis of food folate [31]. The term “free” folate has been used to designate the forms measurable by its ability to support the growth of a folate-dependent organism, Lactobacillus casei, without hydrolysis [14].

23.26 Food folate – digestion and absorption Dietary folates, most of which are PteGlun derivatives, undergo hydrolysis in the gut to PteGlu1 before absorption across the intestinal mucosa. An intestinal enzyme known as folate conjugase (glutamate carboxypeptidase) found in the brush border, catalyses this rate limiting step in the process of luminal digestion of PteGlun. This enzyme is an exopeptidase and is activated by zinc. A second enzyme, an intracellular hydrolase, is found in the lysosomes of intestinal cells, has a pH optimum of 4.5 and is an endopeptidase. The function of this enzyme is still unknown. Reduced PteGlu1 are better absorbed (88–98 percent) than PteGlu(n) as the former are less acidic comparatively. In the absence of protecting agents such as ascorbic acid and reduced thiols, many labile folates may be lost during residence in the acid peptic milieu of the stomach. Other food constituents also affect action of the intestinal hydrolases. The intestinal absorption of folate, as PteGlu1, predominantly occurs in the duodenum and jejunum by active transport in a saturable, pH-dependent process. Monoglutamates are present in portal circulation, which is taken by the liver and converted to polyglutamate derivatives and stored or released into the blood. In plasma, methyltetrahydrofolate (MTHF) is bound to albumin, but about 1/3rd circulates unbound. Cellular transport of folate is mediated through a number of different folate transport systems. Most of them use the folate receptor or the folate carrier protein. Intracellular transport into organelles is only poorly understood, although it is known to be saturable [28–30].

23.27 Functions Many vital steps in nucleic acid metabolism involve the addition of one carbon building blocks. Folate acts as a co-enzyme in several single carbon transfers in the biosynthesis of purine and pyrimidine nucleotides. These one carbon units are derived from the breakdown of serine and glycine and carried by the coenzyme tetrahydrofolate in different chemical forms. Each of these forms participates in different biochemical reactions. 10-formyl THF and 5,10-methylene THF donate the C2 and C8 carbons of purines, respectively. 5,10-methylene THF is also the cofactor for thymidylate synthase which methylates the uracil base (UMP, uracil monophosphate) of RNA to thymidine (dTMP, thymidine monophosphate)

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of DNA (Figure 23.9). It is for this reason that rapidly growing and multiplying cells require an adequate supply of folate. Folate deficiency therefore diminishes and compromises the cell’s ability to synthesize these nucleic acids, resulting in decreased cell division. This effect is most pronounced in the rapidly dividing cells of the bone marrow which are RBC precursors, thus causing megaloblastic anemia [33]. The one carbon fragments can be oxidized and reduced while bound to the coenzyme and inserted into the receiving molecules as formyl groups (most oxidized), hydroxymethyl or methyl groups (most reduced). The immediate methyl-group donor in most reactions is S-adenosyl methionine and S-adenosyl homocysteine is the end product. This homocysteine (Hcy) is converted back to methionine through a series of reactions that requires methyl-THF as the one-carbon donor. Methyl-THF is formed by the reduction of 5,10- methylene-THF and is an irreversible process (Figure 23.8). The enzyme that catalyzes the conversion of homocysteine to methionine (methylation of Hcy) is methionine synthase. This enzyme requires B12 as a cofactor and B12 deficiency drastically reduces the activity of this enzyme. During this reaction, tetrahydrofolate, the biologically active form of folate, is regenerated from N5-methyl-tetrahydrofolate. In the absence of this reaction, all the tetrahydrofolate will eventually end up trapped as N5-methyl-tetrahydrofolate, as N5-methyl-THF has no other biological fate. Thus a primary vitamin B 12 deficiency leads to a secondary folate deficiency. This phenomenon is called the folate trap [5, 6, 8, 33].

23.28 Folic acid and anemia Folic acid deficiency reduces the capacity of proliferating cells to make dTMP thus inhibiting cell division. This effect is most pronounced in the rapidly dividing erythroid precursor cells in the bone marrow leading to cells being larger than normal. Macrocytosis (increased size) of RBCs ensues resulting in increased MCV (mean corpuscular volume) and progresses to decrease in Hb and PCV (packed cell volume). Generally, no change in MCHC (mean corpuscular Hb concentration; Hb/PCV) is observed as both Hb and PCV decrease. This condition is called megaloblastic anaemia. Where iron deficiency is the central problem, the restoration of adequate iron nutriture rapidly replenishes normal red cell mass. As the requirements for synthesis of a new deoxynucleic acid base for rapid cell proliferation place additional demands for folic acid, iron supplements have conventionally been combined with an adjunctive dosage of folic acid [12, 31–32]. Pernicious anaemia, due to primary deficiency of vitamin B12, leads to secondary deficiency of folic acid because all the folate ends up trapped as N5-methyl-tetrahydrofolate (folate trap, explained above).

630 Public health nutrition in developing countries During pregnancy, given the increase in blood volume and growth of the foetus, both of which require rapid cell division, folate deficiency has serious consequences. During early pregnancy folic acid is required for the closure of the neural tube which occurs around the 28th day of pregnancy. Incidence of neural tube defects (spina bifida and anencephaly) is reduced by 400 μg folic acid supplement/day before conception and during the first month of pregnancy [10, 31, 34].

23.29 Assessment of folate status Biochemical assessment of folate nutritional status is most commonly done by measuring serum and RBC folate levels. Serum folate essentially reflects recent intake and red cell levels represent long-term tissue stores. It is generally accepted that serum folate above 14 nmol/L (6 ng/mL) or RBC folate above 360 nmol/L (159 ng/mL) are considered satisfactory; those between 7 and 14 nmol/L (3–6 ng/mL) serum folate and 320–360 nmol/L (141–159 ng/mL) RBC folate are considered to be low and suggestive of risk. Values lower than these indicate clear deficiency of folate. Normal body stores are estimated as 5–10 mg, half of which is in the liver. The turnover rate is estimated to be less than 1% per day [36]. The measurement of plasma concentrations of homocysteine is shown to be a good indicator of folate status. A striking negative correlation between serum folate and protein bound homocysteine is reported [35].

23.30 Vitamin B12 Vitamin B12 (Cobalamin) has been a challenging problem in biochemistry and medicine since the discovery by George Minot and William Murphy in 1926 that pernicious anemia can be treated by feeding the patient large amounts of liver. Cobalamin was first purified in 1948 and crystallized by Dorothy Hodgkin, who elucidated its complex three-dimensional structure in 1956 [5].

23.31 Chemistry The core of cobalamin or vitamin B12 consists of a corrin ring with a central cobalt atom (Figure 23.10). The corrin ring has four pyrrole rings and is similar to the porphyrin ring. The cobalt atom is bonded to the four pyrrole nitrogen atoms. The fifth substituent is a derivative of dimethylbenzimidazole that contains ribose 3-phosphate and aminoisopropanol. One of the nitrogen atoms of dimethylbenzimidazole is linked to cobalt. The sixth substituent of Co atom can be –CH3, OH– or 5’ deoxyadenosyl unit. The cobalt ion can be in the +1, +2 or +3 oxidation states. In the +1 oxidation state, it forms the coenzyme B12 molecule which is the only biological compound known to have a carbon-metal bond [5].

Metabolism of iron, folic acid and vitamin B12

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23.10 Structure of vitamin B 12 .

23.32 Dietary sources and recommended intake All higher animals require the vitamin in their diet and cereals, vegetables and fruits do not contain measurable amounts of the vitamin unless “contaminated” by soil or water containing vitamin B 12. In nature, vitamin B 12 is largely produced by bacteria, fungi and algae. Animals get it from their natural gut bacterial flora or by eating other animals. Therefore, foods of animal origin (including meat, liver, fish, milk, milk products and eggs) constitute the main dietary source for humans. Vegetarians are at risk of B 12 deficiency unless they consume large quantities of fermented foods. The recommended dietary intake is 1.0 μg/day [10, 31, 35, 37].

23.33 Absorption and transport Much of the vitamin B 12 in food is present in bound form and must be released by cooking or acid-peptic and/or tryptic digestion before it is available for absorption. The free vitamin then binds with salivary haptocorrin. Intrinsic factor (IF), a mucoprotein like substance present in

632 Public health nutrition in developing countries gastric juices is essential for the utilization of vitamin B12. The haptocorrinB12 complex is digested by proteases and the released vitamin B12 combines with the intrinsic factor. The intrinsic factor-vitamin B12 complex attaches to receptors in the ileal enterocyte is internalized and subsequently dissociated. The released vitamin B12 binds to a specific B12 binding protein called transcobolamin (TC II) and is actively transported across the ileal basolateral membrane into the bloodstream [35]. When a physiological dose of radioactive cyanocobalamin is given orally, normal people absorb a mean 72% of 0.5 μ dose or 56 percent of a 1 μg dose. Since the absolute amount absorbed depends on the amount of intrinsic factor and the number of receptors available, the percent absorbed decreases as the amount of the vitamin administered increases within the physiological range.

23.34 Bioavailability of dietary vitamin B12 There is relatively little information on the bioavailability of different dietary forms of vitamin B12. In normal subjects, the vitamin in liver, mutton and chicken appears to be absorbed as completely as a similar amount of cyanocobalamin administered in aqueous solution. On the other hand, vitamin B12 in eggs or crystalline vitamin B12 added to eggs is relatively poorly absorbed. The nature of the inhibitory factor(s) in eggs is not known. There is some evidence that the vitamin B12 in food may not be as readily available to individuals with decreased gastric acid secretion (without pernicious anemia) as it is to normal subjects [35].

23.35 Body content Vitamin B12 is stored mainly in the liver in amounts (in omnivorous about 3–5 mg) sufficient to last a couple of years. In humans, the liver contains up to 80 percent of the body’s total store of vitamin B12. At birth, the full-term infant has 25–30 μg of the vitamin which is stored in the liver. As the individual grows, vitamin B 12 is accumulated and in vegetarians the body content is much lower compared to omnivorous adults [10, 31].

23.36 Dietary deficiency of vitamin B12 Dietary deficiency is a widespread problem in the Indian subcontinent due to vegetarian diet. Infants born to vitamin B12 deficient vegan mothers are at high risk of developing the deficiency [37].

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!.!7 Malabsorption of vitamin B 1 Pernicious anemia (PA) is a specific autoimmune disease occurring with increasing age or when antibodies are formed in either the parietal cells or to gastric intrinsic factor or both.

!.!8 Biochemical function Vitamin B12 is required for the recycling of a critical nucleotide base (deoxythymidine) essential for the rapid synthesis of DNA during cell replication. Hence it is indispensable for the proliferation of all of the hematological cell lines in bone marrow, especially the precursors of the myeloid lineage. The absence of vitamin B12 allows these cells to enlarge, but not divide into generations of daughter cells, leading to hypo-proliferative anemia with giant, immature, macrocytic red cells in the circulation. Vitamin B12 is a cofactor for three enzymes, viz. methylmalonyl CoA mutase, leucine aminomutase and methionine synthase. Methylmalonyl CoA is an intermediate in valine catabolism and is produced upon carboxylation of propionyl CoA during the catabolism of isoleucine and cholesterol. Methylmalonyl CoA undergoes a rearrangement to succinyl CoA so as to enter the normal metabolic pathways. This rearrangement is catalyzed by methylmalonyl CoA mutase whose activity is greatly diminished during B12 deficiency. This leads to an accumulation of methylmalonyl CoA which is reflected as increased serum and urine methylmalonyl CoA [35]. Methionine synthase causally links the biochemical basis of megaloblastic anemia of folate and vitamin B12 deficiencies (Fig. 23.11). As mentioned previously, 5,10-MTHF is a cofactor for the very important enzyme, thymidylate synthase, and is responsible for the conversion of the uracil type base found in RNA to the thymine type base which is characteristic of DNA. The reduced rate of cell division results in nuclei that are larger and more poorly differentiated than normal. Identical megaloblastic anemia occurs in vitamin B12 deficiency. The biochemical basis for this is as follows. Recall the folate trap phenomenon explained earlier. Methionine synthase uses the folate cofactor N5-methyl-tetrahydrofolate (N5-M-THF) as part of the methylation cycle. The enzyme that synthesizes N5-MTHF from N5,10methylene tetrahydrofolate, N5,10- methlyene tetrahydrofolate reductase (MTHFR) is known to be irreversible. Methionine synthase, during methylation of homocysteine, converts N5-MTHF to THF and requires vitamin B12 (Fig. 23.11). The activity of this enzyme is severely compromised in vitamin B12 deficiency, thus leading to all folate accumulating as 5MTHF. This creates a pseudo folate deficiency with similar clinical manifestations. As methionine synthase is inhibited, homocysteine accumulates which is reflected as increased serum homocysteine [5, 6, 8].

634 Public health nutrition in developing countries

23.11 Interrelationship between folic acid and vitamin B 12 .

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Due to the above explained metabolic relationship, a moderately high intake of folic acid is not toxic but might mask an underlying vitamin B12 deficiency that only becomes apparent once the irreversible neurological disorders set in. Folate and vitamins B6 and B 12 are essential components in the metabolism of homocysteine, which occurs through remethylation to methionine or trans-sulfuration to cysteine [6].

23.39 Neurological manifestations Vitamin B12 deficiency leads to demyelination of CNS fibers. Peripheral nerves also show axonal degradation without demyelination. The biochemical basis for this is unknown but is attributed to decreased activity of methionine synthase. The myelin sheath is a continually regenerating tissue which would require a continuous supply of methionine. The fully developed neuropathy of B12 deficiency is called subacute combined degeneration; however, not all B12 deficiency presents with neuropathy. On a similar note, it would be expected that folate deficiency would also lead to neuropathy but it is not so as the nervous system preferentially accumulates folates [38].

23.40 Assessment of vitamin B 12 status Serum vitamin B12 level is a specific test for deficiency. Serum vitamin B 12 should possibly be considered a screening test, with high levels ruling out a vitamin B12 deficiency, levels between 150 and 350 pmol/L (203–473 pg/ mL) requiring confirmation, and levels lower than 150 pmol/L (200 pg/mL) probably not needing confirmation. Serum vitamin B12 levels decline 18– 28 pmol/L (24–38 pg/mL) annually in a normal elderly. There may be a marked increase in MCV (normal = 80–96 fL) to 110–140 fL, with no change in MCHC. Serum methylmalonic acid (MMA) and serum homocysteine are two valuable markers for vitamin B12 deficiency as these are only two biochemical pathways that utilize this vitamin in humans. Homocysteine and a 24-hour urine collection for testing MMA can also be performed. Serum levels for homocysteine and MMA may be more specific, elevated levels of MMA are accurate as an indicator for cobalamin deficiency. Therefore if both homocysteine and MMA levels are elevated and the serum vitamin B 12 is low or borderline, vitamin B12 deficiency exists. If the homocysteine level is the only elevated metabolite and the red blood cell folate level is not low, vitamin B12 deficiency also may be indicated. Since elevated levels of homocysteine may also indicate a folic acid deficiency, red blood cell folate levels should be determined before vitamin B12 replacement is begun. It is important to ensure there is no vitamin B12 deficiency before starting folic acid replacement, as this therapy may worsen the associated neurologic symptoms [32, 37, 39].

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of hemoglobin, serum ferritin and serum transferrin receptor during iron supplementation in pregnancy. Nutrition, 20, pp. 896–899. STEVENS RG , JONES DY , MICOZZI MS , TAYLOR PR (1988). Body iron stores and the risk of cancer. New Engl J. Med, 319, pp. 1047–1052. Joint WHO/CDC technical consultation on assessment of iron status at population level. Geneva, 2004, April 6–8. NAIR KM (2001). Alternate strategies for improving iron nutrition: lessons from recent research. Brit J. Nutr, 85 (Suppl 2), p. S187. SRIGIRIDHAR K and NAIR KM (2000). Supplementation with alpha-tocopherol or a combination of alpha-tocopherol and ascorbic acid protects the gastrointestinal tract of iron deficient rats against iron induced oxidative damage during iron repletion. Brit J Nutr, 84, pp. 165–173. SREEDHAR B , NAIR KM (2007). Concurrent repletion of iron and zinc reduces intestinal oxidative damage in iron-and zinc-deficient rats. World J Gastroentrol, 13(43), pp. 5707–5717. COSSINS EA (1984). Folates in biological materials. In: Folates and Pterins. Blakley R.L, Benkovic, (ed.), New York: John Wiley and Sons Inc., 1, pp. 1–60. KRISHNASWAMY K and NAIR KM (2001). Importance of folate in human nutrition. Brit J. Nutr, 85(2), p. S115. PRINZ - LANGENOHL R , BRÖNSTRUP A , THORAND B , HAGES M , PIETRZIK K (1999). Availability of food folate in humans. J. Nutr, 129, pp. 913–916. GREGORY JF (1997). Bioavailability of folate. Eur J. Clin Nutr, 1997; 51: S54– S59. WHO/FAO. Vitamin and mineral requirements in human nutrition, 2nd Edition, WHO, Geneva, 2004. SELHUB J , MORRIS MS , JACQUES PF and ROSENBERG RH . Folate–vitamin B-12 interaction in relation to cognitive impairment, anemia, and biochemical indicators of vitamin B 12 deficiency. Am J Clin Nutr 89: 702S–706S, 2009. KOURY MJ and PONKA P. New insight into erythropoiesis: Roles of folate, vitamin B12, and iron. Annu. Rev. Nutr. 2004; 24: 105–131. CUSKELLY GJ , MCNUTTY H and SCOTT JM (1996). Effect of increasing dietary folate on red cell folate: implications for prevention of neural tube defects. Lancet, 347, 657–659. BOWMAN BA , RUSSELL RM . (eds.) (2006). Present knowledge in nutrition. International Life Sciences Institute, ILSI Press, Washington, D.C. KANG SS , WONG PWK and NORUSIS M (1987). Homocysteinemia due to folate deficiency. Metabolism, 36, pp. 458–462. STABLER SP and ALLEN RH (2004). Vitamin B 12 deficiency as a world problem. Annu Rev Nutr, 24, pp. 299–326. DAWSON DN and WATERS HM (1994). Malnutrition: folate and cobalamin deficiency. Brit J. Biomed Sci, 51, pp. 221–227. QUINLIVAN EP et al. (2002). Importance of both folic acid and vitamin B 12 in reduction of risk of vascular disease. The Lancet, 359, January 19, 2002, pp. 227–28 (research letter).

24 Iron deficiency and iron deficiency anemia in young children Sheila C. Vir and Prakash V. Kotecha

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India. Prakash V. Kotecha, MD, is country representative with A2Z, the USAID Micronutrient Project. Prior to joining USAID, he was the Professor and the Head of Department of Community Medicine at Medical College Vadodara India for over ten years. Besides MD degree in Community Medicine, he has a diploma in Public Health from M.S. University of Baroda and Masters Degree in Community Health from London School of Hygiene and Tropical Medicine, London University, United Kingdom.

".1

Iron deficiency and iron deficiency anemia in young children

24.1.1 Prevalence of iron deficiency and iron deficiency anemia in young children Deficiency of iron is the most common nutrition disorder in the world [1, 2]. In public health terms, iron deficiency is the primary cause of nutritional anemia worldwide. Folic acid deficiency is less widely spread and is in fact observed often along with iron deficiency. Vitamin B12 deficiency is comparatively uncommon. From the public health point of view, prevalence of anemia is taken as a proxy indicator for iron deficiency. It is estimated that when prevalence of iron deficiency anemia of 40% is reported, the prevalence of iron deficiency will be around 100% (Figure 24.1) and when anemia prevalence is 20% iron deficiency is estimated to exist in 50% of the population [3].

638

Iron deficiency and iron deficiency anemia in young children

639

The prevalence of anemia as a public health problem is categorized as follows: <5% no public health problem, 5.0–19.9% mild public health problem, 20–39.9% moderate public health problem, >40% severe public health problem [3]. Table 24.1 presents an overview of the situation of anemia as a public health problem in WHO member states. In 69 of the 192 countries, anemia is a severe public health problem. Only two countries with a low prevalence of anemia are excluded from the public health problem category [4].

24.1 Prevalence of iron deficiency based on prevalence of iron deficiency anemia [3] Table 24.1 Anaemia as a public health problem (a) in WHO member states [4] Level of public health problem

Pre-SAC (b) Number Total of population countries 1000s (%) (c)

None

2

Mild

40

Moderate 81 Severe

69 192

(a)

(b)

(c)

20570

(3.3) 40921 (6.6) 208472 (33.7) 348322 (56.3) 618285

PW Number Total of population countries 1000s (%) 0 33 91 68 192

0 (0.0) 11156 (8.3) 46162 (34.2) 77466 (57.5) 134783

NPW Number Total of population countries 1000s (%) 1 59 78 54 192

4171 (0.3) 647857 (41.7) 441285 (28.4) 459518 (29.6) 1552831

The prevalence of anemia as a public health problem is categorized as follows: <5%, no public health problem; 5.0–19.9%, mild public health problem; 20–29.9%, moderate public health problem; >40%, severe public health problem. Population groups: pre-SAC, pre-school aged children (0.00–4.99 years); PW, pregnant women (no age range defined); NPW, non-pregnant women (15.00–49.99 years) This is the percentage of pre-school-aged children who live in countries where anemia presents this level of a public health problem.

An analysis of anemia status region wise of WHO member countries, representing 99.8% of global population, reveals that 47.4% preschool

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children or 293.1 million preschool child population are anemic [4]. Table 24.2 presents the region-wise situation of anemia. Asia, with 170 million anemic children, has the largest number of anemic pre-school children. Table 24.2 Anemia in pre-school-aged children, pregnant women and non-pregnant women globally and by region [4] Area

Pre-SAC (a) Prevalence Number (%) (c) affected (millions)

PW Prevalence Number (%) (c) affected (millions)

Global

47.4 293.1 (45.7–49.1) (282.8–303.5)

41.8 (39.9–43.8)

56.4 30.2 (53.8–59.1) (28.7–31.6)

468.4 (446.2–490.6)

55.8 (51.9–59.6) 41.6 (39.0–44.2) 18.7 (12.3–25.1) 31.1 (21.8–40.4) 6.1 (3.4–8.8) 30.4 (17.0–43.9)

19.3 (18.0–20.7) 31.7 (29.7–33.6) 1.4 (0.9–1.8) 3.6 (2.5–4.7) 0.3 (0.2–0.4) 0.2 (0.1–0.2)

82.9 (76.5–89.4) 318.3 (302.0–334.6) 26.6 (18.4–34.9) 33.0 (22.4–43.6) 6.0 (4.6–7.3) 1.5 (0.7–2.4)

UN region (b) Africa

64.6 (61.7–67.5) Asia 47.7 (45.2–50.3) Europe 16.7 (10.5–23.0) LAC 39.5 (36.0–43.0) NA 3.4 (2.0–4.9) Oceania 28.0 (15.8–40.2) (a)

(b)

(c)

93.2 (89.1–97.4) 170.0 (161.0–178.9) 6.1 (3.8–8.4) 22.3 (20.3–24.3) 0.8 (0.4–1.1) 0.7 (0.4–1.0)

NPW Prevalence Number (%) (c) affected (millions)

44.4 (40.9–47.8) 33.0 (31.3–34.7) 15.2 (10.5–19.9) 23.5 (15.9–31.0) 7.6 (5.9–9.4) 20.2 (9.5–30.9)

Population groups: pre-SAC, pre-school-aged children (0.00–4.99 years); PW, pregnant women (no age range defined); NPW, non-pregnant women (15.00–49.99 years) WHO member states are stratified by United Nations regions: Africa, Asia, Europe, Latin America and Caribbean (LAC), North America (NA), and Oceania 95% CI

In terms of percentage of anemia in various regions of the world, Africa has the largest percentage prevalence of anemia in the preschool-age group. In fact the percentage prevalence of anemia is higher in pre-school children as compared to pregnant and non-pregnant women in all the regions except Europe and Oceana. On the basis of data profile of vulnerable groups (Table 24.2), it has been proposed that figures for the prevalence of anemia in infants and for very young children in a region is often very similar to those among pregnant mothers when precise data is not available [5]. These surveys provide information only on anemia but iron deficiency is presumed to be the main cause of anemia. A link between anemia prevalence and stage of country’s development is evident [6, 7] when anemia prevalence rate of developing and developed countries is compared. Pre-school children in developing country are at a much higher disadvantage than in the developed world (Figure 24.2). Within the pre-school-age group, iron deficiency and anemia prevalence in children 6–24 months of age is higher than in over two years. This is attributed

Iron deficiency and iron deficiency anemia in young children

641

Non-preg.

24.2 Comparison of prevalence of anemia in India, developing and developed countries [7].

to rapid growth in this phase of life resulting in much wider gap between requirement for iron and dietary iron consumed. Additionally, complementary food consumed by young children in developing countries has low bioavailability of iron since it is often cereal dominated and has low or nil animal food content. It is observed that the prevalence of IDA in children peaks around 18 months of age and thereafter the prevalence tends to decrease as there is often an increase in iron intake through complementary foods. In France, iron deficiency and iron deficiency anemia affect 29% and 4% children younger than 2 years, while in the USA, only 2% children between 1 and 2 years have iron deficiency anemia [3]. Figure 24.3 indicates that the prevalence of anemia in India is 77–78% for under 2 years and about 71% for >2–5 years [8].

24.3 Age-wise percentage prevalence of anemia in pre-school children of India [8]

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Public health nutrition in developing countries

Box 24.1 The problem of anemia in pre-school children in India. Anemia in preschool children is a major public health problem in India. The figures of anemia reported by the Indian Council of Medical Research (ICMR) and the national survey data show no difference in the last two decades [8,9] An analysis of anemia in children in different period between 1950-2001 indicates that the situation has in fact not changed in the last 30 years [2]. Anemia in young children in India has remained stagnant despite a reduction in IMR and decrease in clinical cases of severe malnutrition as well as vitamin A deficiency (Figure 24.4).

24.4 Anemia (percentage) among children in different period [2, 6, 8] Severity of anemia in preschool children 6–35 months, presented in Figure 24.5 [6, 8], indicates that nearly 8 out of 10 children below three years suffer from varying degrees of anemia and every second child suffers from moderate to severe anemia.

24.5 Anemia (percentage) prevalence in children of age 6–35 months [6, 8] State-wise analysis of prevalence of anemia in India (Figure 24.6) indicates a wide variation with only one state (Goa) is reported to have an anemia prevalence marginally below 40 percent and while three other states have anemia prevalence between 40% and 50% (Manipur, Mizoram, Kerala). Anemia

Iron deficiency and iron deficiency anemia in young children

643

prevalence of over 70% is reported from 8 out of the 28 states and UTs surveyed in 2005–06 [8]. These findings confirm that iron deficiency anemia is a public health problem in each and every state of India. Anemia prevalence

State

>70%

Bihar (78%), Madhya Pradesh (74.1%), Uttar Pradesh (73.9%), Haryana (72.3%), Chhattisgarh (71.2%), Andhra Pradesh (70.8%), Karnataka (70.4%) Jharkhand (70.3%) Manipur (41.1%), Mizoram (44.2%), Kerala (44.5%), Himachal Pradesh (54.7%), Arunachal Pradesh (56.9%), Delhi (57.0%), Jammu & Kashmir (58.6%), Sikkim (9.2%), West Bengal (61.0%), Uttaranchal (61.4%), Tripura (62.9%), Maharashtra (63.4%), Tamil Nadu (64.2%), Meghalaya (64.4%), Orissa (65.0%), Punjab (66.4%), Assam (69.6%), Gujarat (69.7%), Rajasthan (69.7%) Goa (38.2%)

>40 to <70%

<40 %

24.6 State-wise anemia prevalence [8]

24.2

Anemia, iron deficiency and iron deficiency anemia

Anemia is the most common indicator used to screen for iron deficiency. However, it is important to distinguish the terms “anemia”, “iron deficiency”, and “iron deficiency anemia” which are often used interchangeably. (a) Anemia A pathological quantitative lower level of hemoglobin than WHOacceptable level is defined as anemia. Iron deficiency is the most common but not the only cause of anemia. Other nutrition causes of anemia include folic acid and vitamin B 12 deficiency, chronic infections (particularly malaria), hereditary haemoglobinopathies and red cell diseases. Multiple causes coexist in an individual or in a population and contribute to the severity of anemia. (b) Iron deficiency (ID) Iron deficiency is a reduction in body iron to the extent that the cellular storage iron required for metabolic/physiological function is fully exhausted with or without anemia. Iron deficiency is usually the result of inadequate bio-available dietary iron, increased iron requirement during rapid growth and blood loss due to any reason. There are no current estimates of total ID cases but based on anemia as an indicator, it is

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Public health nutrition in developing countries

estimated that most pre-school children in developing counties are iron deficient [10]. (c) Iron deficiency anemia (IDA) IDA is defined as iron deficiency with low hemoglobin or anemia. Anemia is the result of inadequate availability of iron for hemoglobin formation. Some functional consequences may be observed in individuals who have iron deficiency without anemia but cognitive impairment, decreased physical capacity, and reduced immunity are commonly associated with iron deficiency anemia. In severe iron deficiency anemia, the capacity to maintain body temperature may also be reduced. Very severe anemia is life threatening. The World Health Organization defined criterion for anemia [10] is for sea level only and will be higher at high altitude for the physiological increase in hemoglobin. Table 24.3 presents the details of hemoglobin and hematocrit cut-offs used to define anemia in people living at sea level. Anemia severity increases as haemoglobin concentration or hematocrit values decrease below the range for the healthy reference of the same age and sex as set by WHO (Table 24.4). Table 24.3 Haemoglobin and hematocrit cut-offs used to define anemia in people living at sea level [10] Age or sex group

Haemoglobin below (g/dl)

Hematocrit below (%)

Children 6 months to 5 years Children 1–5 years Children 12–13 years Non-pregnant women Pregnant women Men

11.0

33

11.5 12.0 12.0 11.0 13.0

34 36 36 33 39

Table 24.4 Classification of anemia in children, based on haemoglobin levels [10] Anemia measured by haemoglobin (g/dl) Children 6–59 months Children 5–11 years Children 12–14 years Non pregnant women above 15 years Pregnant women Men (above 15 years)

Anemia

Mild

Moderate

Severe

<11.0 <11.5 <12.0 <12.0

10.0–10.9 10.0–11.4 10.0–11.9 10.0–11.9

7.0–9.9 7.0–9.9 7.0–9.9 7.0–9.9

<7.0 <7.0 <7.0 <7.0

<11.0 <13.0

10.0–10.9 12.0–12.9

7.0–9.9 9.0–11.9

<7.0 <9.0

Iron deficiency and iron deficiency anemia in young children

".3

645

Iron balance in children

Iron status can be considered as a continuum, which results from longterm negative iron balance when iron stores are progressively lost. Total iron in an adult man is 3.5–4.0 g – 73% of the body’s iron is incorporated into hemoglobin, 12% is in the storage complexes ferritin and haemosiderin, and a very important 15 per cent is incorporated into a variety of other iron-containing compounds, some of them enzymes of vital importance. The heme iron compounds include myoglobin, cytochromes, catalases, and peroxidases. Infants and young children are prone to be affected by iron deficiency since the requirements for iron is high during this stage of rapid growth and development. Almost all iron compounds in the body are continuously broken down and re-synthesized and iron that is released is very efficiently conserved and reutilized. An important consequence of this recycling is that very little iron is lost from the body on a daily basis that is required to be replenished in adult men with normal iron losses in the feces, sweat, and sloughed cells amounting to about 0.9 mg/day, equivalent to <0.1% of iron stores. However, women in their reproductive years need to absorb an average of 1.3 mg/day to make up for the additional iron loss in menstrual blood [11]. In case of infants and children, a large amount of iron is required for growth, i.e. substantially more iron must be absorbed than is lost from the body. For example, a 1-year-old infant loses about 0.2 mg of iron/day, calculated on the basis of body surface area from values measured in adults. The amount needed for growth averages roughly 0.6 mg. Consequently, about 75 % of the 0.8 mg of absorbed iron needed per day during this period is required to meet the needs of accelerated growth.

"."

Patho-physiology of anemia in children under three years of age

Hemoglobin concentrations are normally higher on birth than at any other time of life as a result of the adaptation of the fetus to the hypoxic environment of the uterus. In addition, at full term neonatal reserves of storage iron are relatively generous. Consequently, most newborn infants are well supplied with iron. Between birth and 4 months of age, there is almost no change in total body iron in the term infant. The need for exogenous iron is therefore modest during this period. The abundant iron stores present at birth help to provide for synthesis of hemoglobin, myoglobin, and enzyme iron during the first 4 months. Additional iron from hemoglobin breakdown is also made available to meet iron needs because the concentration of hemoglobin declines from a mean of 17.0 g/dl at birth to a low of 11.0 g/dl at 2 months of age. This low point is also

646

Public health nutrition in developing countries

referred as “the early anemia of infancy” and is distinguished from the “late anemia of infancy” because it is unresponsive to iron treatment. After about 4 months of age, a gradual shift occurs from an abundance of iron to the marginal iron reserves that characterize the period of continued rapid growth. The transition from feast to famine in respect to iron is primarily due to the large amount of iron required to maintain a near constant mean hemoglobin concentration of 12.5 g/dl within a rapidly expanding blood volume between 4 and 12 months. A large amount of iron, about 0.8 mg/day, needs to be absorbed from the diet during this period. Mild maternal iron deficiency and anemia have few significant repercussions on iron status of the newborn, but severe maternal anemia does have a strong influence. The risk of infant developing iron deficiency is further increased if the umbilical cord is clamped before the appropriate stage [12]. Both these risk factors are high in developing countries. In the first two months of life, there is minimal dietary iron absorption and stores are mobilized to meet the iron requirement. Thereafter, dietary iron absorption needs to supply enough iron to facilitate the increased need for more red cell mass. By about 6 months of age, iron stores are usually depleted and diet then becomes the vital source for iron. A low birth weight baby has less iron store and therefore not only such an infant requires extra iron but also needs additional amount of iron intake to be ensured at an earlier age. The overall rapid growth of infancy between 6 and 24 months, include a significant increase in red cell mass and tissue volume. At this stage, requirement for iron is proportionality nearly as high as that for pregnant women. This increase in requirement is difficult to meet through breastfeeding practices or complementary feeding alone unless specific measures are taken to increase iron consumption. Therefore the most common reason for iron deficiency anemia in infants and children is the inadequate supply of iron in the diet. The risk of iron deficiency is high during infancy because only about 50% of the normal iron requirement of a normal six-month old can be obtained from breast milk and by this age the iron stores at birth are likely to have been used up towards providing support for body functions and growth even in children born at term to well-nourished mothers. In case a mother is anemic or a child is of low birth weight (LBW), the stores are depleted much earlier. Continued breastfeeding after six months will provide half of infant’s iron need while the remaining half, approximately 0.4 mg/day, must come from complementary food or iron-containing supplement or use of ironfortified foods for preventing deficiency of iron and iron deficiency anemia [13].

Iron deficiency and iron deficiency anemia in young children

647

The risk factors that contribute to IDA in infants are low or non-iron fortified formula or breast-fed through the later months without supplementation of iron, premature infants or low birth weight (LBW), early cord clamping, maternal anemia, gastrointestinal blood loss due to infection (Helicobactor pylori and helminth infections), limited access to other nutrients that enhance the incorporation of iron into hemoglobin. Additionally, reduced absorption of iron in gastrointestinal disease due to chronic infections, recurrent diarrhea, celiac disease or an intestinal parasite infestation contributes to iron deficiency. However, the most common factor for ID and IDA in infants and children is the low intake of iron in the diet during the rapid growth spurt. Therefore, the two main reasons for IDA in children are (1) increased requirement for iron during rapid growth stage of infancy and early childhood that is between 6 and 24 months; and (2) insufficient intake of iron or poor bio-availability of iron consumed, related to low consumption of absorption enhancers and a high consumption of absorption inhibitors of iron in the second year of life. The situation is aggravated with increase in prevalence of worm infestation.

24.5

Consequences of iron deficiency and iron deficiency anemia in children

Anemia is a public health concern and is the most common cause of morbidity. Anemia, like fever, is a manifestation and not a disease per se. Anemia is most often a hidden problem with few overt symptoms [14]. Children with anemia are denied their rights to optimum physical and mental development before they ever reach a classroom. Anemia in children adds to the burden on health systems, affects learning and school performance, and reduces adult productivity. The massive economic cost of childhood anemia is often underestimated by policy makers while service providers often fail to recognize the “invisible” significant serious health consequences from anemia. The fact that anemia in young children can result in permanent cognitive deficits resulting in children being denied their rights to optimum physical and mental development makes childhood anemia a serious public health concern. The various stages of iron deficiency are presented in Fig. 24.7 [15]. The first stage of iron depletion does not result in functional changes. In the second stage, stores are exhausted and tissues begin to have insufficient iron resulting in iron deficiency. In this stage when there is no outright anemia, negative effects include cognitive impairment, decreased physical capacity, and reduced immunity and these effects are more serious in the last stage of iron deficiency anemia [16].

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Public health nutrition in developing countries

Plasma ferritin (µg/L) 60 Transferrin saturation (%) 35 RBC protoporphyrin (µg/dL) 30 Hemoglobin (g/dL) >12

<12 35 30 >12

<12 <16 <100 >12

<12 <16 <100 >12

24.7 Iron status in relation to iron stores [15]

It is estimated that at least 200 millions of under-five children globally fail to reach their cognitive and socio-emotional development due to undernutrition including iron deficiency and inadequate stimulation [17]. In children less than two years, the most significant negative consequences of IDA are impairment in motor and mental development, which may be irreversible in later life [18, 19]. Poor iron status negatively impacts cognitive as well as motor and social development [20]. Significant adverse effects between 6 and 24 months include decrease in responsiveness and activity as well as increase in body fatigue. Anemia during childhood is serious since it affects cognition and the effects that are observed in first six months of life could often lead to permanent brain damage. Moderate and severe deficiency impairs cognitive performance at any age. In general these effects are corrected with iron supplements but if moderate to severe iron deficiency occurs in infancy during the phase of brain development, the effects on cognition may not be reversible [13]. According to Lozoff et al [21], depending on the age when anemia occurs, some of the development deficits can be improved or even corrected with iron treatment but with iron deficiency in infancy some cognitive and social differences can remain permanent. Box 24.2 [22] presents details of results of a longitudinal study reported on the impact of iron deficiency on cognitive development. An anemic child is likely to remain vulnerable to infections and continues to have lower immunity towards infection. Anemia results in lowering appetite and sets up a vicious cycle which perpetuates to a series of events that need to be corrected and if no corrective action is taken could result in impaired development of mental and physical coordination skills. In older children, iron deficiency leads to impaired scholastic achievement [23].

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Box 24.2 Iron deficiency below age 2 years and cognitive score [22] Children between the ages 1–2 years were enrolled in a study and followed up over a period of 18 years; Anemia was corrected with iron supplements for those children in the intervention group. Children underwent cognitive test in early childhood and at ages 5–8 years, 11–14 years, 15–18 years and 19 years. Bayley tests were used in infancy and age appropriate Wechsler Test and other cognitive tests were applied for later ages. Anemic and non-anemic children were compared, irrespective of being in the intervention or control group. The results revealed that children from the middle socio-economic status (SES) with adequate iron stores scored 8–9 points higher than those who remained anemic in early childhood. This difference was maintained up to 19 years of age. In the lower SES group, children with adequate iron stores had 10 points higher in early childhood. The gap, however, widened substantially with increase in age and a difference of 25 points was noted at the age 19 years. These results indicate that iron deficiency below two years does influence cognitive ability and with such gaps in cognitive score it is expected to adversely influence schooling and earning capacity in future.

While it is well-established that iron deficiency anemia among children is responsible for higher morbidity and subsequent mortality, systemic studies to quantify them are practically difficult for a number of epidemiological reasons and therefore are not available. However, a study as early as 1920s from London has reported impact of iron supplement to infants on reducing bronchitis and gastroenteristis [24]. Infants receiving formula fortified with iron and vitamins were reported to have about 50% less respiratory infections than infants receiving unfortified version of the same formula [25]. Iron deficiency has been reported to be associated with increased diarrhoeal and respiratory diseases [26] while meningitis has been observed to be fatal among those who were anemic [27]. There are other studies which have found no such effect. Interactions of iron and infection reviewed in 2000 concluded that some issues related to iron deficiency and infection remain unresolved [28, 29]. Iron deficiency anemia rarely exists in isolation and to disentangle the role played by anemia from malnutrition and other precipitating factors is difficult to be obtained at the community level.

24.6

Measures for preventing iron deficiency and anemia

One of the goals of the World Summit for Children was reduction in IDA in women by one-third of the 1990 levels by 2010 [30]. There was no reference to address IDA in children in the World Summit Goal since knowledge on impact of ID or IDA on mental development was then not well-appreciated. Since 2000, there is increased concern to address anemia in preschool children with research highlighting the fact that even mild

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Public health nutrition in developing countries

anemia in infants and young children can impair intellectual development and such damage by deficiency of iron to a young child’s brain may not be reversed later in life [22, 31] and therefore priority needs to be accorded to the prevention of iron deficiency in this early stage of life [32]. Iron deficiency anemia can be prevented at low cost, and the benefit/ cost ratio of implementing preventive programs is recognized as one of the highest in the realm of public health. Economic cost of achieving a reduction in nutritional anemia through iron fortification and iron supplementation indicate benefit to cost ratio of 6:1 in case of fortification while economic benefits of supplementation are indicated to far exceed the cost of intervention [33]. Effective and practical interventions are available and poor implementation rather than non-availability of the interventions is the constraint. Anemia-prevention strategies involve synchronized efforts to increase iron intake through supplements to high risk group of population of pre-school children combined with concurrent efforts to provide vitamin A supplements, access to fortified staple cereal or other food items, increasing iron levels in complementary food by promoting use of multi-nutrient mixes as “home fortificants” [34, 35], as well as by implementing measures to reduce parasitic infections and control malaria.

24.6.1 Iron–folic acid supplements Traditionally, for over the last three decades, the IDA programme has focused on iron–folic acid (IFA) supplements to pregnant mothers and comparatively very little attention has been given to address ID or IDA in children, especially for under-two years. Iron deficiency anemia has been viewed merely as “women’s problem” [36]. However, it needs to be recognised that rapidly growing infants need relatively high iron intake. Infants who do not have low birth weight are normally born with sufficient iron but beyond six months of age, iron content of milk is not sufficient. It is virtually impossible for infants over six months to meet the iron needs through diet alone. Higher needs through diet may be met only in situations when the diets contain sufficient amount of fortified foods and heme iron from animal foods or if the iron stores of infant since birth or woman at the start of pregnancy is adequate. With evidence of serious implications of iron deficiency anemia in young children, it has been recommended by INACG/WHO/UNICEF [37] that “in situations where iron-fortified complementary foods are not widely or regularly consumed by young children, all infants should receive iron supplements after six months of age”. In regions where the prevalence of anemia is below 40%, the duration of supplementation for normal birth infants should be from

Iron deficiency and iron deficiency anemia in young children

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six months to until 12 months of age [3]. However, as presented in Table 24.5, in areas where the prevalence is 40% and above, it is recommended to continue supplementation up to 24 months of age [37]. Table 24.5 Guidelines for iron supplementation to children 6–24 months of age [37] Prevalence of anemia in children 6–24 months

Dosage

Birth–Weight Category

Duration

<40%

12.5 mg iron + 50 μg folic acid daily

Normal

6–12 months of age

Low birth weight (<2500 g)

2–24 months of age

12.5 mg iron + 50 μg folic acid daily

Normal

6–24 months of age

Low birth weight (<2500 g)

2–24 months of age

³40%

The most practical iron supplement for use in infants and young children is an aqueous solution of a soluble ferrous salt, such as ferrous sulfate, or a ferric complex, such as iron polymaltose. A single, safe and effective dose for all children under-2-year old that can be easily dispensed by all mothers (literate and non-literate) is required. For the many past decades, oral ferrous sulphate syrup has been the primary strategy to control IDA in infants and young children [38]. However, compliance is adversely influenced due to a combination of factors: the syrup has an unpleasant metallic after taste, leaves dark stains on teeth and high doses cause abdominal discomfort [39]. Additionally, there are technical disadvantages associated with liquid iron such as short shelf-life and practical programme constraint such as high transportation costs due to weight of bottles, and difficulty in adequately dispensing the drops, especially among illiterate population as the care giver is required to measure decimal volume from a dropper [40, 41]. Requirement of iron dosage through supplements for prevention and treatment of IDA depends on the following factors: ●

● ●

●

●

The level of iron stores of the child at the time of birth, which in turn depends on the iron status of the mother during pregnancy. Whether the child born is low birth weight or normal birth weight. Whether the child is on the breastfeeding which is exclusive or along with other foods that contain iron-absorption inhibitors and/or ironabsorption promoters or food consumed is fortified with iron-poor micronutrients. The quantity of the food consumed and whether the bio-availability of iron from it is poor (5%) or good (up to 15%). Level of anemia and the additional factors which contribute to anemia such as infection, worm infestation etc.

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For therapeutic purposes, an adequate and safe hematological response to oral iron intake can be achieved in 4–6 weeks with 3 mg elemental iron per kg body weight/day [42]. However, in a prophylactic program, between 1 and 2 mg of iron per kg body weight/day is appropriate. Assuming 5 percent iron absorption, which is a very conservative estimate of absorption [43], 12.5 mg iron dose is equivalent to 2.5 mg iron per kg body weight for a 6-month-old child with an average weight of 5 kg. The same dose of 12.5 mg iron is adequate in case of 12 month-old infant weighing 8 kg, 1.6 mg iron per kg body weight and for an 18-month-old infant weighing 12 kg, 1.2 mg iron per kg body weight [37]. Table 24.5 presents the guidelines for iron supplementation to children 6–24 months of age [37]. If compliance is poor and children consume iron supplement dose equivalent to consuming the recommended dose only every other day, between 35 and 45 percent of the iron requirement would be available from the iron supplement alone. Iron supplement administration to infants younger than six months of age is recommended in situations where mothers of infants are severely anemic during pregnancy resulting in lower iron stores at birth or infants who are born low birth weight (LBW). In such situations, iron status may be poor in infants at age younger than six months, resulting in adverse impact on growth and development. In poorly nourished populations, 20–30 percent newborns are LBW and these newborns have low levels of iron stores based on lower overall tissue and blood volume at birth. These facts, compounded with increased iron needs associated with rapid weight gain of low birth infants, are the basis for WHO and UNICEF recommendation that LBW babies receive iron supplement beginning at two months of age and the supplementation be continued up to 24 months of age [37, 44, 45]. Operational issues regarding demand, supply and logistics, communications and social mobilization, monitoring, building partnership with private sector needs to be given increased attention for effective implementation of iron supplementation programme for children. Operational feasibility needs to be well-defined following implementation of iron supplement administration programme on a large scale. In India, the revised policy for anemia control includes iron supplementation to children in the form of syrup and small tablets. However, specific guidelines for distribution and monitoring are being finalised. Box 24.3 presents details of iron folic acid supplement programme evolvement in India.

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Box 24.3 Prevention and control of anemia in young children in India Government of India’s 10th five-year plan [46] goals for anemia control for children include 1. Screening of children for anemia wherever required and appropriate treatment of those found anemic. 2. Reducing the prevalence of anemia by 25% and moderate and severe anemia by 50% in children. In India, the National Nutritional Anemia Prophylaxis Program (NNAPP) has been in existence since 1970 [47]. The Prophylaxis programme at the beginning included provision of iron folic acid (IFA) tablets to pre-school children besides pregnant women. Pre-school children with haemoglobin levels over 8 g percent were recommended to be included in the prophylaxis programme while children with hemoglobin less than 8 g percent were recommended to be put on antianaemic treatment. The programme was later revised to include children of 1– 10 years and administration of supplements was changed to 100 days instead of six months. The supplement containing 20 mg of elemental iron (ferrous sulphate) and 100 μg of folic acid for children was provided in two forms – small tablets and 2 ml syrup liquid. The programme was evaluated by ICMR in 1988 [48] and this was followed by a meeting organized by the Government of India at Nirman Bhavan on 21–22 nd Sept in 1989 [49]. The recommendations were reviewed by a core group of experts. The following major policy decisions were taken: (a) The nomenclature of the programme was re-designated as National Nutritional Anemia Control Programme. (NNACP) since it was noted that over 80 percent pregnant mothers were reported to be anemic .It was agreed that the focus of the programme should be on control of anemia rather than on prevention alone. (b) Program priority should be given to vulnerable sections of the population namely pregnant and lactating women, intrauterine device (IUD) users as well as children in the 1–5-year age group. The composition of “big tablet” for pregnant mothers/women in reproductive age was modified with one tablet containing 100 mg elemental iron instead of 60 mg. The amount of folic acid was retained at the dose of 500 μg. The dosage for prophylaxis and treatment was defined – one tablet per woman per day including pregnant women for a minimum of 100 days and two tablets per day for women with severe anemia. (c) Taking into consideration the high cost of syrup recommended for children earlier, usage of syrup in the public health programme was discontinued and only “small IFA tablets” for children between 12 and 59 months was recommended. Each small tablet contained 20 mg elemental iron and 100 μg of folic acid which was recommended to be consumed for a minimum of 100 days in a year by young children. (d) Iron-folic acid tablets were recommended to be supplied not as open tablets in bottles but in a packaged form. Blister packaging was recommended. Based on the above recommendations, a Policy on National Nutrition Anemia Control Programme (NNACP) was formulated in December 1991 [50]. Small “IFA” tablets continued to be supplied under this programme. The NNACP programme was included in the Child Survival Safe Motherhood (CSSM) Programme of the Government of India in 1992 and later as a part of Reproductive Child Health (RCH) programme [51]. In 1998, the NNACP was reviewed at a National Consultation on Anemia organized by the Government of India and UNICEF [52]. No special additional recommendation was made for preschool children. Since

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1992, the NNACP program has continued to be implemented as part of CSSM and later RCH I and RCH II package. The programme is being implemented through the existing health system with support of the Integrated Childhood Development Scheme (ICDS) Programme. However, the focus in implementation has been primarily on pregnant women and not on pre-school children. [53] A nation wide study on usage of IFA supplements was undertaken during early 2000 by the National Nutrition Monitoring Bureau (NNMB) covering 2178 children of the age group one to five years from 8 states (Kerala, Tamil Nadu, Karnatka, Andhra Pradesh, Maharashtra, Madhya Pradesh, Orissa, West Bengal) [54]. The findings highlighted that only 3.8% of children received Iron Folic Acid (IFA) tablets (small iron folic acid tablets) and half of the children received the IFA tablets from the ICDS frontline workers while the remaining half received the supply of the supplements from the multipurpose health worker female. The number of children who received IFA tablets ranged from 0% to 5% in different states except in one state (Maharashtra) where the percentage of children receiving iron folic acid tablet was reported to be almost 12 per cent. In 2002, a technical consultation on “Strategies for Prevention and Control of Iron deficiency Anemia Amongst Under Three Children in India” was organized [54]. Based on the finding of the study as well as the recommendations of the 2002 consultation meeting [55], a consensus was reached that iron and folic acid tablet being supplied to young children under the age of three years is not well-accepted and it was recommended that IFA in the form of syrup should be supplied to children. Iron folic acid supplement was recommended to be administered from six months of age. The above recommendation was endorsed in the Government Policy in the year 2007 [56]. As per 2007 Policy, it was recommended that the NNACP should cover infants aged 6–12 months. The Policy recommends that all children 6–60 months to be given iron folic acid supplements for a minimum of 100 days in a year. The composition of one millilitre of syrup or one small tablet is 20 mg elemental iron and 100 μg folic acid. For safety reasons it was recommended that each bottle of IFA syrup must be supplied with a dispenser that allows only one millilitre to be drawn at a time. Introduction of dispersible tablets has also been proposed. As per these recommendations, both IFA syrup and tablets are being supplied for children in Kit A under the National Rural Health Mission (NRHM) [57]. The Policy guidelines for addressing the public health problem of childhood anemia were revisited at a workshop organized by the Government of India in early 2008 [58]. It was recommended that for children with low birth weight, the IFA supplementation should start from 2 months of age rather than 6 months. It was also recommended that all children should receive the supplement since screening of children for anemia is not considered practical and not recommended. The experts at the meeting agreed that the Government of India guidelines regarding duration of administration of IFA for a minimum period of 100 days, presented in the national guidelines on Integrated Management of Childhood Illness (IMNCI), should be followed [59]. IFA supplementation has been recommended to be discontinued during active episode of illness. Details of delivery and monitoring system have been proposed with emphasis on use of existing health and ICDS systems.

Periodic deworming is simple and safe and has been reported to have significant effect on nutritional status, including iron status. The impact of deworming on nutritional status has been reported from Tanzania where deworming resulted in significant impact on anemia in children less than two-years old whereas the impact of supplementation with iron was not reported to be significant [60].

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In severe malnutrition, supplementation of iron is hazardous [61]. Adequate iron status is essential for preventing and overcoming infections. On the other hand, pathogenic organisms also require iron for their growth and reproduction. In severe malnutrition, the immune system is compromised and iron supplements enhance the growth of pathogenic organism before immunity is restored since the body is not able to continually maintain its overall supply of iron in the forms that are not usable by pathogens or are not free to form compounds that can result in cellular and other damage. Therefore, iron supplementation given to severely malnourished children with impaired immunity can benefit the replication of pathogen before the immune system is rebuilt and restored. Parental iron administered to children with Kwashiorkor has been reported to result in serious illness and death [62]. According to Jackson 2007 [61], “an assumption that anemia found in malnourished individual is a simple consequence of poor or inadequate dietary intake of iron, without a critical consideration of the broader context, gives rise to the potential for serious error in care with inappropriate intervention”. In areas where P.falciparum malaria is hyperendemic, public health recommendations for implementation of a practical low-cost intervention package to correct iron deficiency anemia and promote healthy iron status among infants and young children remains unresolved [14]. The findings from the study in Zanzibar, Tanzania indicate that in the region with stable, perennial, and intense transmission of malaria, iron supplementation administered to children who were iron replete, with or without zinc, resulted in increased morbidity and mortality [63]. Subsequently, WHO consultation recommends that universal iron supplementation should not be used in areas of high malaria transmissions [14].

24.6.2 Obstetric care – delayed cord clamping Cutting-off of the pulsating umbilical cord before iron rich cord blood is transferred to the newborn also results in lower iron in the infant at birth. Delayed clamping of the umbilical cord (most trials defined delayed clamping being soon after cessation of cord pulsation or at 3 minutes after birth) is an effective prophylactic measure for prevention of iron deficiency and anemia. Compared to early cord clamping (defined as immediately after birth or within 10 seconds of birth), delayed clamping results in increase in iron endowment of the child at birth by 50 per cent. The result of delayed clamping is higher blood flow to vital organs in the first week after birth and less cases of anemia at two months of age in full-term infants [64]. A systematic review has confirmed that a higher levels of hemoglobin is observed at 2–3 months of age in children in developing and industrialized countries where the practice of delayed clamping at birth is

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followed. The impact is noted to be higher when mothers are anemic [65]. Delayed clamping is recommended as one of the important measures for prevention of childhood anemia [66].

24.6.3 Fortification and home fortification Food-based approach for increasing iron intake sufficiently to meet the very high requirements for iron for the highest risk group – children under two years and pregnant the mother – has been challenging. Effort is continuously on-going for the fine tuning of technology for iron fortification of traditional staple food, water and beverages, food sauce, table salt as well as commercial foods. A new technology and strategy of adding a fixed amount of fortificant mixture to an individual’s portion of food is referred as “home fortification”, is being experimented since mid1990s [34, 35]. The concept of fortification of complementary food for young children has gained momentum since it has been noted that availability and use of commercial foods fortified with iron and other essential micronutrients in North America have historically been noted to have resulted in disappearance of IDA problem in children [67]. This decrease in IDA in children in western world is recognised as a successful public health accomplishment although specific groups of infants and children, such as infants born prematurely, remain at risk of IDA. Since the use of commercially fortified food for young children is not easily available at affordable cost as well as the fact that regular administering supplements in syrup and drop had not been effective, the concept of home fortification was initiated in 1996 to address childhood IDA [41]. Home fortification pertains to sprinkling of a fixed amount of powder or mixture containing iron and selected micronutrient to cooked food served to a child at home level. One such formulation is Sprinkles. According to Zlottkin and Tondeur (2007) [18], who have pioneered this technology, “In Sprinkles, the iron in the form of ferrous fumarate is encapsulated within a thin lipid layer to prevent the iron from interacting with food, thereby limiting changes to taste, colour or texture of the food. Caregivers are instructed to add the entire content of sachet daily to any semi-solid food prepared for their infant or young child in the household, immediately before serving. Other micronutrients including zinc, iodine, vitamin C, D, A and folic acid may be added to Sprinkles sachets”. The microencapsulate (an edible vegetable-based lipid) masks the taste of iron and prevents colour change by forming a barrier which does not allow an interaction between iron and food to which the Sprinkle is added. Table 24.6 [18] presents the composition of nutritional anemia-prevention formulation in Sprinkles; while Table 24.7 [18] presents the complete micronutrient formulation. The anemia formulation includes ascorbic acid

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to enhance iron absorption, folic acid to prevent megaloblastic anemia and zinc and vitamin A to enhance vitamin A status. Table 24.6 Composition of nutritional anemia formulation Sprinkles [18] Micronutrient

Amount

Iron Zinc Folic acid Vitamin A Vitamin C

12.5 mg 5 mg 160 µg 300 µg RE 30 mg

Table 24.7 Composition of multimicronutrient formulation Sprinkles [18] Micronutrient

Amount

Vitamin A Vitamin C Vitamin D Vitamin E Vitamin B1 Vitamin B2 Vitamin B6 Vitamin B12 Folic acid Niacin Iron Zinc Copper Iodine

400 µg RE 30 mg 5 µg 5 mg TE 0.5 mg 0.5 mg 0.5 mg 0.9 µg 150 µg 6 mg 12.5 mg 4.1 mg 0.56 mg 90 µg

Efficacy trials with anemic children using Sprinkles has demonstrated that the effect on anemia cure rate were comparable to that of standard iron drops [67]. In a period of two months, 58% children who received Sprinkles shifted from anemic to non-anemic stage. A follow-up study also showed that in most children who have been successfully treated for anemia, further intervention was not needed at 12 months postintervention [18]. Box 24.4 presents the details of efficacy trial undertaken in India [68]. The feasibility and acceptability of Sprinkles has also been studied in a large scale trial in Mongolia between 2001 and 2004. The findings demonstrated that usage of Sprinkles in public health programme was feasible. Sprinkles have been successfully used in a wide range of settings ranging from community settings in Bangladesh [69] to emergency setting in Haiti [70]. Adherence and acceptability of Sprinkles has been positive and the only consistently reported side effect is darkening of infants stools. Pilot projects are being scaled up to national level in nine countries in South Asia and Latin America [68].

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Box 24.4 Low-dose Sprinkles – an innovative approach in India to treat IDA in infants and young children [68] In Maharashtra, a state of west India, effectiveness of flexible administration of Sprinkles delivered through existing Integrated Child Development Scheme (ICDS) for reducing the prevalence of anemia in children of age 6 months to 6 years was undertaken. A total of 17,126 children participated in the study where Sprinkles Plus comprising iron and other micronutrients (presented in Table 24.7) was given to children either at the ICDS centre or at home by caregivers/mothers. About 170 ICDS frontline workers were trained to participate in this project. The compliance of flexible administration of 60 sachets of Sprinkles Plus for over 120 days to these children was monitored either under the supervision at ICDS centre or by mother of children who were not attending ICDS centres. Compliance card was maintained by Anganwadi worker/mother. Baseline Hb levels (random sample of 1500 children) was studied while end line Hb levels were estimated on fresh random sample of 1500 children. Sprinkles administration was reported to be well-accepted by mothers and children. Overall anemia reduced from 50.8% to 33.7% and compliance both at ICDS centre and at home was reported to be over 90 percent from the records of ICDS functionary while mothers reported a lower compliance of 56.4%. It was concluded that Sprinkles, flexibly administered through anemia prevention/control program is highly effective in reducing anemia in young children. It was also recognised that the challenge is to establish system to monitor and ensure proper use of Sprinkles and monitor compliance.

24.7

Conclusion

The significance of even mild anemia on intellectual development of infants and young children is of increased concern among the public health experts [32]. There is a need to urgently address the public health problem of anemia in young children, with special focus on under 2 years.

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et al. (2008). For the Maternal and Child Undernutrition Study Group; Maternal and Child Undernutrition 3, What Works? Intervention for Maternal and Child Undernutrition and Survival. Lancet Series I. ZLOTKIN S , ARTHUR P , ANTWI KY , YEUNG G (2001). Treatment of anemia with microcapsulted ferrous fumerate plus ascorbic acid supplied as sprinkles to complementary (weaning) foods. Amer. J. Nutr., 74, pp. 791–795. HIRVE S . Micronutrient and Child Health Workshop, 20–23 October, AIIMS, New Delhi. HYDER SM , HASEEN F , RAHMAN M, ZLOTKIN SH (2005). The effectiveness of flexible administration of sprinkles in anemic and non-anemic infants and young children in Bangladesh. Proceedings of Federation of American Societies for Experimental Biology (FASEB). San Diego (abstract). DE PEE S , MOENCH PFANNER , R, MARTINI E , ZLOTKIN S, DARTON -HILL I, BLOEM MW (2007). Home fortification in emergency response and transition programming: experiences in Aceh and Nias Indonesia. Food nutr Bulletin.

25 Iron and multiple micronutrient supplementation in children: evidence from systematic reviews Tarun Gera

Tarun Gera, MD, is a consultant in the Department of Pediatrics, Fortis Hospital, New Delhi. Following completion of MD (Pediatrics) from Maulana Azad Medical College, University of Delhi, Dr. Gera has been extensively involved in the field of evidence-based medicine and nutrition. He has published seven systematic reviews pertaining to the field of micronutrients.

#.1

Introduction

Anemia is one of the most common nutrient deficiencies in the world. Recent estimates suggest that as many as two billion people are affected by this affliction globally [1]. The problem is especially severe in the South Asian region, particularly India, and more so amongst the children and pregnant women [2]. This is probably because of a combination of factors including inadequate dietary intake, poor dietary patterns, increased requirements and physiologic losses. It has been estimated that more than half the children and as much as 90% pregnant women in India are anemic [3]. Iron deficiency is the main cause of anemia in most settings. The association between the two is strong that anemia is often considered the most common indicator of iron deficiency. However, it is the more severe forms of iron deficiency which contribute to anemia. Iron has a number of other important roles in the developing human’s physiology apart from hematopoiesis. The ill effects of ‘subclinical’ iron deficiency are gradually being recognized and these are often categorized as functional consequences of iron deficiency in the literature. These include poor neurocognitive development, somatic growth and physical or work capacity. In the last decade a lot of research has also focussed on the functional consequences (growth, development, and anemia) of other micronutrients’ deficiencies other than iron, in children. The most well-studied include

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zinc, vitamin A, folate, vitamin B12, vitamin D and vitamin E. It is also argued that multiple micronutrient deficiencies usually coexist largely due to poor quality of the diet and low intake of food from animal sources, mostly in the lesser developed countries. From a pragmatic and economic perspective, it might make sense to combine iron supplementation programs (which are already operational in a number of countries including India) with multiple micronutrient supplementation simultaneously, in order to address the problem of these deficiencies with a unified programmatic approach. Although, such an approach of simultaneous supplementation with multiple micronutrients may seem attractive, there is a strong possibility that there may not be any additional benefit to iron supplementation alone because of the possible negative interactions they may have on each other in vivo. Policy formulation in developing countries, like India, would need convincing documentation of the enhanced benefit of such an approach over isolated iron supplementation. The objective of this chapter is to assess the evidence available in the scientific literature of the advantages of use of multi micronutrient supplement vis-à-vis isolated iron supplementation on anemia, and other functional consequences.

25.2

Iron and multiple micronutrient supplementation and anemia

Anemia continues to be the most well studied outcome of iron deficiency and combating iron deficiency is considered the most important way to control anemia. Several randomized controlled trial conducted in children, with iron being supplemented through either the medicinal route or fortification of food products, have shown a positive beneficial effect in reducing the prevalence of anemia. However, in spite of the fact that iron supplementation programs have been operational in many developing countries, similar reduction in anemia prevalence has not been seen on a public health scale. A possible reason for this apparent lack of effectiveness may be poor compliance and acceptance, low supplies and inadequate penetration of health infrastructure in populations that need them the most. The earlier assumption that iron supplementation might control anemia to a major extent is being increasingly questioned [4, 5]. In a recent metaanalysis (Box 25.1) evaluating the effects of iron supplementation on anemia in developing countries, the authors concluded that ‘there is a suggestion in the data, not well documented except in a couple of studies, that something other than iron may be operating to limit hemoglobin response and anemia control’ [4]. In another meta-analysis of randomized controlled trials (RCTs), the increase in hemoglobin with iron supplementation alone was modest (0.74 mg/dl), the response being even

Iron and multiple micronutrient supplementation in children

665

Box 25.1 Meta-analysis In statistics, a meta-analysis combines the results of several studies that address a set of related research hypotheses. Resulting overall averages when controlling for study characteristics can be considered meta-effect sizes, which are more powerful estimates of the true effect size than those derived in a single study under a given single set of assumptions and conditions. Meta-analysis provides a systematic overview of quantitative research which has examined a particular question and is helpful in providing insight into the overall effectiveness of interventions, the relative impact of independent variables, and the strength of relationship between variables.

poorer in malaria endemic regions [6]. Projections from this analysis suggest that in under six children, on an average between 37.9% and 62.3% (mean 49.2%) anemia is responsive to iron therapy; the corresponding figures for malarial regions being 5.8% and 31.8% (mean 22.2%). A probable reason for this is that apart from iron, several other micronutrient deficiencies can cause anemia [7–9]. For example, it is now established that vitamin A deficiency can cause anemia. Riboflavin, folate, ascorbic acid, zinc and vitamin B12 deficiencies are also known to impair hemoglobin synthesis. A number of randomized controlled trials have been done to assess the impact of multiple micronutrient (including iron) supplementation on hemoglobin levels and anemia prevalence in children. The data from these trials has been synthesized in two large systematic reviews to help one arrive at an intelligible conclusion. Allen et al. [10] extracted data from 26 studies that studied the effect of multiple micronutrient supplementation on hemoglobin levels and showed that it had a significant positive effect on the hemoglobin levels (Effect Size = 0.39 mg/dL; 95% CI 0.25, 0.53; p<0.001) (Figure 25.1). Younger children and studies using fortification as the method of supplementation showed better improvement in the hemoglobin levels. The reduction in point prevalence of anemia was reported in fewer studies and ranged from 10% to 40%. The reduction in anemia prevalence was greater in children with lower baseline anemia and in those who received a higher amount of iron in the supplement. The most important lacunae in this systematic review was that it failed in making distinction in the composition of the supplement provided. Thus studies that provided multiple micronutrients with iron were combined with those who did not. Similarly, the placebo groups included iron as well as placebo controls. Thus, the review failed to assess the additive effect of multiple micronutrient supplementation on hemoglobin over and above the hematinic effect provided by iron supplementation alone. These issues were addressed by a more comprehensive review [11]. Randomized controlled trials evaluating change in Hb levels with interventions that included Fe and multiple-micronutrient supplementation in comparison

25.1 Effect of multiple micronutrient supplementation on Hb levels in children [10]

–1.2

–0.8

–0.4

0.0

0.4

0.8

1.2

1.6

2.0

2.4

666 Public health nutrition in developing countries

Iron and multiple micronutrient supplementation in children

667

to placebo alone or Fe alone were analysed in two separate systematic reviews. Twenty-five trials were included in the review comparing Fe and micronutrient supplementation with placebo. The pooled estimate (random effects model) for change in Hb with Fe and micronutrient supplementation (weighted mean difference) was 0.65 g/dl (95% CI 0.50, 0.80, P<0.001). Lower baseline Hb, lower height-for-age Z score, non-intake of “other micronutrients” and malarial non-hyperendemic region were noted to be significant predictors of greater Hb response and heterogeneity. These results were similar to a systematic review that had evaluated the effect of iron supplementation alone on hemoglobin levels in children [6]. Thirteen trials were included in the review comparing Fe and micronutrient supplementation with Fe alone. The pooled estimate for change in Hb with Fe and micronutrient supplementation (weighted mean difference) was 0.14 g/dl (95% CI 0.00, 0.28, P= 0.04) (Figure 25.2). Stratified analyses suggested at the possibility of a decremental response in hemoglobin with some micronutrients.

25.2 Effect of iron and multiple micronutrient supplementation versus iron alone on hemoglobin levels in children [11].

From these two meta-analyses [6, 11], it may be postulated that the effect size of the change in hemoglobin is not likely to alter much with addition of multiple micronutrients to iron supplementation. Similar reductions in the prevalence of anemia in children may be expected (37– 62% in non-malarial endemic areas and 5–31% for malarial endemic areas) despite the addition of multiple micronutrients to the iron supplement. These analyses indicate that an unselected addition of multiple micronutrients to iron supplementation will not result in a significant improvement in hemoglobin response in children.

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Public health nutrition in developing countries

The interaction of many of these micronutrients is still poorly understood. The possibility of negative and unpredictable interactions with co-administration of several micronutrients may therefore exist. This possibility is suggested by a decremental hemoglobin response with addition of “other micronutrients”. In conclusion, synthesized evidence available at present does not indicate that an unselected addition of multiple-micronutrients to iron supplementation will result in a significant improvement in hemoglobin response in children. There is a suggestion that some micronutrients may even have a negative effect on the hematinic effect of iron. Routine addition of unselected multiple micronutrients to iron therefore appears neither appropriate nor justified for nutritional anemia control programs. There is an urgent need to evaluate the interactive effect of individual micronutrients with iron on the hemoglobin response to provide programmatic direction.

25.3

Effect of iron and multiple micronutrient supplementation on mental development in children

The role of single micronutrients on cognitive performance of children has been investigated in many nutrition interventions. From these studies, it can be concluded that there is strong evidence for a beneficial effect of iron and iodine on cognition, while evidence for other micronutrients such as B-vitamins and zinc is plausible given their biological role in brain function [12]. Iron is required for proper myelination of the spinal cord and white matter of cerebellar folds, and it is a cofactor for a number of enzymes involved in neurotransmitter synthesis (serotonin, norepinephrine and dopamine) [13, 14]. Iodine is needed for the production of the thyroid hormones triiodothyronine (T3) and thyroxin (T4), which are essential for growth and development of the fetal brain [15]. Zinc is essential for neurogenesis, neuronal migration, and synaptogenesis and its deficiency could interfere with neurotransmission and subsequent neuropsychological behaviour [16]. B vitamins have a role as coenzymes in numerous metabolic processes, including formation of neurotransmitters (communication in the brain), neural tube formation, and synthesis of myelin basic protein (myelination of nerves) [12]. Amongst all these the strongest evidence of benefit of supplementation through well conducted RCTs and systematic reviews is restricted to iron and iodine supplementation. In a systematic review assessing the effect of iron supplementation on mental and motor development in children, the authors showed that iron supplementation did have a significant positive effect on mental development, albeit modestly [17]. The positive effects of iron were more pronounced in older and iron deficient, anemic children.

Iron and multiple micronutrient supplementation in children

669

The mental development in children less than 2 years of age and the motor development were not affected by supplementation, indicating an irreversible effect of iron deficiency in this subgroup. There is a possible preventive role of iron supplementation in preventing cognitive deficits even in children who are apparently iron replete. Previously conducted qualitative reviews have shown multiple micronutrient supplementation to be beneficial in neurocognitive development of children [18]. Recently a systematic review assessing the effect of multiple micronutrient supplementation on cognitive performance in children was conducted by Eilander et al [19]. This review synthesized data from 20 RCTs and concluded that there was a marginally positive effect of multiple micronutrient supplementation on fluid intelligence in children (statistically not significant) and no effect on crystallized intelligence. There was a statistically significant effect on academic performance in older children but the number of studies (four) found to be too few to derive any intelligible conclusions. These conclusions were very much in agreement with previously conducted reviews that had focussed on individual domains of mental development [18].

25.3 Effect of multiple micronutrient supplementation on fluid intelligence in children [19].

Looking at the currently available data, there is definitely a case for iron supplementation in improving mental and motor development, more so, as preventive therapy. However, no robust evidence links routine multiple micronutrient supplementation with improvement in cognitive performance in children so as to suggest recommendation for supplementation as a public health measure.

670

#.4

Public health nutrition in developing countries

Iron and multiple micronutrient supplementation in children and growth

Given the widespread prevalence of stunting and wasting in the world, especially in South Asia and Sub-Saharan Africa, its appropriate management has occupied many a scientific minds. It is obvious that the most needed therapies would include ensuring adequate protein and caloric intake, and access to health care for timely treatment of morbidities. However, despite addressing these concerns in large public health interventions has not always yielded the expected results. This led to two major interventions apart from the ones already stated – exclusive breastfeeding and micronutrient supplementation. Regarding the latter, a large number of trials have been conducted globally that have assessed the effect of both individual micronutrient and multiple micronutrient supplementation on growth in children, and these have been followed by meta-analyses as well that have tried to synthesize the available information quantitatively. The most widely cited meta-analyses was the one conducted by Brown et al [20] that showed zinc supplementation to be associated with a beneficial effect on the linear growth in children. Systematic reviews on the same topic with reference to iron and vitamin A, however, failed to show any such benefit. In fact, one of these reviews even indicated at the possibility of a negative effect of iron supplementation in iron replete children and with longer duration (>6 months) of iron supplementation [21, 22]. One meta-analysis suggests the possibility of a beneficial effect with multiple micronutrient supplementation [10]. Some of these systematic reviews are more than 5 years old and a number of trials have been conducted on this topic since then, the most notable amongst which is the International Research on Infant Supplementation Initiative (IRIS) trial which is a large multicentric trial that evaluated the effect of multiple micronutrient supplementation in young children. In order to incorporate the new data available, a systematic review was conducted on the effect of individual and multiple micronutrient supplementation on growth in children [23]. The findings of this review were almost similar to the previously conducted reviews. Iron (27 trials) and vitamin A (17 trials) had no effect on physical growth. Zinc supplementation (43 trials) had a small positive effect on WAZ (weight for age) scores but no effect on linear growth, in contrast to the Brown meta-analyses. Multiple micronutrient supplementation was associated with an improvement in height but the effect size was very small.

Iron and multiple micronutrient supplementation in children

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25.4 Effect of multiple micronutrient supplementation on height gain in children [23]

The results from these reviews suggest that though micronutrient interventions (single and multiple) may have a marginal effect on anthropometric parameters, the effect on height is small. The series of systematic reviews conducted so far suggest that iron supplementation alone has a positive effect on hematological parameters and mental development in children. The effect on growth and anthropometry is minimal. This, to a certain extent, justifies the need for mass scale iron supplementation programs for amelioration of anemia and to achieve optimal mental development, albeit with realistic expectations.

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However, the addition of multiple micronutrients does not seem to offer any additional benefit as far as the specific outcomes on anaemia, mental development and growth is concerned. Furthermore, in some cases indiscriminate addition of micronutrients may even have a deleterious effect. This may be attributed to a number of reasons – the limited number of studies that differentiate between a therapeutic and preventive effects of supplementation, short duration of most of the supplementation trials, lack of uniformity of the composition of the combination of micronutrients used, variation in the settings in which the trials were conducted, the lack of understanding of the physiologic role of some of the micronutrients in developing human body and the interactions that occur in vivo when a number of micronutrients are given simultaneously, and the limiting role of other factors like poor complementary feeding, poverty and lack of food security, infections and infestations, inadequate stimulation etc. A better understanding of these issues and a clearer elucidation of micronutrient interactions is required. Presently, there is no scientific basis to support routine multiple micronutrient supplementation in children as a public health measure.

References 1. United Nations Administrative Committee on Coordination Sub-Committee on Nutrition (ACC/SCN) (2000). Fourth Report on the World Nutrition Situation. Geneva: ACC/SCN in collaboration with International Food Policy Research Institute. 2. MASON JB, et al. (2001) The micronutrient report: Current progress and trends in the control of vitamin A, iodine, and iron deficiencies. Ottawa, The Micronutrient Initiative (Accessed at http://www.micronutrient.org on September 8, 2004). 3. SINGH P and TOTEJA GS (2003). Micronutrient profile of Indian children and women: summary of available data for iron and vitamin A. Indian Pediatr, 40, pp. 477–479. 4. BEATON GH and MCCABE GP (1999). Efficacy of intermittent iron supplementation in the control of iron deficiency anaemia in developing countries: an analysis of experience. Ottawa, The Micronutrient Initiative. 5. SCHOLL T and HEDIGER M (1994). Anaemia and iron deficiency anaemia: compilation of data on pregnancy outcome. Am J Clin Nutr. 59, pp. 492S–500S. 6. GERA T, SACHDEV HP, NESTEL P , SACHDEV S (2007). Effect of iron supplementation on haemoglobin response in children: systematic review of randomised controlled trials. J Pediatr Gastroenterol Nutr., 44(4), pp. 468–486. 7. HODGES RE, et al (1978). Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr, 31, pp. 876–885. 8. CAMPBELL TC, BRUN T , JUNSHI C , ZULIN F , PARPIA B (1990). Questioning riboflavin recommendations on the basis of a survey in China. Am J Clin Nutr, 51, pp. 436–445. 9. BAKER SJ (1981). Nutritional anemias. Part 2: Tropical Asia. Clinical Haemat. 10, pp. 843–871.

Iron and multiple micronutrient supplementation in children 10.

11.

12. 13. 14. 15.

16.

17.

18. 19.

20.

21. 22.

23.

ALLEN LH , PEERSON JM , OLNEY DK

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(2009). Provision of multiple rather than two or fewer micronutrients more effectively improves growth and other outcomes in micronutrient deficient children and adults. J Nutr, 139, pp. 1022–1030. GERA T , SACHDEV HP , NESTEL P (2009). Effect of combining multiple micronutrients with iron supplementation on Hb response in children: systematic review of randomized controlled trials. Public Health Nutr, 12(6), pp. 756–773. BRYAN J , et al (2004). Nutrients for cognitive development in school aged children. Nut Rev, 62, pp. 295–306. BEARD JL , CONNOR JR , JONES BC (1993). Brain iron: location and function. Prog Food Nutr Sci, 17, pp. 183–221. BEARD JL, CONNOR JR , JONES BC (1993). Iron in the brain. Nutr Rev; 51, pp. 157–70. MELSE -BOONSTRA A , JAISWAL N (2010). Iodine deficiency in pregnancy, infancy and childhood and its consequences for brain development. Best Pract Res Clin Endocrinol Metab, 24(1), pp. 29–38. BOURRE JM (2006). Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging, 10, pp. 377–385. SACHDEV HPS , GERA T, NESTEL P (2005). Effect of iron supplementation on mental and motor development in children. Public Health and Nutrition, 8(2), pp. 117–132. BENTON D (2001). Micro-nutrient supplementation and the intelligence of children. Neurosci Biobehav Rev, 25, pp. 297–309. EILANDER A , GERA T , SACHDEV HS , TRANSLER C , VAN DER KNAAP HC , KOK FJ , OSENDARP SJ (2010). Multiple micronutrient supplementation for improving cognitive performance in children: systematic review of randomized controlled trials. Am J Clin nutr, 91, pp. 115–130. BROWN KH , PEERSON JM , RIVERA J , ALLEN LH (2002). Effect of supplemental zinc on the growth and serum zinc concentrations of prepubertal children: a metaanalysis of randomized controlled trials. Am J Clin Nutr; 75, pp. 1062–1071. RAMAKRISHNAN U , ABURTO N , MCCABE G , MARTORELL R (2004). Multimicronutrient growth: results of 3 meta-analyses. J Nutr, 134, pp. 2592–2602. SACHDEV H , GERA T , NESTEL P (2006). Effect of iron supplementation on physical growth in children: systematic review of randomised controlled trials. Public Health Nutr, 9, pp. 904–920. RAMAKRISHNAN U , NGUYEN P and MARTORELL R (2009). Effects of micronutrients on growth of children under 5 y of age: meta-analyses of single and multiple nutrient interventions. Am J Clin Nutr, 89, pp. 191–203.

26 Nutritional anemia during pregnancy, early childhood and adolescence: the critical development periods Subadra Seshadri

Subadra Seshadri MSc, MS, PhD, a senior nutrition consultant, was formerly Professor and Head of the Department of Foods and Nutrition at M S University of Baroda. She is the recipient of Dr S G Srikantia Memorial Lecture Award 2005 of the Nutrition Society of India. Her significant research contributions to nutritional anemia, especially iron deficiency anemia and cognition, are widely recognized. Dr Seshadri has served as a technical expert on micronutrient research and development to WHO, UNICEF and others.

$.1

Introduction

Nutritional anemia is a major public health problem worldwide, affecting an estimated 2 billion people, most of them in the developing world [1–2]. Given the impact that nutritional anemia has on psychological and physical development, behavior and work performance, it is a problem of serious public health significance. Iron deficiency is by far the commonest cause of nutritional anemia [3–4]. Iron deficiency occurs when an insufficient amount of iron is absorbed to meet the body’s requirements. This insufficiency may be due to inadequate iron intake from the diet, to reduced bioavailability of the dietary iron, or to increased needs of iron as occurs during infancy and pregnancy. Only when iron deficiency is prolonged does it lead to anemia, a condition in which hemoglobin level in the blood falls below normal for a given age and sex group. Iron deficiency is usually diagnosed with the help of several laboratory tests. These include serum iron, iron binding capacity, transferrin saturation, serum ferritin, transferrin receptors and erythrocyte proto porphyrin concentration in blood. In iron deficiency anemia, in addition to the changes in the above parameters, there is a gradual fall in blood hemoglobin level below

674

Nutritional anemia during pregnancy, early childhood ...

675

normal resulting in different degrees of anemia from mild to moderate to severe. While iron deficiency is the most common cause of anemia in India and the other developing countries, other nutritional deficiencies such as low intake of folic acid, vitamin B 12, riboflavin, vitamin A and vitamin C can all influence the etiology of anemia [3, 5, 6]. Important among these is folic acid deficiency. Combined folate and iron deficiency is especially common in women in the second half of pregnancy, in India [7]. Anemia is common in children suffering from severe protein energy malnutrition. Vitamin B12 deficiency in strict vegetarians leads to anemia which is usually megaloblastic (the red cells are larger than normal in size) as against the microcytic anemia of iron deficiency (the red cells are smaller in size compared to normal). Folate deficiency also manifests as a megaloblastic anemia. If iron, folate and vitamin B 12 deficiencies co exist, the latter will become apparent only after iron deficiency has been corrected, thus making it necessary to use laboratory tests other than hemoglobin and red cell morphology for the diagnosis of these deficiencies. Besides folate and vitamin B12 deficiencies, two other nutrient deficiencies involved in the causation of anemia, are riboflavin and vitamin A. Thus, multiple nutrient deficiencies may be involved in the pathogenesis of anemia. However, it is important to appreciate that iron deficiency is the major cause of anemia in the developing world, with some recent studies suggesting that 50% of all the anemias may be estimated to be due to iron deficiency. Additionally, there are a similar number of people manifesting iron deficiency without anemia, thus placing iron deficiency as the most common public health nutritional deficiency the world over [3].

26.1.1 Definition of nutritional anemia Nutritional anemia in general is defined as a condition that results in a lowering of hemoglobin (Hb) levels below what is considered to be normal for specific demographic groups regardless of the underlying nutritional deficiencies that may be the cause. A WHO group of experts in 1971 defined normal hemoglobin concentration in the following terms: “It is recognized that there is a homeostatic mechanism that sets the hemoglobin level in each individual. Whereas it is not known whether this is the optimum level for health it is accepted as ‘normal’ for the individual.The distribution of such normal values in the population should be derived from a representative sample of healthy persons in whom the presence of nutritional deficiencies has been excluded by specific laboratory determinations or by prior administration of hematinics.This distribution of normal values is likely to be the same throughout the world when allowance is made for factors such as age, sex, pregnancy and altitude” (WHO, 1972).

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Nutritional anemia is thus defined “as a condition in which the hemoglobin level is below the level that is normal, for a given individual due to deficiency of one or more of the nutrients required for hemopoiesis and conversely as a condition in which the hemoglobin concentration can be raised by increasing the amount of nutrients absorbed”. “In a community in which there is no anemia, the frequency distribution curve of hemoglobin concentration follows a nearly normal distribution, but in a community with a high prevalence of anemia the frequency distribution curve will be skewed to the left” [8]. The criteria for determining the presence of nutritional anemia, was first recommended by WHO in 1968. A subsequent WHO committee has recommended that 11.5 g/dl be considered as the cut-off for anemia for school children aged 5–11 years. In addition, there is also defined hemoglobin cut-off values for various degrees of anemia. Moderate anemia is defined as hemoglobin levels below 10 g/dl and severe anemia as hemoglobin levels below 7 g/dl in individuals and population groups. Table 26.1 Hemoglobin values below which anemia is likely to be present in populations living at sea level as proposed by WHO in1968 [9] and modified for 5–11 year-old children later in 1998 [10] Groups

Hemoglobin level below which anemia is considered to be present (g/dl)

Children 6 months to 6 years Children 5–11 years Children 12–13 years Adult males Adult females (non-pregnant) Adult females (pregnant)

11.0 11.5 12.0 13.0 12.0 11.0

Additionally, epidemiological criteria for assessing the severity and the magnitude of nutritional anemia in populations [11] have also been proposed. Population prevalence for defining the severity of the problem Parameters

Magnitude High

Moderate

Low

Percent of population with Hb level less than the above cut-off points

>40

10–39

<10

Percent of population with Hb level less than 7 g/dl especially women and children

>10

1–9

<1

While the causes of anemia have been known for a long time, the multiple adverse functional effects of anemia have been brought to light only recently. Physical work capacity, mental functions and cognitive development, immune functions and pregnancy outcome are all affected adversely in iron deficiency

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anemia [12–17], thus contributing to the erosion of human resources in a country like India, making it imperative to have clear policies and programs for the prevention and correction of anemia. This chapter would first outline the global prevalence of anemia in different age, sex and physiological groups, followed by prevalence in India. The various factors in the etiology of nutritional anemia will then be discussed, followed by iron requirements of different age groups and physiological conditions, focusing on why some demographic groups are much more vulnerable to anemia than the others. This is followed by methods for assessment of anemia, indicators of iron, folic acid and B12 deficiencies and the functional consequences of anemia. In the final section public health approaches for the prevention and control of anemia will be discussed. Through out this chapter, the term anemia is used to refer to nutritional anemia, i.e. anemia caused by nutritional deficiencies directly through inadequate diets or indirectly through conditions that increase the iron requirements. Anemias of other etiology, such as genetic anemia, are not within the scope of this chapter.

26.2

Prevalence of anemia: global and the Indian population

26.2.1 Global prevalence of anemia Global and regional prevalence of anemia has been reported recently in a WHO publication for preschool-age children (<5 years) and for pregnant and non pregnant women [1]. These figures represented in the Table 26.2 below show that globally the prevalence of anemia is the highest in pre school age children, 47.4%, followed by pregnant women, 41.8% and lowest in non pregnant women, 30.2%. The prevalence figures are reported for 6 regions, namely Africa, Asia, Europe, Latin America, North America and Oceania. Highest prevalence in all the three groups is seen in Africa which is followed by Asia. Table 26.2 Global and regional prevalence of anemia [1] Area

Global Africa Asia Europe Latin America North America Oceania

Preschool age children

Pregnant women

Non-pregnant women

Prevalence % in millions

Number

Prevalence Number % in millions

Prevalence % in millions

Number

47.4 64.6 47.7 16.7 39.5

293.1 93.2 170.0 6.1 22.3

41.8 55.8 41.6 18.7 31.1

56.4 19.3 31.7 1.4 36.0

30.2 44.4 33.0 15.2 23.5

468.4 82.9 318.3 26.6 33.0

3.4

0.8

6.1

0.3

7.6

6.0

28

0.7

30.4

0.2

20.2

1.5

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Public health nutrition in developing countries

However within Asia, the prevalence of anemia is quite high in South and South East Asia as seen from the 5th Report of the World Nutritions situation by the ACC-SCN, 2004 [18] (Table 26.3). Table 26.3 Prevalence of anemia in women (15–45 years) (5th Report of the World Nutrition Situation, ACC-SCN, 2004) [18] Regions and countries

Mild anemia (%)

Moderate anemia (%)

Severe anemia

Any anemia (%)

40.7 39.1 22.1

21.8 20.8 7.5

1.8 2.8 0.7

64.3 62.7 30.4

10.2 22.7

2.0 4.6

0.3 0.3

12.4 27.7

26.6

7.7

1.2

35.5

27.7

9.0

1.5

38.1

37.8

8.4

1.1

47.3

44.8 35.0

12.7 14.8

1.3 1.9

58.8 51.8

Bolivia, 1998 Haiti, 2000 Peru, 2000

20.7 36.3 25.4

5.6 15.8 5.9

0.9 3.0 0.3

27.1 55.1 31.6

Mild anemia women Moderate anemia

Hb 10–10.9 g/dl for pregnant women; Hb 10–11.9g/dl for non pregnant Hb 7–9.9 g/dl; Severe anemia Hb <7 g/dl

Sub-Saharan Africa Benin, 2001 Mali, 2001 Uganda 2001 North Africa West Asia/ Europe Armenia,2000 Egypt,2000 Central Asia Kazhakhastan 1999 Krygez Republic, 1997 Turkmenistan, 2000 South and south east Asia Cambodia,2000 India 1998–99 Latin America and Caribbean

Nationally representative data on iron deficiency and iron deficiency anemia has been reported for adolescents by the National Health and Nutrition Examination Survey III (NHANES-III) in the USA [19]. Iron deficiency was defined as having an abnormal value for at least two out of the three l a b o r a t o r y t e s t s o f i r o n s t a t u s ( e r y t h r o c y t e protoporphyrin, transferrin saturation, or serum ferritin); and iron deficiency anemia was defined as iron deficiency plus low hemoglobin. Prevalence was determined based on the 5 th percentile value of these parameters in the NHANES III data. Nine to eleven percent of adolescent girls and women of childbearing age

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were iron deficient; of these, iron deficiency anemia was found in 3% and 2–5%, respectively. Iron deficiency was found in no more than 1% of adolescent boys and young men. Among women of childbearing age, iron deficiency was more likely in those who were minority, low income, and multiparous. Table 26.4 Prevalence of iron deficiency and iron deficiency anemia in adolescent males and non-pregnant females [19] Gender and age (years)

Iron deficiency (%)

Iron deficiency anemia (%)

Females 12–15 16–19

9 11

2 3

Males 12–15 16–19

1 <1

<1 <1

As against this situation in US, an example of a well developed country, the prevalence of anemia in India among all demographic groups is high.

26.2.2 Prevalence of anemia in India Prevalence of anemia in India, in the different demographic groups is shown in Table 26.5. Table 26.5 Prevalence of anemia in India Group

Reference

Prevalence (%)

Pregnant women

ICMR ICMR NFHS NFHS

87 85 50 58

Early childhood to pre-school

NFHS II, 1998–99

1989 [20] 2001 [21] II 1988–89 [22] III, 2006–07 [23]

74

Children (6 to 35 months)

NFHS III, 2006–7

79

Adolescent girls

SESHADRI, 1999, Rural Gujarat [24] SESHADRI, 1999, Urban affluent [25] ICMR, 2001, Rural India

62 22

NFHS II 1998–99

52

NFHS III 2006–07

56

90

Adult women Ever married women (15–49 years) Ever married women (15–49 years)

Pregnant women Nationally representative data on prevalence of anemia in pregnant women in India were generated in the year 1989 through a country wide evaluation

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Public health nutrition in developing countries

of the anemia control program that was launched in 1975 but had not been evaluated since then. For the study of hemoglobin by the cyanmethemoglobin method, 4775 pregnant women at or beyond 20 weeks of gestation from 10 states and the union territory of Delhi were examined. The prevalence of anemia defined as Hb less than 11 g/dl was 87%. Other large scale studies since then have found the prevalence to be quite high, in the range of 80% and above [21]. However, the National Family Health surveys II and III [22, 23] have reported a somewhat lower prevalence of anemia which is attributed to a different method used for assessment of Hb rather than a fall in the prevalence rates. Early childhood Studies prior to 1985 in India gave an average prevalence rate of 68% in pre-school children [26]. More recently ICMR carried out a prevalence survey of anemia in preschool children from four regions of India. The NFHS II and III have also carried out Hb assays in a large sample of pre school children. The prevalence rates in children remain high, above 70 % and have shown no decline since the last four decades. See Table 26.4 for details. Adolescent females The prevalence of anemia in adolescent girls has been reported by a number of studies recently in India and all of them point to high prevalence, in the range of 60–90% in girls aged 11–18 years (Table 26.5), much higher than the 20% population prevalence cut-off for nonpregnant women in reproductive age group that was identified by WHO to classify the problem as one of public health significance. Thus there is enough evidence to establish that anemia is a major public health problem among adolescents also in India and needs to be tackled by appropriate public health measures.

26.3

Causes of nutritional anemia

While the major cause of nutritional anemia in India and the world over is related to dietary inadequacies, often these dietary inadequacies are aggravated by environmental factors such as poor sanitation leading to helminthic and protozoal infestations and infection with malarial parasites. Therefore, dietary factors as causative agents will have to be seen in conjunction with the other environmental factors while talking of preventive public health approaches.

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26.3.1 Deficiency of several nutrients involved in etiology of anemia Dietary deficiency of several micro nutrients can lead to anemia. These include, iron – a major dietary factor in the causation of anemia while other nutrient deficiencies such as folic acid, vitamin A [27–29], riboflavin [30] and vitamin B12 [31] contribute in a secondary manner. The cellular events in iron deficiency that eventually lead to anemia are well documented. Iron is needed for the synthesis of hemoglobin, the main oxygen carrier in the blood; for the synthesis of myoglobin that serves as a ready source of oxygen for the oxidative processes in muscle, and for the synthesis of heme and non-heme proteins involved in cellular processes. Deficiency of iron results in impaired production of these molecules eventually leading to low hemoglobin levels and anemia.

26.3.2 Low dietary intake of iron – a major cause of anemia in India Several dietary intake studies have been carried out in India, using a diet history, a 24 h dietary recall or weighed food intakes. Such larger studies have been done as a part of the National Nutrition Monitoring Bureau surveys [32–34]. In general, these studies indicate that iron intakes as a percent of the recommended dietary allowances set by the ICMR in 1989 is no more than 50. Thus low intakes are the order of the day. Even on these low intakes, the anemia prevalence figures need not be so high if the dietary iron bioavailability is high. Unfortunately, the iron bioavailability from Indian diets is one of the lowest in the world.

26.3.3 Low iron bioavailability is another major cause of anemia in India Bioavailability of iron is defined as the fraction of the dietary iron absorbed and utilized for specific functions such as the synthesis of hemoglobin, heme containing enzymes and other iron containing functional proteins [35]. It is dependent on a variety of dietary factors such as the chemical form in which iron is present in foods, i.e. heme iron versus non-heme iron, its solubility in the gastro intestinal tract and the various iron absorption promoters and inhibitors in the foods which decide what fraction of the dietary iron will be absorbed and utilized [36]. There are two major chemical forms of iron in a mixed diet, and each is absorbed by a different mechanism. Heme, containing iron in a porphyrin ring structure is found in hemoglobin and myoglobin and accounts for

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nearly 40% of the iron present in animal tissue including fish and poultry [37]. Because of the porphyrin ring structure the iron in heme containing molecules is protected from the action of complexing agents present in the meal and is taken up by the mucosal cells as the intact protoporphyrin complex. Absorption of heme iron is therefore high averaging 15% in iron replete individuals to 35% in those lacking iron stores [38]. Once absorbed by the cell, iron in the heme molecule is split by a specific enzyme, xanthine oxidase. After this, the iron from the heme and non-heme sources form a common pool with in the cell. The other chemical form of iron, namely non-heme iron is present largely in foods of vegetable origin and in non cellular animal foods such as eggs and dairy products. In addition, approximately half of the iron in meat, fish and poultry is non heme. The specific rate of non heme iron absorption depends upon other dietary constituents ingested concomitantly as well as the iron status of the individual [36]. Hence absorption of non-heme iron ranges widely from 2% to 20% depending on the above two determinants [38]. The various dietary factors affecting non heme iron bioavailability are shown in Table 26.5 below. The two major enhancers of iron absorption are: ascorbic acid and flesh foods like meat, poultry and fish, where as the inhibitors far outnumber the enhancers, especially in the Indian dietaries. Table 26.6 Food components affecting dietary non heme iron bioavailability [36] (Potency is indicated in terms of + signs. The sign +++ indicates highest positive effect for enhancers and highest negative effect for inhibitors. For example tea has a most potent inhibitory effect on iron absorption while ascorbic acid is a very potent enhancer of iron absorption.) Food Components – The Enhancers and Inhibitors

Potency

ENHANCERS Ascorbic acid Animal tissue

+++ +++

INHIBITORS Tea Soy products Coffee EDTA Calcium/Phosphate salts

+++ +++ ++ ++ ++

Eggs Yolk Albumen Wheat bran Phytate Fiber

++ ++ +++ + +

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Ascorbic acid has been shown to be a powerful enhancer of iron absorption. Several in vivo studies have been carried out using crystalline ascorbic acid as well as ascorbic acid from food sources [39–42]. The major findings that emerge from these studies are: 1. Ascorbic acid enhances iron absorption from both low and high bioavailability meals, when added as crystalline ascorbic acid or from food sources. 2. The magnitude of increase is much higher in the low availability non heme iron containing meals than in the high availability heme iron containing meals. 3. The increase in absorption that occurs with ascorbic acid is influenced by the ascorbic acid to iron molar ratio, larger the ratio, higher the absorption. 4. Further the ascorbic acid effect has also been shown to be dose dependent, up to a level of 1000 mg. However, the enhancing effect of ascorbic acid at lower dose level is much higher than the enhancing effect at higher levels. Thus although dose dependent, it is not necessary in practical diets to have high levels of ascorbic acid to bring about a significant increase in absorption of iron. In vivo absorption studies have shown that 30 mg of ascorbic acid can increase the iron absorption twofold while 50–75 mg can bring about 3–5 fold increases in iron absorption. In other words within the range of physiological intakes, iron absorption especially from typical non heme iron containing diets can be increased very significantly, a finding that needs to be translated into dietary practices much more vigorously. Ascorbic acid operates in multiple ways to increase iron absorption, by forming a soluble complex at the acidic pH in the stomach that remains soluble as the pH rises in the small intestine, by reducing the ferric to more readily absorbed ferrous ions, by preventing the formation of insoluble complexes with the inhibitors and by preferentially donating its iron to the brush border receptors to increase iron uptake by mucosal cells. Meat and flesh foods in addition to containing better bioavailable iron, also possess the ability to enhance non heme iron absorption from primarily vegetarian diets [43–44]. The potency of 100 g of cooked meat in enhancing iron absorption has been graded as equal to that of 100 mg ascorbic acid [37]. Given the economic constraints to the consumption of flesh foods, the only enhancer of significance in the predominantly vegetarian Indian dietaries is ascorbic acid. The inhibitors of iron absorption on the other hand far outnumber the enhancers, as is evident from Table 26.5. In general, the enhancers form soluble complexes with non-heme iron which readily give up their iron to iron binding proteins present on the

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microvilli of the intestinal lumen that in turn facilitate absorption across the lumen into the mucosal cells. On the contrary, the inhibitors form insoluble complexes with non-heme iron that remain insoluble and do not release the iron for absorption. Extensive studies on iron absorption from typical diets have shown that the Indian vegetarian diet high in cereals and pulses and low in fruits and vegetables, accompanied by tea, has the lowest iron bioavailability. Table 26.7 shows iron bioavailability in some typical meals estimated in vivo. Table 26.7 Iron bioavailability in some typical meals [45–49] S. Type of meal no.

Ingredients

Bioavailability In vivo

Reference

1.

Wheat flour, oil, potato Onion, tea, milk and sugar, Rice, red gram dhal, potato, onion, brinjal, oil, milk Ragi, potato, onion, brinjal, oil, tea, milk, and sugar Sorghum, potato, onion, brinjal, oil Tea, milk and sugar Commercial product containing minced meat, bread, onion sauce, Brussels sprouts Potatoes, maize, black beans, rice, Rice, cat fish, spinach, fish paste, beans and spices Maize, butter, cheese, oats, milk Maize, black beans, fish paste, plantain, tomato, potato, carrot, meat Maize, rice, plantain, fish, avocado, tomato, onion, water melon Maize, milk, plantain, fish, pumpkin, papaya, coffee, sugar

1.8

45

4.5

45

0.9

45

0.8

45

38.8

46

3.2

47

12.0

48

1.3

49

3.9

49

6.7

49

11.1

49

2. 3. 4.

Indian wheat break fast Indian rice lunch Indian Ragi breakfast Indian break fast

5.

Hamburger meal

6.

Latin American meal South East Asian rice and fish meal Venezuelan breakfast Venezuelan lunch

7. 8. 9.

10. Venezuelan lunch 11. Venezuelan supper

In addition to the dietary factors, iron status of the individuals also plays a crucial role in determining the amount of iron absorbed. Iron deplete individuals absorb more iron from the same meal compared to iron replete individuals. The molecular basis of iron absorption is discussed under the section on iron homeostasis. Thus to summarize, the chemical form of iron, the balance of the enhancers and inhibitors of iron absorption in the diet and the iron status of the individual are the three major factors that influence the amount of iron absorbed and transported to the body for specific functions which is

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defined as iron bioavailability. Given that the predominant chemical form of iron in the Indian dietary is non-heme iron and the inhibitors far outnumber the enhancers, in addition to the intake of enhancers being highly seasonal and very low most of the time, the absorption of iron is considered to be not more than 3–5% in most regional diets in India [50].

26.3.4 Parasitic infestations Parasitic infestations aggravate the already existing states of nutritional deficiencies, especially iron, and may push the affected individuals into overt anemia. In this context, hook worms (Ancylostoma duodenale and Necator Americanus) are the most deleterious followed by whip worms (Trichuris Trichuria), both of which cause blood losses. Blood loss due to hook worms may vary from 2 ml to 100 ml per day [51] according to the severity of infestation. In a population whose iron status is already compromised by low dietary intake of iron and poor bioavailability, a small load of hook worms can precipitate anemia. Over a period of time, even small hookworm loads can cause blood losses sufficient to deplete iron reserves, placing these individuals at high risk of developing anemia. For example, blood loss of 1ml per day equivalent to 0.347 mg of iron at a Hb level of 10 g/dl can cause a loss of 250 mg of iron over two years which approximates the total body iron stores in an adult woman in India. The reported prevalence of hook worm infestation increases with age in children. Therefore the greatest effect of hook worm infestation is seen in school aged children and adults. Approximately 20% of the world’s population is reported to be infected by hook worms [52] Further some work places are particularly prone to hookworms such as the tea plantations where the moist unsanitary conditions coupled with walking bare foot makes the workers contract the infestation easily [53]. The other parasites like round worms (Ascaris lumbricoides) act by impairing absorption, the effect not confined only to iron but extend to other nutrients such as vitamin A; severe round worm infestation is reported to act by reducing the appetite and food intake. Poor sanitary and environmental conditions, over crowding and illiteracy, all favor the spread of helminthic infestations.

26.3.5 Chronic recurrent infections, malaria and human immunodeficiency virus Chronic recurrent infections could also be one of the causes of anemia. A trend towards lower hemoglobin levels is reported in infections and inflammatory processes. Malaria is a major factor causing severe anemia in pregnancy and infancy, common in African countries [52, 54]. Malaria

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is thought to be the primary cause of severe anemia in at least 50% of subjects living in malaria endemic areas. A recent study in Tanzania confirmed malaria as the largest contributor to severe anemia in infants, 60% severely anemic due to malaria as against 30% due to iron deficiency [55]. Anemia associated with malaria is caused by hemolysis of the red blood cells, suppressed erythropoiesis, and secondary folate deficiency due to increased folate requirement consequent to acute hemolysis [52]. Longitudinal studies have shown that pregnant women are more susceptible to malarial parasites, compared to non pregnant women. A group that appears to have particularly lowered immunity to malaria in endemic areas is women in their first pregnancies [56]. Malaria in pregnant women is associated with low birth weight, pre mature deliveries and still births. Although a direct effect of malaria on these adverse effects cannot be ruled out, it appears that for the most part, these effects are due to the severe anemia caused by malarial parasitosis [57]. Malaria chemoprophylaxis is shown to be effective in abolishing parasitemias and in prevention of anemia, in pregnant women and young children living in malaria endemic areas [52]. However, the chemoprophylaxis for pregnant women should be given only after 19th week of pregnancy [57]. Malaria induced hemolysis increases the requirement for folic acid and results in megaloblastosis that can be corrected by chemoprophylaxis. HIV infection is another cause for concern in the anemia situation, particularly in Africa [52]. A WHO report on severe anemia recommends that when anemia is associated with leucopenia (an abnormal lowering of white cell count) and thrombocytopenia (an abnormal drop in the number of blood cells, called platelets, involved in forming blood clots), the possibility of HIV infection must be suspected [57] . Cytopenias (low count of different types of blood cells) of all major blood cell lines are common in Acquired Immune Deficiency Syndrome (AIDS). In one early series of patients with AIDS, anemia was noted in approximately 70 percent, lymphopenia in 70 percent, neutropenia in 50 percent, and thrombocytopenia in 40 percent [58]. The incidence of the various cytopenias correlates directly with the degree of immunosuppression. Anemia is the most common hematologic abnormality associated with HIV, affecting 60 to 80 percent of patients in late stage disease. While it may be a mere laboratory abnormality in some individuals, in others typical symptoms may be present – fatigue, dyspnea, reduced exercise tolerance, and diminished functional capacity – that are directly related to a reduction in hemoglobin. In a review of more than 32,000 patients infected with HIV, the yearly incidence of developing anemia was reported to increase with disease progression, affecting 3% of all patients with asymptomatic HIV infection, 12% of asymptomatic patients with CD4 cell counts below

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200/μL, and 37% of patients with an AIDS-related illness [59]. Another source reports that up to 70% of people with AIDS are anemic [52]. Anemia of HIV is multifactorial. HIV infection per se causes anemia. Other common causes are anemia of chronic disease as a result of opportunistic infections secondary to HIV, suppression of the bone marrow by anti retroviral therapy and hemolytic anemias induced by oxidant drugs [60]. Treating reversible causes of anemia including treatment of opportunistic diseases, correcting deficiencies in vitamin B 12 or folic acid, changing myelosuppressive medications if feasible and appropriate, may all improve anemia in the appropriate setting. Effective antiretroviral therapy administered to all patients is expected to correct the anemia substantially if not completely.

26.4

Iron homeostasis

Iron homeostasis is maintained in the body by internal factors primarily by modulating iron absorption. Unlike other nutrients, iron is unique as once absorbed it is held within the body tenaciously with no physiological mechanism for its excretion. Excess iron accumulation within the body results in iron overload which is toxic while iron deficiency results in anemia of varying severity and causes several functional impairments. Both these are averted under normal conditions by a set of internal factors that regulate body iron stores primarily through regulation of iron absorption. Iron status of the individuals plays a very crucial role in determining the amount of iron absorbed. Iron deplete individuals absorb more iron from the same meal compared to iron replete individuals. The molecular basis of iron absorption and the different factors involved in the regulation of iron absorption are briefly reviewed. Iron absorption involves the uptake of iron from the lumen of the intestine into the enterocytes and transfer across the baso lateral membrane into the portal blood circulation. Each step involves the participation of a transmembrane transporter coupled to an enzyme that changes the oxidation state of iron. Several key proteins are needed for the absorption and transport. These are duodenal cytochrome b (Dcytb), divalent metal iron transporter 1 (DMT 1), hephaestin and ferroportin [61]. Dcytb is a ferri reductase attached to the micro villi on the outer surface of the enterocytes. It reduces the ferric ions into the more readily absorbable ferrous ions and forms a tiny door way for the passage of iron into the body of the enterocyte. DMT 1, a divalent metal ion transporter is a brush border transmembrane transporter for several divalent cations including iron, copper and zinc. It pumps iron into the enterocyte by an active proton coupled transport mechanism requiring energy. DMT 1 transports only

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ferrous ions and so reduction of ferric ions to ferrous ions by Dcytb is a pre requisite. The amount of DMT 1 in the apical membrane is regulated by body iron requirements. Once inside the enterocytes iron can take one of the two path ways .It may be incorporated into ferritin and stay within the enterocytes until the enterocytes are sloughed off and the iron is lost from the body. Alternately the iron may be taken to the baso lateral membrane across which it is transported into the blood stream by means of a specific iron carrier protein, ferroportin. It is then oxidised by a membrane bound ferroxidase, hephaestin, yielding ferric ions that are bound by plasma transferrin for distribution around the body via the blood. Expression of DMT1, ferritin and ferroportin mRNA’s is posttranscriptionally controlled by the IRP/IRE system to protect enterocytes from iron excess or depletion while allowing efficient iron flux across these cells. The mRNAs which code for these proteins have a region (iron responsive element, IRE) which can bind to iron regulating protein (IRP). The extent of binding will up or down regulate the production of DMT 1, ferritin or ferroportin. In iron excess, DMT 1 and ferroportin are down regulated while ferritin is up regulated resulting in removal of iron from the body along with the senescent enterocytes. In iron deficiency, the converse occurs resulting in greater absorption of iron into the blood stream [62]. Ferroportin as well as hephaestin are under the control of hepcidin, a peptide hormone secreted by the liver in response to three major stimuli: (1) body iron stores, (2) demand for erythropoiesis, and (3) hypoxia. The expression of hepcidin, the principal hormone involved in iron regulation, offers a unified mechanism to account for changes seen in iron deficiency, hereditary hemochromatosis and in chronic inflammatory disorders. When body iron stores tend to fall or demand for erythropoiesis is increased, hepcidin is down regulated, with its secretion falling to low levels. When body iron stores are adequate and or demand for erythropoiesis is reduced, hepcidin is upregulated, resulting in increased secretion of the hormone. Hepcidin acts by binding to ferroportin and blocking the transport of iron across the baso lateral membrane, thus regulating the amount of iron absorbed depending on the iron status of the individual. Hepcidin expression is under the control of at least three genes, HFE (hemo chromatosis gene), TFR 2 (Transferrin receptor 2) and HJV (hemo juvelin). The molecular mechanism of action of these is yet to be unraveled [61]. Figure 26.1 provides a schematic representation of the regulation of iron absorption by the various proteins involved and by hepcidin. Heme iron absorption is less well understood. Heme is taken into enterocytes by a carrier mechanism. A folate transporter, PCFT (also called HCP1) may contribute to this process. Heme is degraded in enterocytes by heme oxygenase releasing iron ions for efflux via ferroportin.

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26.1 Schematic representation of iron absorption.

26.5

Iron requirements

In addition to the factors discussed under the causes of anemia that contribute to the high prevalence in the Indian population, increased iron requirements during pregnancy, early childhood and adolescence and the inability of the habitual diets to meet these increased requirements are also responsible for the high prevalence of anemia in these groups.

26.5.1 Iron requirements in pregnancy Studies on normal healthy pregnant women have shown that there is hardly any increase in iron requirements in the first trimester of pregnancy. However, during the second and third trimesters, there is an increase in

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maternal blood volume and transfer of iron to the fetus that impose a high demand for iron that cannot be met by the existing diets. The total iron cost of a pregnancy has been worked out to be 1100–1200 mg [63–65]. Table 26.8 Iron cost of pregnancy Requirements Fetus (at term) Expansion of red cell mass Placenta and umbilical cord Maternal blood loss during delivery Obligatory loss (wear and tear) Total iron cost 15 m of amenorrhea saves

Iron (mg) 280 450 90 150 230 1200 240–480

If the iron saved due to amenorrhea is taken into account, the net requirement of iron for a pregnancy is about 700–850 mg, which translates into an iron requirement of 4 mg/d over the last two trimesters. Since it is difficult to obtain the entire requirement through the diet, iron supplements need to be provided during pregnancy. It is the practice in developed countries like US to provide supplements of 30 mg iron per day while under the National Anemia Control Program in India, pregnant women are provided 100 mg elemental iron and 0.5 mg folic acid daily for at least 100 days during the second and third trimesters of pregnancy.

26.5.2 Iron requirements in infancy and early childhood During the first two years of life, there is rapid physical growth and brain development that increases the demand for tissue iron deposition. Iron content of breast milk is low (0.78 mg/l); however the iron in breast milk is well absorbed to the extent of 50% [70]. In a normal birth weight infant, this level of iron absorption from the breast milk ensures adequate amount of iron if the infant is exclusively breast fed. However, the iron stores of a healthy normal birth weight infant are exhausted by 6 months; while the iron requirement continues to remain high. With complementary feeding remaining very inadequate, infants from 6 months to 2 years are particularly highly vulnerable to anemia. A critical aspect of iron nutrition in infancy, as compared to adults, is the greater dependency of the infant on external sources of iron for red cell production. It has been calculated that in a 10kg, one year old infant the diet must provide 30% of the iron needed for hemoglobin turn over as against only 5% in an adult [66]. Estimated requirements of absorbed iron for infants in the first year and for children 1–8 years is shown in the Table 26.9 below. As seen, total absorbed iron requirements for 6–12 months old infants is 0.9 mg, which at the rate of an average bioavailability of 5% translates into 20 mg iron

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per day. It is evident that either supplemental iron will be needed or the dietary iron bioavailability should increase if the iron requirements of infants are to be fully met in developing countries. Beyond 1 year the total absorbed iron requirement drops to about 0.8 mg per day. Table 26.9 Estimated requirements of absorbed iron for children (mg/day) [66] Age

0–6 months

6–12 months

1–2 years

2–8 years

Requirements for growth

0.25

0.53

0.29

0.23

Iron losses Total requirements

0.24 0.49

0.37 0.90

0.46 0.75

0.56 0.79

One third of all infants born in India are of low birth weight (LBW), defined as birth weight less than 2500 g. Low birth weight occurs due to premature birth, pre term delivery, i.e. before 37 w of gestation, or full term birth but small for gestational age due to intra uterine growth retardation. Thus LBW includes a heterogeneous group of infants. Very low birth weight infants are defined as having birth weights less than 1500 g, including mostly premature births. Low birth weight infants have poorer stores of iron, exhaust their iron stores before 6 months of age; in some cases as early as two months, but their iron requirements remain high. Low birth weight infants are much more vulnerable to anemia due to these factors. Most of the data on iron requirements of LBW infants are derived from studies on pre term births. Pre-term and full-term infants have on an average 74 mg iron per kg body weight at birth, about 75% of it is in the circulating hemoglobin, constituting a true iron reserve. Pre term infants birth weight however is low to very low, thus total body iron in a pre term infant at birth may only be one fourth of that in a full term infant. For instance, one of the studies by Siimes (1984) [67] showed that a very LBW infant with a body weight of 0.8 kg had a total body iron of only 50 mg. Pre term infants often become anemic a few months after birth. The iron stores in a pre term infant gets depleted by two months with the result that most such infants become anemic by two months or soon after that. A full term normal birth weight infant increases body weight from 3.2 kg at birth to 10 kg at 1 year. At the same time the total body iron content increases from 210mg to 365mg. Thus the estimated increase in iron content is about 50% although the body weight triples during this time. As against this, very low birth weight infants may increase their body weight up to 5–10 fold by one year, with an accompanying fivefold increase in body iron during this period. The following Table 26.10 shows the available data on increase in growth and iron content of pre-term and full-term infants.

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Table 26.10 Influence of growth on estimated iron needs of pre-term and full-term normal weight infants [67] Initial birth weight (kg)

Increase in body weight over 12 months

Increase in body iron over 12 months

Ratio – iron/weight (mg/kg)

0.8 1.6 3.2

7.2 7.9 6.8

210 215 155

29 27 23

As seen from the above Table 26.10, the need for iron is higher per kg body weight gain in pre term infants compared to full term normal birth weight infants. This is considered applicable to all low birth weight infants as well. The current recommendation is to supplement all low birth weight infants with oral iron, in the form of ferrous fumarate or ferrous gluconate at the level of 2–3 mg/kg body weight per day from 6 to 8 weeks of age until 12 months [68].

26.5.3 Iron requirements of adolescent boys and girls Adolescence is characterized by a large growth spurt. During this period iron requirements are increased dramatically in both boys and girls, and this occurs due to expansion in blood volume, increase in muscle mass, and in girls due to onset of menstruation. Overall the iron requirements nearly double in boys, from 0.7 to 0.9 mg per day to 2.2 mg/d, as they move from preadolescent to adolescent stage and the increase is even higher in girls, especially if they are heavily menstruating. [65]. These increased requirements are associated with the timing and size of the growth spurt as well as sexual maturation and the onset of menses. The available data on iron intakes in adolescents suggest that adolescent girls are unlikely to acquire substantial iron stores during this time period because intakes tend to be low. The bioavailability from diets in developing and industrialized countries indicates a negative iron balance is likely in many female populations. The low iron stores in these young women of reproductive age will make them susceptible to iron deficiency anemia during pregnancy because dietary intakes alone are insufficient, in most cases, to meet the requirements of pregnancy. Iron losses in adolescents through different routes such as urinary, bile and desquamated gastro intestinal cells are assumed to be similar to the losses in adults as there are no clear data to indicate otherwise, once body size is considered [69]. Iron requirement for expansion in blood volume is estimated to be 0.18 mg/d for boys and 0.14 mg/d for girls. Increase in total body essential iron pool is estimated as 0.55 mg/d for boys and 0.33 mg/d for girls. To this must be added the increase due to increase in hemoglobin levels. In girls allowances should be made for menstrual losses of blood. Overall, the

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requirement for absorbable iron in boys is estimated to be 1.8 mg/d and for girls 2.1 mg/d. [65] Taking into account the predominantly cereal pulse based diets of Indians and the bioavailability of these diets, the Indian Council of Medical Research has proposed the following as iron requirements for different age and sex groups in its most recent revision [70]. The earlier ICMR expert committee in 1988 [71] used three levels of iron absorption, 3% for adult men, children and adolescent boys, 8% for pregnant women and 5% for all other women including girls above 10y to determine the dietary iron requirements for these groups. Recent studies on iron absorption in Indians using stable isotopes have indicated that iron absorption on habitual diets may not be as low as 3–5%. With a typical rice-based diet, iron absorption was found to be 17.5% in iron deficient adult women and 7.3% in normal women [72]. Therefore the present committee revised the absorption figures upwards and have used only two levels, 5% for men, and for children below the age of 18 both boys and girls and 8% for women including pregnant and lactating [70]. The principles of estimating the requirements for different age groups remain the same as described in earlier ICMR reports. Table 26.11 Daily iron requirement of Indians (ICMR, 2009) [70] Group Adult M (5%) W (8%) Pregnant women (8%) Lactating women (8%) Infants Children (5%) Adolescents (5%)

Adolescents

Male/Female/ Body weight Age group Kg Man Woman

0–6 months 6–12 months 1–3 years 4–6 years 7–9 years 10–12 years Boys Girls 13–15 years Boys Girls 16–18 years Boys Girls

Iron Iron Dietary iron requirement requirement requirement Mcg/kg/d Total mg/d Mg/d

64 58 58

14 30 47

0.89 1.74 2.72

18.0 22.0 34.0

58

22

1.27

16

5.5 8.4 13.7 18.1 25.2

46 48 28 35 32

0.23 0.40 0.38 0.63 0.80

(a)

8.0 13.0 16.0

34.3 35.3

30 37

1.03 1.30

21.0 26.0

47.4 46.6

32 29

1.51 1.35

30.0 27.0

56.2 52.0

22 25

1.23 1.30

25.0 26.0

(a)

Note – Data are insufficient to establish RDA for iron for infants from birth through 6 months of age and therefore recommended iron intake for this group is based on the average intake of healthy infants fed breast milk. Iron enriched solid food should complement breast milk from 7 to 12 months of age [70]. (a)

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Assessment of anemia

26.6.1 Estimation of hemoglobin levels By definition, anemia is a condition in which hemoglobin levels are lower than the normal for a given age, sex and physiological state. Therefore most assessments of anemia are based on hemoglobin levels. However hemoglobin level per se does not tell us anything about the causes of anemia. In order to have information on the cause of anemia, other parameters need to be defined. The major cause of anemia is iron deficiency either due to dietary deficiency or increased requirements due to growth or specific conditions like infections, blood losses, etc. Unlike hemoglobin which can be estimated with relative ease in the field situation, parameters of iron deficiency are dependant on laboratory facilities and are not practical or feasible in many settings especially in the developing countries. Fortunately the proportion of anemia that is due to iron deficiency can be estimated in many situations by assessing the hemoglobin response to iron therapy, provided that no other supplements are given during this period and that the diet does not change substantially. Thus hemoglobin has been the major criterion for determining anemia, both due to all cause as well as iron deficiency. Methods of estimating hemoglobin can be broadly divided into qualitative and quantitative [73]. The qualitative methods provide information on broad range of hemoglobin values. Generally these are based on comparing the color of a drop of blood on a filter paper strip with standard color charts. Alternately a drop of blood is allowed to fall into a solution of copper sulphate of known specific gravity and observed to note if the drop floats or sinks for the first 10–15 seconds, indicating the specific gravity of the blood is lower or higher than that of the copper sulphate solution. A series of copper sulphate solutions of different specific gravities corresponding to defined hemoglobin levels are used in the estimation. The third qualitative method does not require blood samples but depends on clinical symptoms of pallor. While the skill required for conducting these tests is low to medium, the accuracy and precision are low, making them unsuitable for assessing prevalence of anemia. However for deciding whether an individual should be placed on a therapeutic or preventive iron supplementation at the field level they are quite useful. The quantitative methods use either undiluted whole blood or diluted blood samples. Although different diluting agents and different technologies are available, four of these are credited with high level of accuracy and precision. One of these four involves centrifugation of whole blood to determine the volume of the red cells expressed as hematocrit. This is seldom used in the field condition in India as it does not give a direct estimate of

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hemoglobin. Of the other three, the cyanmethemoglobin and the oxyhemoglobin methods are based on dilution of a very small amount of blood and require high level of skill and training. The hemocue uses a drop of whole blood and does not require carefully calibrated amount; nor does it need dilution. Therefore it calls for low levels of skill but the cost of instrument and the cost per estimation is high. Most anemia assessments in India have used the standard cyanmethemoglobin method using calibrated amount of blood diluted in a suitable agent, while the large scale surveys of NFHS II and III have used the hemocue. Unfortunately the data obtained by the hemocue are not comparable with those of the cyanmethemoglobin method, based on dilution of the blood sample. It is now well established that the hemocue overestimates hemoglobin levels and therefore the method provides an under estimation of the anemia levels. Thus we have to balance the high level of skill needed for the standard cyanmethaemoglobin method that calls for dilution of blood with the high cost of hemocue that under estimates anemia levels. A field level adaptation of the cyanmethemoglobin method has been used in situations where laboratory facilities are severely limited. In this method, a calibrated amount of blood is collected on a whatman filter paper circle of specified dimension, allowed to dry and transported to a lab within a week for elution and estimation. The difference between this and the standard laboratory method has been shown to be low and is of little consequence in assessing anemia prevalence.

26.6.2 Indicators of iron, folate and vitamin B12 deficiencies Iron deficiency is considered to occur in three stages [74]. When the intake of iron is insufficient to meet the daily iron losses and the need for growth, iron reserves start getting depleted. In the first stage referred to as the iron deficient stores, iron reserves are essentially absent but the supply to erythroid marrow is not yet curtailed. This is reflected in the absence of ‘stainable iron’ in the bone marrow and a reduction in serum ferritin levels. Iron lack is the only condition in which there is a reduction in serum ferritin levels and therefore this parameter is highly specific for iron deficiency. However, inflammatory conditions produce an increase in serum ferritin making it difficult to interpret serum ferritin values in the presence of infections. Studies have shown that 1 mcg per liter of serum ferritin is equal to 10 mg of storage iron. More recently, transferrin receptors in blood have been shown to be a more sensitive indicator of iron stores as this parameter is not affected by infections and inflammation. Unlike serum

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ferritin, transferrin receptors are increased in iron deficiency, as a response to bind more of the serum iron so that it can be delivered to the bone marrow and other tissues. In the second stage of iron deficiency referred to as iron deficient erythropoiesis, there is a reduction in iron supply to the erythroid marrow. Serum iron is reduced and total iron binding capacity is increased in this stage. The more useful index of stage 2 deficiency is the transferrin saturation (TS) which is the ratio of serum iron to total iron binding capacity. When the transferrin saturation falls below 15%, hemoglobin production in the developing red cells is curtailed. Transferrin saturation, however, suffers from three major limitations as an indicator of iron deficiency. First, serum iron measurement in the laboratory is highly susceptible to iron contamination, particularly with manual methods, resulting in erroneously high serum iron values if contamination is not scrupulously avoided. Secondly, the diagnostic ability of TS is reduced because of wide diurnal variations of serum iron in normal subjects, and finally the level of TS falls within hours of onset of even mild inflammation, leading to erroneous interpretation. Erythrocyte protoporphyrin is another measurement that can be used to detect iron deficient erythropoiesis. When the iron supply to the bone marrow is curtailed, protoporphyrin in its free form increases in the erythrocytes, i.e. protoporphyrin not bound with iron and the protein globin. An advantage of the erythrocyte protoporphyrin is that it is a more stable index of iron supply to the bone marrow as elevation occurs only after several weeks of restricted iron supply to the bone marrow. A disadvantage of this indicator especially with children is that the level increases with lead poisoning. The third and final stage of iron lack is iron deficiency anemia in which there is a fall in hemoglobin levels, below what is normal for the individual. The parameters for diagnosing iron deficiency with normal and abnormal values are portrayed in the Table 26.12 below. Table 26.12 Stages of iron deficiency and the normal and abnormal range of values for the indicators [74]. Stage if iron deficiency/ indicators

Normal iron stores 600 mg

Depleted iron stores

Restricted supply of iron to erythroid marrow

Anemia

Plasma ferritin µg/L

60

<12

<12

<12

Transferrin saturation (%)

35

35

<16

<16

RBC Protoporphyrin µg/dl

30

30

>70

>70

Hemoglobin (g/dl)

>12

>12

>12

<12

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In addition, values indicative of iron excess have also been defined. Serum ferritin in excess of 300 mcg/l and transferrin saturation in excess of 60% are indicatives of iron over load [75–76]. The concurrent presence of folate and vitamin B 12 deficiencies may be identified by the red cell folate, serum folate and serum vitamin B12 levels. Red cell folic acid level below 100 nanogram per ml; serum folic acid levels below 3 nanogram per ml; and serum vitamin B12 level below 100 pico gram per ml are all indicative of deficiencies of these vitamins [8].

26.7

Functional effects of anemia

Although nutritional anemia may result due to deficiencies of several nutrients, the focus of research has been on anemia due to iron deficiency as this is a major cause of anemia world over. The aspects discussed in the next section pertain mainly to iron deficiency anemia, as all studies have addressed the reversibility of the adverse effects of anemia on functional effects with iron therapy.

26.7.1 Anemia, iron deficiency and physical performance Iron in the body plays an essential role in oxidative energy production; this iron is known as functional iron as against iron that serves as a reserve which is known as storage iron. Functional iron is found in hemoglobin in red cells, myoglobin in muscles, iron dependent enzymes and respiratory chain proteins in the mitochondria. Table 26.13 below summarizes their functions in energy production, which make it apparent that iron deficiency and anemia produce a range of impairments in oxidative energy production that gets reflected in impaired physical performance and working capacity [76]. Table 26.13 Role of iron in energy production Name of protein

Functional site

Major function

Hemoglobin

Red blood cells

Oxygen transport

Myoglobin

Cytoplasm of muscle cells

Diffusion of oxygen to the mitochondria

Oxidative enzymes

Mitochondrial membrane

Oxidation of substrates

Respiratory chain proteins

Mitochondrial membrane

Electron transfer

Studies in human adults have shown that iron deficiency and anemia, both limit physical capacity measured by tests of aerobic capacity and endurance tests. Anemia, with lower hemoglobin levels reduces oxygen delivery to the tissues and impairs primarily the aerobic capacity. Iron deficiency on the other hand, by reducing tissue oxidative capacity is

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considered to have a major adverse effect on the endurance capacity especially at sub maximal work loads. Iron deficiency anemia by virtue of low Hb levels and tissue iron deficiency affects both aerobic capacity and endurance. Endurance tests typically involve sub maximal work loads and time to exhaustion is determined under standard conditions, while aerobic capacity is measured either in a treadmill or a bicycle ergo meter at maximum exertion levels. A recent review [12] which evaluated nine laboratory studies in human adults that were either unblinded or double blind randomized placebo controlled trials, found that both severe and moderate iron deficiency anemia impaired aerobic capacity. The impairment could be corrected by increasing hemoglobin concentration. Iron deficiency without anemia was not found to affect aerobic capacity but had a significant adverse effect on endurance capacity in adults. The lack of effect of iron deficiency without anemia on aerobic capacity was attributed to the strong dependence of maximum oxygen consumption (VO2 Max) on oxygen delivery which in turn is affected only when hemoglobin levels are reduced. Several field studies in male and female tea pickers have shown strong positive association between anemia and aerobic capacity, measured either as heart rate during a step test or during tread mill tests [77–79] .These studies also demonstrated that work time and work load were proportional to hemoglobin. Most importantly, increases in various measures of aerobic capacity were found with increase in hemoglobin. Impaired physical performance can adversely affect productivity, especially in income earning activities that are dependent on physical efforts. Most consistent data comes from tea and rubber plantation workers in whom productivity could be quantified. These studies in India, Indonesia and Sri Lanka have shown that there is a fall in productivity in anemic subjects that shows up in income earned as well as in the quality of the diets [80–82]. Economic losses expected due to iron deficiency is estimated to be 1.47% of the GDP in India which when translated into absolute terms is equivalent to 4294 million US dollars, a huge loss indeed [83]. Most laboratory and field studies of anemia versus physical performance have focused on adults with only a few that has investigated this aspect in children. The results of these studies have indicated that both aerobic capacity and endurance were impaired in anemic children, consistent with the observations on adults [84–85]. Animal studies provide extra ordinarily consistent data. Most severely anemic rats have the lowest aerobic capacity, severity of anemia directly proportional to decline in aerobic capacity from hemoglobin levels of 140 to 80 g/l [86]. A similar finding was also reported from tea pickers in Sri Lanka [77].

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Taken together, these data provide clear evidence of compromised physical performance in adults while more studies are indicated in children [87]. Reduced ability to engage in physical activities in children can have other ramifications such as an adverse effect on learning due to limited scope for exploratory activities and the lack of activity stimulus for optimum development of motor skills. In anemic adults, impaired physical work capacity, lower productivity, lower earnings, and poor quality of diets can set up a vicious cycle that result in severe losses at the national and individual level. Iron supplementation to correct anemia results in a significant improvement in physical capacity as well as in income earned [80–82, 88] and has the potential to reverse the huge losses in GDP.

26.7.2 Anemia and cognitive functions in children In the last four decades several studies have addressed the issue of anemia versus cognitive development in children. While these studies in general are consistent in indicating impairment in cognitive development due to anemia in young infants and children, the reversibility of this with nutritional therapy, chiefly with iron has been conclusively shown only for older children, i.e. above the age of two years. The first indication that cognitive development may be compromised in iron deficient anemic children came from co relational studies that showed a significant association between tests of cognitive development and hemoglobin levels, the anemic children performing poorly on a wide range of psychological tests compared to the non anemic children [89–91]. Several longitudinal observational studies that have tried to link cognitive development or school achievement in later childhood with anemia in infancy or early childhood have been consistent in showing that formerly anemic children continued to be at a developmental disadvantage at one or more of the follow up assessments, even after adjusting for some social background variables such as gender and birth weight. Deficits were noted in formerly anemic children in pre school skills, fine and gross motor skills, and visual motor integration [13]. Randomized supplementation trials provide final convincing evidence linking anemia with poorer cognitive development and the promising prospect of reversal of the adverse effects with nutritional therapy. The studies reported in the literature have measured a wide variety of cognitive functions in older children. These have included visual perception, memory, concentration, problem solving skills and discrimination learning. Almost all the studies have shown poorer performance of the anemic children and a significant improvement after iron supplementation or iron and folic acid supplementation to correct anemia. The poorer performance

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in a variety of tests was seen in infants as well as in older children. However, the reversal of the adverse effects with iron supplementation was demonstrated convincingly only in the older children, i.e., in children above the age of two years [13, 92–94]. This has raised two questions in relation to the younger children: one that iron deficiency anemia when it occurs at a very young age (i.e. in the first year of life) may leave a permanent deficit that may not be corrected by supplementation later in life and the second relates to the tests used that they may not be sensitive enough to detect the improvements. Available evidence appears to indicate that the former rather than the latter may be the case which underscores the importance of effective public health measures to prevent anemia in the young children.

26.7.3 Effects of anemia on pregnancy outcome An association between anemia and adverse pregnancy outcome has been found in many studies. Birth weights have been reported to be lower at both ends of hemoglobin, the relationship being U shaped [95]. Unfavorable pregnancy outcomes consequent to anemia have included lower mean birth weight, lower gestational duration, and increased perinatal mortality [96]. Oral iron supplementation during pregnancy increases weight at birth and reduces the incidence of low birth weight [97–98]. Accumulating evidence suggests an association between maternal iron status during pregnancy and iron status of infants post partum. Although anemia, especially severe anemia has been reported as an associated cause of maternal mortality in several countries around the world, prospective trials are lacking. Other effects of anemia such as maternal morbidity, well being and infant health also need further documentation [95].

26.7.4 Lowered cellular immunity and increased morbidities Anemia has been shown to result in impairment in cell mediated immunity and lymphocyte proliferation response to mitogens in pregnant women that is corrected by iron therapy [99]. In young children, both cell mediated immune response and bactericidal activity of leucocytes, was found to be impaired in anemia, especially when hemoglobin levels fell below 10 g/dl [100] both of which were corrected by iron therapy [101]. The effect of anemia on morbidities is less clear [102].

26.7.5 Impaired thermo regulation There are some studies to show that ability to withstand cold temperatures is compromised in iron deficient and anemic women. It appears likely that

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this effect is mediated by thyroid hormone. Lack of iron may result in a lack of adequate stores of thyroid hormone which curtails increased cellular metabolism on exposure to cold, leading to increased intolerance [103].

26.7.6 Child growth deficits Only a few studies have investigated the effect of anemia on child growth [104, 105]. These have reported a positive effect of iron supplements on growth which will need to be pursued further to clearly document if child growth can be improved with iron supplements in anemic young children [106].

26.8

Approaches for the prevention and control of anemia

There are broadly two approaches for the control of iron deficiency anemia: one is to increase the amount of absorbable iron by one or more of the following means: (a) fortifying common foods with iron; (b) increasing the bioavailability of the dietary iron by increasing the enhancers in the diet and reducing the inhibitors; (c) by providing iron through medicinal supplementation; the other is one of controlling infestations and infections that cause lowering of hemoglobin. While food based strategies may be adequate in areas where anemia prevalence is less than 10% in the population, medicinal supplementation in addition to food fortification will be needed in areas of high prevalence, i.e. more than 40%. In new borns, umbilical cord clamping, delayed for at least two minutes after birth, can increase body iron stores of the infant at birth and improve iron status in the first few months. Therefore it is an important additional measure specific to this age group for prevention of iron deficiency anemia

26.8.1 Food fortification Food fortification refers to the addition of iron to foods over and above what is naturally present in them. Food fortification can take many forms; mass fortification refers to the fortification of foods consumed widely by the general population; targeted fortification is the fortification of foods consumed by specific sub population groups such as complementary foods meant for young children; and market driven fortification where the food manufacturer voluntarily fortifies foods with nutrients, an example is the wheat atta fortified with iron and marketed by private food companies [107]. Besides these, bio fortification of staple foods, i.e. breeding and genetic modification of plants so as to improve their nutrient contents and or absorption of the nutrients is a novel approach that is currently being researched. The golden rice is an example of genetically modified rice

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grains containing beta carotene. Much more work is needed in this area before the foods can become a part of our daily diet. For food fortification to be successful, the food vehicle chosen should be consumed by a vast majority of the needy population, it should be possible to fortify the entire required quantities in a few places to assure quality, the selected fortificant should have a high bioavailability and must not react with other foods when cooked or mixed, and the fortified food must be consumed in fixed amounts daily so that wide variations do not occur in intakes. Staple foods like rice and wheat and others such as salt, soy sauce and fish sauce have been developed as food vehicles for iron fortification [107]. Among these, salt is a good vehicle for iron in the developing countries for the general population. Efforts to fortify salt with iron and iodine has been successful in India and else where. The double fortified salt developed by the National Institute of Nutrition in India, using a low cost technology, provides 1mg iron and 100 mcg iodine per g salt, i.e. 1000 ppm of iron and 40 ppm of iodine. The average daily salt consumption by adults in India is estimated as 8 g which, at the level of fortification described above provides 8mg iron /d. The bioavailability of the iron in the DFS has been shown to be good, 6.1% [108]. The stability, safety and acceptability at the community level have all been satisfactorily demonstrated. Impact data on residential school children who consumed the double fortified salt for two years showed a decline in anemia prevalence from 42% to 30% [109]. Currently, production of double fortified salt has been floated in India in some of the southern states [110].

26.8.2 Increasing bioavailability of dietary iron There are basically two ways in which the bioavailability of iron in the diets can be improved. The first is by increasing the enhancers, namely ascorbic acid and, meat, fish and poultry (MFP) in the diet and the other is to reduce the content of inhibitors in the diet. A large body of literature is available which demonstrates convincingly that under controlled conditions, MFP and ascorbic acid increase the absorption of non heme iron in humans [36–39, 111]. As little as 10 mg of ascorbic acid can increase the absorption of iron two fold. There are many foods in the Indian context that are high in ascorbic acid. These are usually the fruits and vegetables. It is important to note here that ascorbic acid is easily lost at high temperatures and in the presence of oxygen. Therefore, the fruits should be consumed in fresh uncooked forms for best effects and immediately after the meals. The important fruits that are good sources of ascorbic acid are citrus fruits of any kind, guavas, papaya, and among the vegetables all green leafy vegetables, cauliflower, Indian gooseberry are all good sources of ascorbic acid.

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The typically vegetarian Indian dietary is known for its high content of inhibitors of iron absorption. These are phytic acid present in whole grain cereals and flours, fiber in wheat bran, tannins in tea and ragi, calcium in milk, soya bean products, and egg yolk. The inhibitors reduce iron absorption by forming insoluble complexes with iron that get precipitated in the alkaline environment of the small intestine which do not release the iron for absorption. Reduction of inhibitors of iron absorption such as phytic acid, concomitantly with an increase in ascorbic acid content of foods, by processes such as germination and fermentation have also been shown to result in increased bioavailability of iron. There are two approaches by which these can be integrated into a public health policy and program. One is to augment the production of fruits and vegetables which are good sources of ascorbic acid so that access and availability of these foods to the general population is increased. The other is to promote, through nutrition education and counseling, the consumption of these fruits and vegetables and processes at the household level such as germination and fermentation that can reduce the inhibitors in the diet. Germination and fermentation are traditional food processing methods extensively used in India at the household level until recently but are showing a decline in the current period. Thus it is important that diet practices at the household level are preserved/modified in a manner as to allow for better iron absorption and improved iron bioavailability.

26.8.3 Nutrient supplements This approach involves provision of the missing nutrient as a supplement to the population at risk. Iron and folic acid supplements have received the most attention as these are two nutrients that contribute to the high prevalence of anemia. Far fewer studies have been done with other nutrients such as vitamin A or vitamin B 12. Many developing countries have used iron folic acid supplementation as the main public health approach to control anemia, although with only limited success [20,112], primarily due to several limitations in the implementation of the program. The current recommendations by WHO [76] for iron supplementation are shown in Table 26.14. The anemia control program in India provides iron-folic acid supplements (IFA) consisting of 100 mg iron and 500 μg folic acid daily for a minimum of 100 days to pregnant women, starting as early in pregnancy as possible and continuing for the rest of pregnancy. The same dosage and tablets are provided to lactating women in the first three months post partum. Young children receive 20 mg iron and 100 μg folic acid.

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Table 26.14 Guidelines for the use of iron supplements to prevent anemia Age groups

Indications for supplementation

Dosage schedule

Duration

LBW infants

Universal supplementation

Iron: 2 mg/kg body weight per day

from 2 to 23 months of age

Children 6–23 months of age

Where anemia prevalence is above 40%

Iron: 2 mg/kg body weight per day

From 6 to 23 months

Children 24–59 months of age

Where anemia prevalence is above 40%

Iron: 2 mg/kg body weight per day up to 30 mg

3 months

School-age children above 60 months

Where anemia prevalence above 60 months is above 40%

Iron: 30 mg/d Folic acid : 250 μg/d

3 months

Women of child bearing age

Where anemia prevalence is above 40%

Iron: 60 mg/d Folic acid: 400 μg/d

3 months

Pregnant women

Universal supplementation

Iron: 60 mg/d Folic acid: 400 μg/d

As soon as possible after gestation starts – no later than the 3rd month – and continuing for the rest of pregnancy

Lactating women

Where anemia prevalence is above 40%

Iron: 60 mg/d Folic acid 400 μg/d

3 months post partum

Adolescents are prescribed the same adult tablets as for pregnant and lactating mothers. However, bi-weekly administration of the adult supplement is recommended for adolescent girls and women in the reproductive age. Recently the World Health Organization has issued a position statement on weekly supplementation of iron for reproductive age women. This position statement is based on the consensus of a World Health Organization (WHO) Global Consultation on Weekly Iron and Folic Acid Supplementation [113]. While recommending that the strategies to combat iron deficiency and anemia should be integrated, the consultation recognized that weekly iron folate supplementation (WIFS) is an important strategy for the prevention of iron deficiency, improvement of pre-pregnancy iron reserves and the improvement of folate status in women. In population groups where anemia prevalence is above 20% in women of reproductive age and in the absence such data where anemia prevalence is above 40% in pregnant women, the consultation recommended that WIFS should be considered.

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The weekly supplement should contain 60 mg iron in the form of ferrous sulfate (FeSO 4.7H2O) and 2800 mcg folic acid, although the dose level recommended for folic acid is supported by very limited evidence. Since folic acid supplementation may reduce the efficacy of anti malarial treatment, it may be prudent to use iron only as a weekly supplement in this setting. Upon confirmation of pregnancy, the dose schedule mentioned in Table 26.12 for pregnancy should be followed. It is intended that WIFS programs will be integrated with other efforts to control iron deficiency and anemia and will be planned in such a way that it will become a self sustaining long term program that the women of reproductive age will use during their child bearing years.

26.8.4 Parasite and malaria control As hookworms and malaria contribute to anemia and iron deficiency in a significant way, especially in pregnant women [114] and in young children, deworming using appropriate drugs will be the choice, until such a time when sanitary conditions can be improved. Albendazole and Mebendazole are reported to be effective against most of the helminthic infestation seen in the south Asian region. They are also considered relatively safe if administered in the 2nd or 3rd trimester of pregnancy and in children above 1 year of age. These drugs are not to be given in the first trimester of pregnancy. The dosages as recommended by the WHO[10] are: for pregnant women in endemic areas (prevalence 20–30% or more), a single dose of albendazole (400 mg) or mebandazole (500 mg) is considered effective and safe if given in the 2nd trimester. It is recommended that this be repeated in the 3rd trimester if the women live in highly endemic areas (prevalence of helminthes more than 50%). If plasmodium falsiparum malaria is endemic and transmission of infection is high, the women in their first or second pregnancies should be given curative anti malarials on the first pre natal visit, followed by prophylaxis as per local recommendations. Single dose albendazole (400 mg) or mebendazole (500 mg) twice a year is recommended for children above 5 years in endemic areas. Malaria prophylaxis is reported to improve hemoglobin levels, reduce prevalence of anemia and improve birth weights in the first and second pregnancies in malaria endemic areas. Malarial prophylaxis and anti malarials should be administered as per the local recommendations [10].

26.9

Summary

Nutritional anemia is a major public health problem in the world affecting an estimated 2 billion people of which 90% are in the developing countries,

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especially in South East Asia and Africa. Dietary iron deficiency and low availability are the two major causes of anemia on such a wide scale; however other nutritional deficiencies such as vitamin A, folic acid, vitamin B12 and riboflavin may contribute to the prevalence of anemia in certain settings. It is estimated that on a world wide basis, iron deficiency accounts for 50% of the total anemia in the population and where prevalence is high, iron deficiency would account for a much higher percentage of the total anemia seen in the population. Dietary iron exists in two chemical forms; heme iron present in flesh foods and non heme iron present in foods of vegetable origin. Diets in developing countries comprise predominantly of non heme iron that is absorbed poorly compared to heme iron. Three major factors influence the amount of iron absorbed and transported to the body for specific functions which is defined as iron bioavailability. These are the chemical form of iron, the balance of enhancers and inhibitors of iron absorption in the diet and the iron status of the individual. Given that the predominant chemical form of iron in the Indian dietary is non-heme iron and the inhibitors far outnumber the enhancers, the absorption of iron is about 5% in most regional diets in India. Increased iron needs during pregnancy, early childhood, and adolescence make these population groups particularly vulnerable to anemia, especially in a situation of dietary deficiency and poor bioavailability. Regulation of iron absorption at the intestinal level is the chief mechanism for iron homeostasis, as there is no physiological mechanism for excretion of iron once it is absorbed into the body. Iron homeostasis is a complex process that involves several proteins, hepcidin secreted by the liver being the principal hormone involved in iron regulation. Assessment of anemia is usually done by measuring hemoglobin level in the blood. However, the relative role of different nutrients in the causation of anemia calls for other laboratory investigations of iron, folate and vitamin B12 status. Anemia is of grave public health concern in view of its wide ranging adverse functional consequences that include impaired physical work capacity and a resultant reduced productivity and income in adults; impaired cognitive functions in children with the possibility of a permanent deficit in children below the age of one year; adverse pregnancy outcomes that include low birth weight, increased pre mature births and higher perinatal mortality. Maternal mortality is significantly higher in anemic pregnant women. Other functions affected by iron deficiency anemia include the ability to mount an appropriate immune response to infections, poor thermo regulation and possibly impaired growth in young children. The serious consequences of anemia require that there is a need for a clear public policy in support of integrated efforts for the control of anemia in all developing countries, which should focus on appropriate food

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fortification, methods to improve iron availability, nutrient supplements, and control of infections and infestations.

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(eds.) (2008). Worldwide prevalence of anemia 1993–2005: WHO global database on anemia. Geneva, WHO and CDC. DEMAEYER E and ADIELS -TEGMAN M (1985). The prevalence of anaemia in the world. World Health Statistics Quarterly, 38, pp. 302–316. HURRELL RF and HESS SY (2004). Role for micronutrient interactions in the epidemiology of micro nutrient deficiencies: Interactions of iron, iodine and vitamin A. In: Micronutrient Deficiencies During the Weaning Period and the First Years of Life. Pettifor JM, Zlotkin S (eds). Basel (Switzerland): Nestle Nutrition/Karger, pp. 1–19. WHO (2002). The World Health Report: Reducing risks, promoting healthy life: overview. World Health Organization, Geneva (WHO/WHR/02.1). FISHMAN SM , CHRISTIAN P, WEST KP (2000). The role of vitamins in the prevention and control of anemia. Public Health Nutrition, 3, pp. 125–150. ALLEN LH , CASTERLINE - SABEL JE (2004). Prevalence and causes of nutritional anemias. In: Nutritional Anemias. Ramakrishnan U. (ed.). Boca Raton FL: CRC Press, pp. 17–21. RAMAN L , SUBBALAXMI PV , VASUMATI N , RAWAL A , VASANTHI G , PARVATHI CH , ADINARAYANA K , RAO KV (1989). Iron and folic acid nutritional status of women in slum. Nutr Rep Internat 39, pp. 73–80. BAKER SJ and DE MAEYER EM (1979). Nutritional anemia: its understanding and control with special reference to the work of the World health organization. Am J Clin Nutr, 32, pp. 368–417. WHO (1968). Technical Report Series No 405, Nutritional Anemias, Geneva. STOLTZFUS RJ and DREYFUSS ML (1998). Guidelines for the use of iron supplements to prevent and treat iron deficiency anemia. Geneva: International Anemia Consultative Group/ UNICEF/WHO. FAO / WHO (1992). International Conference on Nutrition: Major issues for Nutrition Strategies. Italy: Food and Agriculture Organization and World Health Organization, Theme paper No 6, p. 12. HAAS JD and BROWNLIE T (2001). Iron deficiency anemia and reduced work capacity: A critical review of the research to determine a causal relationship. J Nutr, 131, pp. 676S–690S. GRANTHAM MC, GREGOR S, ANI C (2001). A review of studies on the effect of iron deficiency on cognitive development in children. J Nutr, 131, pp. 649S–668S. SESHADRI S (2005). The persistent problem of iron deficiency anemia and its consequences: A life cycle approach is critical for its control. Proc Nutr Soc India, 52, pp. 19–36. OPPENHEIMER SJ (2001). Iron and its relation to immunity and infectious disease. J Nutr, 131, pp. 616S–635S. PREMA K , NEELA KUMARI S , RAMALKASHMI BA (1981). Anemia and adverse obstetric outcome. Nutr Rep Internat, 23, pp. 637–643. ALLEN LH (2000). Anemia and iron deficiency: Effects on pregnancy outcome. Am J Clin Nutr, 71, pp. 1280S–1284S. ACC / SCN (2004). 5th Report on the world nutrition situation – Nutrition for improved development outcomes. Geneva: ACC/SCN/WHO, p. 20.

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(1991). Impact of anemia prophylaxis in pregnancy on maternal hemoglobin, serum ferritin and birth weight. Ind J Med Res 94, pp. 277–280. C O G S W E L L M E , PA RVA N TA I , I C K E S L , Y I P R , B R I T T E N H A M G M (2003). Iron supplementation during pregnancy, anemia and birth weight: a randomized controlled trial. Am J Clin Nutr, 78, pp. 773–781. PREMA K , RAMALAKSHMI BA , NADHAVAPEDDI R , BABU S (1982). Immune status of anemic pregnant women. Brit J Obst Gynecol, 89, pp. 222–225. SRIKANTIA SG , BHASKARAM P , PRASAD JS , KRISHNAMACHARI K (1976). Anemia and immune response. The Lancet, 309, pp. 1307–1309. BHASKARAM P, SIVA PRASAD J , KRISHNAMACHARI K (1977). Anemia and immune response. The Lancet, 309, p. 1000. GERA T and SACHDEV HPS (2002). Effect of iron supplementation on incidence of infectitious illneses in children: systematic review. Brit Med J, 325, p. 1142. BRIGHAM D and BEARD J (1996). Iron and thermo regulation: A review. Crit Rev Food Sci Nutr, 36, pp. 747–763. AUKET MA, PARKYA SCOTT PH, WHARTON BA (1986). Treatment with iron increases weight gain and psychomotor development. Arch Diseases Childhood, 61, pp. 847–849. BHATIA D and SESHADRI S (1987). Growth performance in anemia and following iron supplementation. Ind Ped 30, pp. 195–200. SACHDEV HP , GERA T , NESTEL P (2006). Effect of iron supplementation on physical growth in children: systematic review of randomized controlled trials. Public Health Nutrition, 9, pp. 904–920. ALLEN L , BENOIST DE B , DARY Q , HURRELL R (2006). Guidelines on food fortification with micronutrients. Geneva, WHO/FAO. NARASINGA TAO BS (1994). Fortification of salt with iron and iodine to control anemia and goiter: Development of a new formula with good stability and bio availability. Food and Nutrition Bulletin, 15, pp. 32–39. MADHAVAN NAIR K , BRAHMAM GNV , RANGANATHAN S , VIJAYARAGHAVAN K , SIVAKUMAR B, KRISHNASWAMI K (1998). Impact evaluation of iron and iodine fortified salt. Ind J Med Res108, pp. 203–211. NIN and ICMR (2005). Double fortified common salt (DFS) as a tool to control iodine deficiency disorders (IDD) and iron deficiency anemia (IDA). A Technical report. Hyderabad. TAYLOR PG , MÉNDEZ -CASTELLANOS H , MARTÍNEZ -TORRES C, JAFFE W, BLANCO ML , JIMÉNEZ ML , LEETS I , TROPPER E , RAMÍREZ J , NIEVES ML , CASAL G , LAYRISSE M (1995). Iron bio availability from diets consumed by different socio economic strata of the Venezuelan population. J Nutr, 125, pp. 1860–1868. ACC /SCN (1991). Controlling iron deficiency. Nutrition policy discussion paper no 9. Administrative Committee on Co-ordination- Sub Committee on Nutrition, Geneva. WHO (2009). Weekly iron–folic acid supplementation (WIFS) in women of reproductive age: its role in promoting optimal maternal and child health. Position statement. Geneva, World Health Organization, (http://www.who.int/nutrition/ publications/micronutrients/weekly_iron_folicacid.pdf, accessed [date]). DREYFUSS ML , STOLTZFUS RJ , SHRESTHA JB , PRADHAN EK , LECLERQ CL, KHATRY SK, SHRESTHA SR , KATZ J , ALBONICO M , WEST KP JR (2000). Hookworms, malaria and vitamin A deficiency contribute to anemia and iron deficiency among pregnant women in the plains of Nepal. J Nutr, 130, pp. 2527–2536.

27 Iron deficiency and iron deficiency anemia in adolescent girls Sheila C. Vir

Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

%.1

Prevalence of iron deficiency and anemia among adolescent girls

Adolescence, between the ages of 10–19 years [1], contributes to almost 20% population in developing countries. Adolescence is a stage of accelerated growth and development [2, 3, 4] when requirements for iron increases significantly. Iron deficiency and iron deficiency anemia (IDA) in adolescence is a major public health problem. As per the global estimates, 23% adolescent girls are anemic [5]. Incidence of anemia in school age children tends to increase with age and corresponds with acceleration in growth during adolescence (Figure 27.1). Studies indicate that the prevalence of anemia in school children increases from 10 years old upwards and remains high until 18 years of age during the growth period (Figure 27.1). The highest prevalence is between the ages of 12–15 years with over 50% girls reported to be anemic [6, 7]. This trend in prevalence of IDA with age is due to inability to meet the higher requirement for iron with increase in body mass which is correlated to variations in velocity of growth of adolescents [8, 9].

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27.1 Age-wise prevalence of anemia multi-centric study on adolescent girls [10]

In most South–East Asian countries almost half of the adolescent girls are anemic [11-21]. On the other hand, the prevalence of anemia in adolescent girls in USA and Norway is less than 6% (Figure 27.2).

27.2 Anemia prevalence in adolescent girls [11–21]

The high prevalence of anemia in adolescent girls in a region often corresponds with a high level of anemia during pregnancy. As indicated in Table 27.1, in all South Asian countries, except Thailand, one-third of adolescent girls were anemic while prevalence of anemia in pregnant mothers was over 40% (Table 27.1). Anemia is primarily due to iron deficiency and is in fact the long end stage of a relatively long process of deterioration in iron stores. Many more adolescents are in fact suffering from iron deficiency (ID) with its adverse effects on health and physical

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stamina, than are frankly anemic [22]. UNICEF/UNU/WHO/MI [23] indicate that there are approximately 2.5 cases of iron deficiency for each case of anemia. The functional consequences are known to occur prior to onset of clinical stage of iron deficiency. Table 27.1 Prevalence of anemia in adolescent population as compared to pregnant women in South East Asian Region countries Country

Prevalence of anemia (percentage) Adolescents girls Pregnant women

Bangladesh [10] Bhutan [11] India [12, 13] Indonesia [14] Maldives [15] Myanmar [16] Nepal [17] Sri Lanka [18] Thailand [19, 20] (a)

40.0 26.4 90.0 30.0 50.0 45.2 46.0 40.0 17.0

75.0 68.0 58.7 (a) 51.0 68.0 52.0 68.0 40.0 12.0

Only India data specifies inclusion of adolescents.

27.2

Causes of iron deficiency and iron deficiency anemia in adolescent girls

Adolescent girls are at high risk of iron deficiency and anemia due to accelerated increase in requirements for iron, poor dietary intake of iron, high rate of infection and infestation as well as the social problem of adolescent pregnancy and conception. (a) Accelerated increase in requirement for iron during adolescence – Iron deficiency anemia (IDA) occurs when iron stores in the body are depleted and supply to tissues is compromised resulting in fall of hemoglobin levels. Iron needs for the body increases sharply with accelerated growth spurt – adolescents on an average gain weight equivalent to 65% of their weight at the beginning of the period or 40% of their final weight, and a height gain equivalent to 15% of their adult height or 25% of an individual’s attained height during adolescence [24, 25, 26]. The accelerated increase in lean body mass, blood volume and red cell mass results in increase in requirement for iron for the synthesis of myoglobin in muscles and hemoglobin in blood [27]. Figure 27.3 presents the continuous increase in the median requirements for absorbed iron for both boys and girls during adolescence [27]. The requirement peaks between the ages of 14–15 years. As shown in Table 27.2, the overall iron requirement increases two to three folds from a preadolescent level of approximately 0.6– 0.9 mg iron per day to as much as 1.37–1.88 mg per day in adolescent

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27.3 Median requirements for absorbed iron (mg/day) during adolescence stage [27] Table 27.2 Iron intakes required for adolescent boys and girls, median basal iron losses, menstrual losses in women, and total absolute iron requirements as compared to children [22] Group

Age

Body weight Mean

(Years) Children 0.5–1.0 1–3 4–6 7–10 Males 11–14 15–17 18+ Females 11–14 (b) 11–14 15–17 18+ (a)

(b) (c)

Required Basal Iron intakes iron for growth losses Median

(kg)

(mg/day)

9 13.3 19.2 28.1 45 64.4 75 46.1 46.1 56.4 62

0.55 0.27 0.23 0.32 0.55 0.60 0.55 0.55 0.35

Menstrual losses

Total absolute requirements(a)

95th Median 95th percentile percentile (mg/day) (mg/day) (mg/day) (mg/day) (mg/day)

0.17 0.19 0.27 0.39 0.62 0.90 1.05 0.65 0.65 0.79 0.87

Median

0.48(b) 0.48(b) 0.48(b)

1.90 (c) 1.90 (c) 1.90 (c)

0.72 0.46 0.50 0.71 1.17 1.50 1.05 1.20 1.68 1.62 1.46

0.93 0.58 0.63 0.89 1.46 1.88 1.37 1.40 3.27 3.10 2.94

Total absolute requirements = Requirement for growth + basal losses + menstrual losses (females only) Non-menstruating Effect of the normal variation in hemoglobin concentration not included in this figure

boys and 1.40–3.27 in adolescent girls [22, 27]. Additional iron is therefore required by both adolescent boys and girls for the expanding red cell mass and growing body tissue. The risk of iron deficiency increases significantly during the adolescent growth spurt for both boys and girls. In boys, following the phase of growth spurt, the need for iron decreases and there is a scope for overcoming

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deficiency of iron, However, in case of adolescent girls, the situation differs with requirements for iron continuing to remain high through the reproductive life to replace iron that is lost during menstruation – there is a regular loss of 12.5–15.0 mg iron per month or 0.4–0.5 mg iron per day in menstrual blood. Therefore in girls, following the growth spurt, the risk of iron deficiency continues to be of a public health concern through the entire reproductive age but this risk subsides for boys [28]. (b) Low dietary intake and bio-availability of iron – The primary cause of IDA in adolescence is lack of iron available to the body to meet the high requirements due to low dietary intake and poor bioavailability of iron consumed against the significant increase in requirements [29]. The data from India indicates that the diets of girls aged between 13 and 18 years provide much lower level of iron than the diets of boys in the same age group [30]. Low consumption of nutrients by adolescents reported from India indicates that over 50% adolescent girls consume less than 50% RDA for energy while over 70% girls consume less than 50% RDA of iron [31]. Similarly the Bangladesh study on adolescent girls attending school in Dhaka city [32] reveals that 31% of these girls consume less than 50% RDA of iron and 10% less than 50% energy. Similar findings of low intake of iron and energy are reported from other studies in adolescent girls in Bangladesh, Indonesia and India [33, 34, 35]. Besides low consumption of total dietary iron, the source of iron is important. Routine intake of monotonous diets based on cereals along with consumption of low quantities of meat, fish or fresh vegetables and fruits results in poor availability of iron. Such diet with high concentration of inhibitors and low concentration of enhancers lowers the bio-availability of dietary iron from cereal based diet. This is evident from data of India [36] where the prevalence of anemia is higher in Indian adolescents consuming a vegetarian diet (45.8%) as compared to those consuming a mixed diet, which includes animal food (30%). Daily recommended intake of dietary iron varies widely when bioavailability of iron is taken into consideration (Table 27.4). Women in reproductive ages require only 19.6 mg daily of iron when diet is 15% bio-available compared to about 58.8 mg when diet is poor in vitamin C and animal protein and the bio-availability is only 5% [37]. Poor total intake of iron as well as low bioavailability of iron consumed results in iron deficiency and subsequently IDA. In adolescents, there is also a tendency to frequently consume snacks prepared from cereals as well as a habit to consume carbonated drinks while there is a lower desire to eat fruits and vegetables. Moreover, habitual consumption of tea/coffee immediately after meals by adolescent girls also contributes to higher prevalence of anemia of 50% as compared to 34% in

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Table 27.3 Dietary intakes (energy, protein and iron) by adolescent girls in Bangladesh, Indonesia and India [33, 34, 35] Bangladesh (Adolescent girls)

Energy (kcal)

Intake (RDA)

Indonesia (Adolescent girls 10–12 years)

1005 (1970 kcal (10–12 years) 2060 kcal (13–15 years)

India

Non-IDA

IDA

1122 (1900)

1126 (1900)

2060 kcal (16–18 years))

Protein (g)

Intake (RDA)

44 (-)

43.8 (54)

45.3 (54)

Iron (mg)

Intake (RDA)

18 (28)

6.9 (14)

8.3 (14)

1389 (10–12 yrs) (1970) 1566 (13–15 yrs) (2060) 1630 (16–17 yrs) (2060)

37.8 (10–12 yrs) (57) 42.0 (13–15 yrs) (65) 43.9 (16–17 yrs) (63) 11.5 (10–12 yrs) (19) 13.0 (13–15 yrs) (28) 13.5 (16–17 yrs) (30.0)

* Figures in parenthesis indicate recommended dietery allowances (RDA) Table 27.4 Selected recommended daily intakes for iron by estimated dietary iron availability [37] Dietary iron Children Children Women Women bioavailability (1–3 years) (4–6 years) (19–50 years) during (Percentage) pregnancy (2nd trimester) (mg)

Women Men (19– during 50 years) breast feeding (0–3 months lactation) (mg) (mg)

(mg)

(mg)

(mg)

15

3.9

4.2

19.6

>50.0

10.0

9.1

10 51

5.8 11.6

6.3 12.6

29.4 58.8

>50.0 >50.0

15.0 30.0

13.7 27.4

Recommended daily intake for iron depends on the bio-availability of the diet: diet rich in vitamin C and animal protein = 15%; diet rich in cereals, low in animal protein, but rich in vitamin C = 10%, diet poor in vitamin C and animal protein = 5%.

those who do not consume tea/coffee after meals [33]. Although the iron density in the diets of both boys and girls is similar, the lower total food intake or energy intake by adolescent girls compared to boys, combined with menstrual losses cause adolescent girls to be at greater risk of iron deficiency and IDA [12]. In fact, in developing countries, 20% of women with normal menstruation have serious problems in meeting their iron requirements by food alone [34]. Social discrimination towards girl child as well as the frequent tendency of dieting play a crucial role in worsening

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the quality and quantity of diet and the dietary iron consumed by adolescents. (c) Frequent infectious disease and parasitic infections – The frequent occurrence of infectious diseases and parasitic infestations in developing countries further increases requirements for iron and increases the chances of negative iron status and IDA. In a study in India, one-third of adolescents had a history of passing worms [38]. The prevalence of anemia was double in these girls (53.6%) compared to those who were not reported to be infested (25%). Infections and infestations interfere with food intake, assimilation and absorption, storage and use of many nutrients such as iron, vitamin B12, folic acid, vitamin C, vitamin A etc which contribute to anemia. IDA during adolescence is primarily due to deficiency of iron resulting from low availability of dietary iron and less often due to deficiency of other nutrients and other conditions such as hookworm infestations, schistosomiasis and other infections [28]. However, the role of infestation and infection in contributing to iron deficiency and anemia cannot be ignored. (d) Adolescent pregnancy – Added to the problem of poor dietary iron intake is the traditional practice of early marriage. Social pressure often results in most women conceiving within a year of marriage [39]. An onset of pregnancy during adolescence period of life further increases demands for iron and contributes to aggravating the iron deficiency and IDA. Table 27.5 indicates that in India, Bangladesh and Nepal [12, 35–37, 39, 40] over 50% girls are married by 18 years of age. In Indonesia, Thailand and Sri Lanka, 26, 22 and 12 per cent girls, respectively are married by 18 years of age. Studies on adolescent pregnant girls in Nepal and tribal India indicate risks and outcomes of pregnancy increases in such adolescent mothers with higher prevalence of anemia [41, 42]. Table 27.5 Percentage of women aged 20–24 married by age 15 and 18 in selected countries of South East Asia Region South East Asian Countries Bangladesh (1999–2000) [39] India (2005–2006) [12] Indonesia (2002–2003) [40] Nepal (2005) [36] Sri Lanka (2000) [35] Thailand (1987) [37]

Married by age 15 years (%) 32.3 18.2 4.3 14.1 1.5 2

Married by age 18 years (%) 66.2 47.4 22.0 56.1 10 20

Figure 27.4 presents an overview of the factors leading to higher iron requirements during adolescence and precipitation of anemia.

27.4 Adolescence, a silent phase of iron deficiency and iron deficiency anemia – prevention is critical

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Iron deficiency and iron deficiency anemia in adolescent girls

27.3

721

Consequences of iron deficiency and iron deficiency anemia

Since 16th century, there are references to diseases commonly affecting adolescent girls which are characterized by pallor, fatigue, poor appetite and menstrual disturbances which seem to be related to iron deficiency [42]. In fact iron deficiency anemia during adolescence sets up a vicious cycle of anemia during pregnancy and childhood with serious consequences (Figure 27.5). Iron deficiency anemia adversely affects transportation of oxygen to tissues and accounts for the diminished work capacity and physical performance. IDA during adolescence has serious implications for a wide range of outcome: impaired physical growth, weakened cognitive development, reduced physical and work performance/capacity and diminished concentration in daily tasks and school performance, loss of appetite resulting in reduced food intake as well as irregular menstruation [12]. Iron deficiency adversely affects the immune system. It has been estimated that each 1% decrease in hemoglobin results in a 1.5% decrease in work capacity and a 1–2% decrease in work output with economic consequences [23]. Anemic children exhibit poor attentiveness, poor memory and poor academic performance. It has been reported that anemia results in poor attention, concentration and scholastic performance [43, 44] and is associated with disturbances in attention and perception resulting in poor academic achievements [43]. Other clinical symptoms due to IDA include anorexia, flatulence, nausea, dimness of vision and headache which may ultimately affect school attendance, school retention and overall performance [28]. The serious implications of IDA needs to be seen with reference to its impact on lack of incentive to remain in schools, academic under achievements, poor school attendance and poor physical condition leading to poor economic productivity [45]. Iron deficiency in adolescent girls has serious implications on the future generation by adversely affecting the health of the fetus. Iron deficient adolescent girls have a higher risk of preterm delivery and having babies with low birth weight (LBW) [46, 47]. In fact anemia during adolescence limits growth and delays onset of menarche which may lead to cephalopelvic disproportion. IDA combined with early onset pregnancy results in increased maternal morbidity and mortality, increased risk of low birth weight, increased fetal morbidity and mortality as well as higher neonatal mortality [21, 48, 49]. These serious consequences are of special public health significance in developing countries where one third of adolescent girls are reported to be anemic [50] and 12 % of all women aged 15–19 years and 44% of married women aged 15–19 years are reported to have atleast one child [12]. In fact, severe anemia increases the risk of mortality of pregnant mothers with poor iron stores [51]. Investment in

27.5 Consequences of iron deficiency (ID) and iron deficiency anemia (IDA) during the life cycle [52].

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Iron deficiency and iron deficiency anemia in adolescent girls

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building iron nutriture during adolescence is therefore critical not only for prevention of anemia and ill health during the adolescence phases of life itself but is crucial for mother’s health and fetal development as well as child growth and development later in life (Figure 27.5). With such serious adverse effect of iron deficiency and iron deficiency anemia, overcoming iron deficiency has significant impact on Millennium Development Goals (MDGs) as presented below in Box 27.1[52]. Box 27.1 Iron deficiency and iron deficiency anemia (IDA) prevention in Women of Reproductive Age (WRA) help to achieve the MDGs [52] MDG goals

Impact of IDA prevention

MDG # 1 Eradicate Extreme Poverty and Hunger

• Increases body’s capacity to do work (for every 10% increase in HB – 15% increase in physical work) • Reduces low birth weight • Reduces undernutrition in under 5 year MDG # 2 Achieve Universal • Reduces frequency and severity of Primary Education infections/morbidity and mortality • Improves School attendance, retention, learning capacity and school achievement MDG # 3 Promote Gender • Anemia in girls – often more severe than Equality and Empower Women in boys. Adversely influences school attendance and achievement. • Reduces Gender disparity MDG # 4 Reduce Child • Reduces serious consequences on child Mortality health, including LBW, still birth • Reduces Child mortality MDG # 5 Improve Maternal • Reduction of maternal anemia Health • Reduces MMR (20% of maternal deaths are directly attributed to anemia)

27.4

Prevention and control of iron deficiency and iron deficiency anemia

The most effective public health approach to prevent and control iron deficiency and iron deficiency anemia is a multiple integrated intervention comprising the following three main strategies – food-based approach, iron supplementation and public health interventions (Figure 27.6). The country strategy, however, needs to be based on analysis of the local situations. The most cost-effective means of determining whether iron deficiency is the cause of anemia is to measure changes in hemoglobin or hematocrit status in response to oral iron supplementation [53]. For addressing iron deficiency and IDA, participation of sectors other than health sector such as education, food industry and horticulture is important. Dietary diversification is the most sustainable approach, but is a difficult

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intervention to implement as a public health measure since both the actual quantity of iron intake and bioavailability of iron consumed is important. Foods with high bio-available iron (animal food) or foods that enhance the absorption of iron such as foods rich in vitamin C are expensive. Dietary measure such as iron fortification of basic food has been shown to be effective in reducing prevalence of iron deficiency anemia. Fortification aims to increase the intake of nutrient without bringing a change in customary diet. Many developing countries are in the process of introducing consumption of foods fortified with iron and other micronutrients. Wheat flour and maize meal are two major food vehicles that have been successfully used for fortification with iron in developed and developing countries. Standards for levels of iron used for fortification vary in different countries. For example fortification of wheat flour with Ferrous Sulphate used in Canada is 29–43 parts per million (ppm), Chile 30 ppm and Nigeria 35 ppm [54]. Regular use of cereal foods fortified with iron and salt fortified with iodine and iron as well as use of micronutrient mix as home or institutional fortificant is cost-effective and important to be promoted for addressing anemia in population including adolescent girls.

27.6 Integrated strategy to address iron deficiency and iron deficiency anemia in adolescent girls

For improving iron status and prevention of iron deficiency anemia, regular use of iron-folic acid supplements is recommended as a public health approach. A joint consensus statement by UNICEF/UNU/WHO/ MI emphasizes that in countries where anemia prevalence exceeds 40% in pregnant women or is above 20 percent among women in reproductive

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age group, universal iron supplements of adolescent girls (minimum those aged 12–16 years) and women of child bearing age is warranted [55]. In 1999, a meta-analysis was undertaken to study the efficacy of intermittent iron supplementation in the control of iron deficiency anemia in developing countries [56, 57]. The analysis was based on the results of a total of 22 completed trials of iron supplementation, including 9 studies with adolescent groups (Table 27.5). The results indicated a positive impact with weekly supplements in 5 of the 9 studies. The meta-analysis study concluded that “it appears under highly controlled conditions, supplementation can have an impact on anemia prevalence and that the daily and weekly approaches may have similar impact”. Based on this conclusion, weekly supplementation with iron-folic acid was then recommended only in situations where there is a strong assurance of supervision and high compliance. Table 27.6 Efficacy of Daily and Weekly Iron Folic Acid Supplementation (WIFS) in various countries – meta-analysis study [55] Countries East Jakarta India Baroda Delhi Mumbai Malawi Malaysia Mali Peru Sri Lanka

% Prevalence of Anemia** Weekly Daily Control (B)* (E)* (B) (E) (B) (E) (B) (E) (B) (E) (B) (E) (B) (E) (B) (E) (B) (E)

17.9 6.7 53.8 66.2 49.0 48.2 65.0 33.9 11.1 12.0 49.8 9.0 29.6 38.0 18.4 17.3 25.0 9.5

15.6 7.8 63.5 44.4 47.0 30.9 61.6 26.2 12.8 11.9 NA* NA* 37.1 30.9 19.8 10.9 18.5 8.6

17.3 21.3 62.7 60.1 44.6 57.8 64.8 58.4 NA NA 0 10.1 28.9 39.0 15.5 22.7 19.8 13.4

* (B) refers to Baseline and (E) refers to Endline ** Anemia criteria – Hb < 12 g/L

This global meta-analysis study was followed by a number of efficacy trials on use of weekly iron-folic acid (IFA) supplements for the adolescent girls population in Asia, Africa and South America [57–60]. Based on the results of these projects , weekly and not daily iron–folic acid supplement consumption is proposed as a preventive approach to improve iron status and for reducing the prevalence of anemia. The positive impact of weekly consumption of iron supplement is explained on the basis of the “mucosal

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block” hypothesis wherein administration of iron every seven days is assumed to allow time for shedding of cells loaded with iron from a previous dose, thereby increasing iron absorption [61, 62]. Additionally, weekly dosage instead of daily dosage is considered to result in avoiding a constant luminal and mucosal overload and thus preventing likely stimulation of gastro-intestinal symptoms [61–64]. Weekly dosage is expected to have fewer side effects with a positive impact on increasing compliance and reduction in anemia. The impact of weekly iron folic acid supplements (WIFS) in reducing prevalence of anemia is evident in a short period of 6–12 months from a study undertaken in non-school going adolescent girls in the state of Uttar Pradesh, India (Figure 27.7) [65].

27.7 Impact on hemoglobin levels following 6 and 12 months of weekly IFA consumption on adolescent girls [65]

Targeting adolescent girls with WIFS is critical for prevention of anemia since their high requirements, if not met, could lead to depleted iron stores even before the onset of pregnancy [66, 67]. WIFS is a low cost intervention and this is of advantage since consumption of supplements is recommended throughout the reproductive period. Menarche often sets in by 12 years of age and it is beneficial to ensure that adolescent girls regularly consume iron-folic acid tablets right from the onset of menarche. Intervention to address anemia at younger age of 10–14 years as compared to 15–18 years has been demonstrated to give a better response in weight gain and Body Mass Index (BMI) and in the regularization of menstrual cycle. Regular consumption of IFA influences not only adolescent growth, physical output and educational performance but WIFS regime during adolescence is an investment for future and safe pregnancy [13]. Iron requirements during pregnancy are high and it is not always possible to

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absorb an adequate amount of supplementary iron, especially by those women who are iron deficient during pregnancy. Pregnancy itself is too short a period for addressing pre-existing anemia and in fact, it is noted that longer the pre-pregnancy preventive supplementation, the better its impact on iron nutrition during pregnancy [63]. Effort to improve iron status and anemia after the onset of pregnancy is therefore late and inadequate to meet the high requirements [65, 68]. Building pre-pregnancy iron stores contributes in lowering the risks of low birth weight, miscarriages and premature delivery since iron deficiency anemia as early as the first trimester itself increases the risks of premature delivery and low birth weight [36]. Building folic acid stores along with iron, prior to pregnancy, has the additional advantage of reducing the risks of neural tube defects (NTD) [69]. Regular consumption of WIFS during adolescence is envisaged to contribute to a set of behavior which is expected to have a beneficial effect in improving the acceptability as well as high compliance of IFA tablets during pregnancy. It is therefore obvious that actions for prevention of anemia need to be taken during adolescence itself and adequate iron status built up prior to the onset of pregnancy. Regular use of WIFS with the onset of menstruation is of special significance in developing countries where a very high percentage of girls enter pregnancy during the adolescence age itself. Along with WIFS, efforts to delay conception to over 18 years needs to be intensified for promotion of adolescent health and nutrition. WIFS programme for adolescent girls implemented on a large scale in a few countries demonstrated a high compliance of supplement ranging from 42% to 94% and a reduction in anemia prevalence of 9.3% to 56.8% in a period of 6–12 months of intervention (Table 27.7) [65–68, 70–76]. In these programmes, the use of a fixed day approach (Iron day or WIFS day) facilitated in addressing the problem of forgetfulness which was noted to be the primary cause of poor compliance (Table 27.8). Table 27.7 Large scale WIFS programme from six countries [65–68, 70–76]

(a) (b) (c)

Case study

Intervention period (months)

Compliance c (%) (Baseline) Reduction in anemia anemia prevalence (%) prevalence (%)

Indiaa Cambodia b Egyptb LAO PDR b Philippines b Vietnam b

12 6–12 6 6 12 9–12

70–94 98–100 92.2 74.5 64–99 80–93

73.3–93.0 58.0 30.0 43.0 33.3 37.5–45.6

WIFS composition – 100 mg elemental iron and 500 µg folic acid WIFS composition – 60 mg elemental iron and folic acid 0.3–3.5 mg All six countries – “Fixed” Day strategy used for WIFS Programme.

8.9–46.8% – 20.0 53.4 – 48.0–56.8

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The programme issues considered important for effective implementation and outcome of the WIFS programme are political commitment to control anemia and resources allocated for procuring good quality supplements, regular supply of IFA tablets in attractive blister packs, effective logistic management, use of a fixed day in a week as “Iron Day” for effective programme management and promoting regular weekly consumption of tablet, appropriate communication and social mobilisation strategy for ensuring community support and improving compliance [70]. Table 27.8 WIFS programme of India and Laos – percentage compliance [65, 70, 72]

India (UP) (Adolescent girl – non-school)(a) WIFS routinely taken (%) WIFS not taken (%) ● Forgetfulness ■ Side effects (vomiting, stomach ache, health problem) ● Onset of pregnancy ● Others (a) (b)

86.0 14.0 52.4 28.6(a) – 19.0

Lao PDR (WRAs)b

74.5 25.5 50.0 5.8 16.7 27.5

Only 4% of total adolescent girls studied complained of adverse side effects Women in reproductive age (WRA).

A regular quality and quantity supply of IFA supplements along with a good delivery system and consistent efforts for creation of demand for supplements through social mobilisation and education activities is essential. Regular supply and linkage with suitable delivery systems, which involves not only health sector but other sector such as education and groups of adolescent girls ,youth and community groups is useful [70, 77, 78]. A social marketing strategy used in WIFS pilot project in India [79] and three large studies in Cambodia, Vietnam, the Philippines have demonstrated that a well planned communication strategy combined with attractive packaging has a substantial “value addition” effect [61–65, 80]. Blister packaging of 4 tablets/blister or 10 tablets/blister for meeting requirements of one–two months supply is practical for distribution and monitoring of WIFS. Large scale unsupervised trials indicate that counseling of adolescent girls on positive attributes of WIFS and consuming tablets on a weekly designated day is effective in increasing compliance [68]. A study in Tanzania and India presents scientific evidence that a comprehensive communication strategy is effective for increasing acceptability and compliance even in the absence of supervision [65, 68]. Project findings

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demonstrate that adolescents who are reached through a well planned communication strategy view advantages for continuing WIFS to be much more important than discontinuing WIFS due to some minor side effects experienced. Communication strategy with a focus on the various benefits of WIFS such as improved learning, increase in concentration at school and work, higher level of energy, enhancement in skin glow or appearance as well as regularity of menstruation have been reported to be useful for mobilizing community and adolescent girls to regularly consume weekly dose of IFA tablets rather than information only on the side effects or emphasis on the future implications of WIFS on reproductive health. Monitoring distribution and consumption of IFA tablets through a special supplement record register as well as individual monitoring card has proved effective in improving compliance [68, 78]. In addition, periodic process and impact evaluation is recommended to be institutionalized to facilitate in programme adjustment and to check whether desired outcomes are being achieved. WHO (2008) has recommended regular consumption of weekly ironfolic acid supplements for the women in reproductive age [81]. Box 27.2 presents details. Box 27.2 The WHO statement 2008 on WIFS for women in the reproductive age (WRA) group [81] In 1998, a joint statement of UNICEF/UNU/WHO/MI emphasized universal regular iron-folic acid supplementation in regions where anemia prevalence is over 20% among women in reproductive age group or over 40% in pregnant mothers. In 2008, WHO issued a position statement on WIFS for women in the reproductive Age (WRA) Group [81]. The position statement is based on the consensus of a WHO Global Consultation on ‘Weekly Iron and Folic Acid Supplementation (WIFS) for Preventing Anemia in Women of Reproductive Age’ held in Manila, in April 2007 [82]. The WHO position statement is intended for a wide audience including implementing partners, scientists and governments involved in the design and implementation of public health interventions. Strategies to combat both iron deficiency and anemia, and to improve iron reserves and folate status of women of reproductive age (WRA) are emphasized to be integrated. In summary the statement highlights the following; ●

●

●

In population where the prevalence of anemia in WRA is over 20% (or >40% in pregnant woman or children under 5 years) and mass fortification programme of staple foods with iron and folic acid are unlikely to be implemented within 1–2 years, WIFS should be considered a strategy. Recommended composition of WIFS being 60 mg elemental iron and 2800 μg folic acid (although evidence for the effective dose of folic acid for weekly supplementation is very limited). Upon confirmation of pregnancy, daily supplementation with 60 mg iron and 400 μg folic acid during pregnancy and first 3 months postpartum is recommended. WIFS programme must be integrated with other efforts to control iron deficiency and anemia and should be planned as long term self sustained interventions that woman of child bearing WRA will utilize during their child bearing years.

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27.5

Anemia in adolescent girls in India and efforts launched at state level

Anemia prevalence rate in India is reported to vary between 48% and 90% [19, 83, 84]. A recent study on anemia prevalence in adolescent girls aged 10–19 years residing in eastern state of Assam, India [85] reported cent percent girls were anemic – 29.3% were mildly anemic (10–11 g%), while 58.5% girls had moderate anemia (7.0–9.9g%) and 12.3% had severe anemia (Hb <7g%). As per the national survey data [13] 55.8% adolescent age girls aged 15–19 years are anemic and of these 39% are reported to be mildly anemic. Prevalence of anemia is high across all socio-economic groups and 46.1% women in the highest economic group are anemic while in the lowest socio economic group, anemia prevalence is 64.3% [13]. Data from National family Health Survey [13] indicates 55.3% women in the reproductive age (WRA) are anemic and in only five states (Punjab, Manipur, Goa, Kerala and Mizoram) anemia prevalence is less than 40% while in 7 of the 28 states surveyed anemia prevalence is reported to be over 60% (Table 27.9). This India profile of anemia in WRA could be considered a proxy indicator of the situation of anemia in adolescent girls in various states of the country. Table 27.9 Anemia prevalence in women 15–49 (a) years in India (b) – state-wise profile [13] Percentage prevalence of anemia

States of India

< 40% (5 states) > 40–60% (16 states)

Punjab, Manipur, Mizoram, Goa, Kerala Delhi, Haryana (a), Himachal pradesh, Jammu & Kashmir, Uttaranchal, Chhattisgarh (a), Madhya Pradesh (a), Uttar Pradesh, Arunachal Pradesh, Meghalaya, Sikkim, Gujarat, Maharashtra (a), Karnataka, Tamil Nadu Bihar (a), Jharkhand (a), Orissa (a), West Bengal(a), Assam (a), Tripura (a), Andhra Pradesh (a)

> 60% (7 states) (a) (b)

Ten states have anemia prevalence over the national average of 55.3%. All India anemia prevalence is 55.3%.

A National Anemia Consultative Meeting of Government of India in 1997 recommended “adolescent girls on attaining menarche should continue one IFA tablet containing 100 mg elemental iron and 500 μg folic acid once a week. This should be accompanied by appropriate dietary counseling” [86]. The recommendations were based on the findings of the efficacy trails implemented in three regions of India with UNICEF support – Baroda, Delhi and Mumbai [83, 84, 87]. These trails compared the administration of daily iron folic acid (IFA) supplementation with weekly IFA. Additionally, the Consultation also reviewed the experience of social marketing of IFA tablets to adolescent girls, undertaken by a professional

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non government agency, Parivar Seva Sansthan for the State government of Delhi [79]. The Consultation highlighted the need for implementation of district level pilot projects for defining programme operational strategy. The Consultation recommended “The total duration for consumption of weekly dose of iron supplementation and its cost effectiveness and operational feasibility should be examined. These pilot projects should be carried out in 8–10 states in different regions of the country to facilitate in the formulation of the national policy for control of nutritional anemia among adolescents”. Following the National Consultation Meeting, WIFS programme was implemented in selected states of India [59]. The composition of the supplement used for WIFS was the same as that is supplied under the Reproductive Child Health (RCH) programme of the Government of India for the antenatal care (ANC) services, i.e. each tablet contains 100 mg elemental iron and 500 μg Folic Acid. The cost of annual supply of 100 tablets for a pregnant mother is estimated to be about 25 US cents while the cost for an adolescent girl consuming weekly iron supplement is estimated to be 12 US cents. The state programmes on anemia control in adolescent girls focus on weekly administration of IFA supplements to adolescent girls in school and out of school. The supplements are distributed free of cost. In some states biannual deworming is administered along with WIFS while in some states nutrition or family life education is also included in the package of services. For improving management and compliance, a “fixed WIFS day” approach is used [65, 66, 71, 84]. The health and education departments play a leading role in the WIFS programme for school going girls. The strategy for reaching girls out of school is noted to be more challenging and the system of Integrated Child Development Services (ICDS) is used along with the health sector for the distribution and monitoring of iron-folic acid supplement as well as for conducting education and community mobilisation activities. With one year’s intervention, a substantial decrease in anemia prevalence has been reported – the decrease varies from 5% in the state of Jharkhand to 43% in state of Andhra Pradesh and 50% in the state of Uttar Pradesh [59]. These state level implementations demonstrated that routine consumption of weekly iron folic supplements is a cost-effective intervention to address anemia in adolescent girls and it is critical that WIFS programme for adolescent population is accorded a high priority in the public health programmes of the country. Box 27.3 presents experience of an adolescent anemia project implemented in one of northern states of India.

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Box 27.3 Uttar Pradesh – UMANG (Uplifting Marriage Age, Nutrition and Growth) Project [65] A 4-year project UMANG was launched in the state of UP in 2003 with the objective of preventing iron deficiency and reducing anemia in adolescent girls in school and out of school. The intervention included weekly iron–folic acid tablets, family life education, and deworming tablets every 6 months. A total of 150,700 adolescent school and non-school girls in a district (Lucknow) were reached. Girls in school were reached through teachers in the school system and both education and health departments played active roles. Girls out of school were reached through the ICDS Programme. IFA supplement were distributed directly to adolescent girls by ICDS workers (AWW) through formation of an adolescent girls group and a “girl to girl” approach. Consumption of iron–folic acid tablets was supervised for schoolgirls but not for non-school girls. Hemoglobin levels were improved and anemia prevalence was reduced significantly at 6 months. No difference in the impact on hemoglobin levels or anemia prevalence was observed between supervised and unsupervised girls. Counseling on the positive effects of regular weekly iron–folic acid intake contributed to a high compliance rate of over 85%. Supervision in non-school system was not feasible but routine recording of distribution and consumption of IFA contributed to high compliance. The effect of supplementation on the prevalence of anemia and the compliance rate were assessed over a 4-year period. In 4 years, the overall prevalence of anemia was reduced from 73.3% to 25.4%. The cost of implementation was estimated to be US$0.36 per beneficiary per year. The results lead to the conclusion that weekly iron–folic acid supplementation combined with monthly education sessions and six monthly deworming is cost-effective in reducing the prevalence of anemia in adolescent girls. Appropriate counseling and effective monitoring system, irrespective of supervision, is critical for achieving positive outcomes. Following the success of UMANG project, the state government of Uttar Pradesh has included the weekly iron–folic acid supplementation programme for adolescent girls in schools as in the state implementation plan of the National Rural Health Mission (NRHM).

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(2007). Global consultation on Weekly Iron-Folic Acid Supplementation for preventing Anemia in women of Reproductive Age Group. 35. Sri Lanka Demographic and health Survey (2000). 36. UNICEF (2005). Early marriage, a harmful traditional practice: A statistical exploration. 37. CHOI JW, PAI SH, IM MG, KIM SK (1999). Change in transferrin receptor concentration with age. Lin Chem., 45, p. 1562. 38. RAWAT CMS (2000). An epidemiological study of anaemia in adolescent girls in the rural areas of Meerut. MD thesis, Chaudhary Charan Singh University, Meerut, India. 39. Bangladesh Demographic and Health Survey (2007). 40. Indonesia Demographic and Health Survey (2007). 41. SHARMA AK, VERMA K, KHATRI S , KANNAN AT (2001). Pregnancy in adolescents: a study of risks and outcome in Eastern Nepal. Ind Paed., 38, pp. 1405–1409. 42. SHARMA V and SHARMA A (1992). Health profile of pregnant adolescents among selected tribal population of Rajasthan. Ind J. Adol Health, 13(8), pp. 696–699. 43. LEVIN HM (1986). A benefit-cost analysis of nutrition program for anaemia reduction. Res Observer, 1, p. 219. 44. WEBB TE and OSKI FA (1974). Behavioural status of young adolescents with iron deficiency anaemia. J. Spec. Educ, 8, pp. 153–156. 45. DAMAYANTI D, SOEKARJO DD, SASKIA DE PEE, KUSIN JA, MARTIN W , BLOEM MW (2006). School-based supplementation: lessons learned in Indonesia. SCN News, 31, pp. 14–18. 46. SCHOLL TO, HEDIGER ML, FISCHER RL, SHEARER JW (1992). Anaemia vs iron deficiency: Increased risk of preterm delivery in a perspective study. Am J Clin Nutr, Adolescent nutrition (5), pp. 985–988. 47. SCHOLL TO and HEDIGER ML (1994). Anaemia and iron deficiency anaemia: complications of data on pregnancy outcome. Am J Clin Nutr, 59(2), pp. 492S500S, discussions 500S–501S. 48. BRABIN L and BRABIN BJ (1992). The cost of successful adolescent growth and development in girls in relation to iron and vitamin A status. Am J Clin Nutr, 55, p. 955. 49. VIR S (1998). Control of iron deficiency anaemia – a public health programme priority, Proceedings of XXXVI Nutrition society of India meeting, 26–27th Nov. 50. DEMAEYER E and ADIELS– TEGMAN M (1985). The prevalence of anaemia in the world. World Health Statistics, 38, p. 302. 51. BRABIN BJ, HEKIMI M and PELLETIER D (2001). An analysis of anaemia and pregnancy related maternal mortality. J. Nutr., 131, pp. 604S–614S. 52. CAVALLI- SFORZA T, BERGER B, SMITASIRI S , VITERI F (2005). Weekly iron folic acid supplementation of women of reproductive age: impact overview, lessons learned, expansion plans, and contributions toward achievement of the millennium development goals. Nutrition Reviews, 63(12), pp. S152–S158. 53. YIP R, STOLTZFUS R , SIMMONS W, (1996). Assessment of prevalence and nature of iron deficiency for population .The utility of comparing hemoglobin distribution. In: Iron Nutrition in Health and Disease. Hallberg L and Asp, N (eds).: John Libby and Co. Ltd, London, pp. 31–48. 54. L O T F I M et al, Fortification of Foods: Current Practice, Research and Opportunities. The Micronutrient Fortification of Foods: Current Practices, Research and Opportunities. The Micronutrient Initiative and International Agriculture Centre, Ottawa, Canada. VITERI

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(1998). Technical workshop on preventing iron deficiency in women and children – technical consensus on key issues. BEATON GH and MCCABE GP (1999). Efficacy of Intermittent Iron Supplementation in the Control of Iron Deficiency Anaemia in Developing Countries: An Analysis of Experience. Final report to the Micronutrient Initiative. BERGER J , THANH HTK , TOMMASO CS , SUTTILAK S , KHAN NC , MILANI S, HOA PT , QUANG ND , VITERI F (2005). Community Mobilization and Social Marketing to Promote Weekly Iron-Folic Acid Supplementation in Women of Reproductive Age in Vietnam: Impact on Anemia and Iron Status. Nutrition Reviews, 63(12), pp. S95–S108. BOTHWELL TH (2000). Iron requirements in pregnancy and strategies to meet them. Am J Clin Nutr, 72, pp. 257S–264S. DWIVEDI A and SCHULTINK W (2006). Reducing anaemia among Indian adolescent girls through once-weekly supplementation with iron and folic acid. SCN News, 31, pp. 19–23. ANGELES - AGDEPPA I , SCHULTINK W, SASTROAMIDJOJO S , GROSS R, KARYADI D (1997). Weekly micronutrient supplementation to build iron stores in female Indonesian adolescents. Am J Clin Nutr, 66, pp. 177–183. W R I G H T A J and S O U T H O N S (1990). The effectiveness of various iron supplementation regimens in improving the Fe status of anaemic rats. Br J Nutr. 63, pp. 579–585. VITERI FE (1995). Iron deficiency in children: New possibilities for its control. Int Child Health, 6, pp. 49–61. SCHULTINK W (1997). Iron Supplementation Programme Compliance of target groups and frequency of tablet intake. FNB, 18, pp. 64–70. GROSS R et al (1997). Daily versus weekly iron supplementation: Programmatic and economic implications for Indonesia. FNB, 18, pp. 64–70. VIR SC, SINGH N, NIGAM A , JAIN R (2008). Weekly iron and folic acid supplementation with counseling reduces anaemia in adolescent girls: A large scale effectiveness study in Uttar radish, India. Food and Nutrition Bulletin, 29(3), pp. 186–194. KOTECHA PV , PATEL RZ , KARKAR PD , NIRUPAM S (2002). Impact evaluation of adolescent girl’s anaemia reduction program, Vadodara district. Government of Gujarat and UNICEF. SHARMA K and GANDHI H . A study on assessing the impact of adolescent anaemia control project among out of school adolescent girls, a midterm evaluation in Shivpuri district, Madhya Pradesh. Department of Women and Child Development, State Government of Madhya Pradesh, India and UNICEF. Egypt’s Adolescent Anemia Prevention Program (Ref – Ministry of Health and Population, Health Insurance Organization, 1999). BOTTO LD et al (1999). Neural-tube defects. New England Journal of Medicine, 341, pp. 1509–1519. VIR SC (2009). Micronutrient and Child Health Workshop, 20–23rd October 2009, AIIMS, New Delhi. SAIYED F (2008). UNICEF Patna field office report, India. Preliminary report of operational trial of weekly iron folic acid supplementation (2007). Sekong province, Lao People’s Democratic Republic. Ministry of Health and WHO. PASRICHA SR, CARUANA SR , PHUC TQ , CASEY GJ , JOLLEY D , KINGSL S, TIEN NT, MACGREGOR L , MONTRESOR A , BIGGS BA (2008). Anemia, iron deficiency, meat consumption

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Public health nutrition in developing countries and hookworm infection in women of reproductive age in Northwest Vietnam. Am. J. Trop. Med. Hyg., 87 (3), pp. 375–381. KANAL K , HALLEN JB , SFORZA TC , CRAPE B , SMITASIRI S and the Cambodian weekly iron folic acid program team (2005). Weekly iron folic acid supplements to prevent anemia among Cambodian women in three settings: process and outcomes of social marketing and community mobilisation. Nutrition Reviews. 63(12), pp. S126–S133. PAULINO LS, AGDEPPA IA , ETORMA UMM , RAMOS AC , SFORZA TC (2005). Weekly iron folic acid supplementation to improve iron status and prevent pregnancy anemia in Filipino women of reproductive age: The Philippine experience through government and private partnership. Nutrition Reviews. 63(12), pp. S109–S115. KHAN NC , THANH HTK , BERGER J , HOA PT , QUANG ND , SMITASIRI S, SFORZA TC (2005). Community mobilisation and social marketing to promote weekly iron folic acid supplementation: a new approach toward controlling anemia among women of reproductive age in Vietnam. Nutrition Reviews. 63(12), pp. S87–S94. NORSWORTHY B et al (2004). Effects of once-a-week or daily folic acid supplementation on red blood cell folate concentrations in women. European Journal of Clinical Nutrition, 58, pp. 548–554. GILLESPIE S (1998). Major issues in the control of iron deficiency. MI/UNICEF. PARIVAR SEWA SANSTHAN , UNICEF ( INDIA ) (1997). Project on Social marketing of Iron Tablets, personal communication. ADANK C , GREEN TJ , SKEAFF CM , BRIARS B (2003). Weekly high dose folic supplementation is effective in lowering serum homocysteine concentration in women. Annals Nutr Metabol, 4, pp. 55–59. WHO (2008). Weekly iron and folic acid supplementation (WIFS) in women of reproductive age: its role in promoting optimal maternal and child health. WHO (2007). Global Consultation on weekly iron and folic acid supplementation (WIFS) for preventing anaemia in women of reproductive age, 25–27th April 2007, Manila, Philippines. MEHTA MN (1998). Effectiveness of daily and weekly iron and folic acid supplementation in anaemic adolescent girls. Final report of the UNICEF research project, Bombay. SESHADRI S (1998). Oral iron supplementation to control anaemia in adolescent girls. MS University of Baroda and UNICEF, India. VIR SC (2008). Report on nutritional status of women and children in tea estate of Dibrugarh, Assam, UNICEF consultancy report. Department of Family Welfare, Maternal Health Division, Ministry of Health and Family Welfare, Nirman Bhawan, New Delhi. National Consultation on control of nutritional anaemia in India 16–17th October 1997, GoI (1998). AGARWAL KN (1998). Assessment of the prevalence of anaemia and iron stores in response to daily and weekly iron and folic acid supplementation in adolescent girls (10–18 years) from urban slums of northeast Delhi. UNICEF project report.

28 Zinc – an essential micronutrient for health and development Sunil Sazawal and Pratibha Dhingra

Sunil Sazawal, MD, MPH, PhD, is an Associate Professor, Johns Hopkins Bloomberg School of Public Health; Visiting Professor, Annamalai University, India; and the Director, Center for Micronutrient Research, New Delhi, India. Dr Sazawal is a physician by profession and has more than 20 years of research experience in conducting clinical and community-based trials of micronutrient interventions, especially in role of zinc and iron in reducing infectious diseases and mortality in children. Pratibha Dhingra, PhD, is a Senior Research Scientist at the Center for Micronutrient Research, New Delhi, India. Dr Dhingra has more than 16 years of research experience in community-based health projects, with a special focus on role of micronutrients in preventing and improving the health, growth and development of children.

&.1

Introduction

Zinc is an essential micronutrient for all forms of life and plays a critical structural and functional role in multiple enzyme systems involved in gene expression, cell division and growth, immunologic and reproductive functions. Clinical zinc deficiency in humans was first described in Iran in 1961, when the consumption of diets with low zinc bioavailability due to high phytic acid content was associated with delayed sexual development and “adolescent nutritional dwarfism” [1] and later recognized in a group of patients from Egypt with hypogonadism, anemia and hepatosplenomegaly [2]. Since then, zinc insufficiency has been recognized as an important public health issue, especially in developing countries [3].

&.

Biological functions of zinc

Zinc occurs in divalent state (Zn++) and is a bluish white metallic element (atomic number 30, atomic weight 65.4), which makes up about 0.002%

737

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of the earth’s crust and is the 23rd most abundant element. Zinc is associated with more than 200 distinct metalloenzymes, which have a diverse range of functions, including the synthesis of nucleic acids and specific proteins, such as hormones and their receptors [4]. Zinc also chelates with the amino acids cysteine and histidine, forming ‘zinc fingers’ that are important for protein transcription. Additional processes that are regulated by zinc include expression of the metallothionein gene, apoptosis and synaptic signaling. Zinc plays an important role in human metabolism and in the perpetuation of genetic material, including transcription of DNA, translation of RNA, and ultimately cellular division. Zinc deficiency at the gene regulatory level probably provides the common mechanism for many of the clinical signs of zinc deficiency such as growth failure, skin abnormalities and other signs that occur in various organs and organ systems. Of auxiliary interest is the absence of redox properties in zinc, which allows it to be transported in biological systems without inducing oxidant damage, as can occur with other trace elements, such as iron and copper.

28.3

Public health significance

Zinc Investigators’ Collaborative Group, 2000 [5] has emphasized the significance of zinc in human nutrition and public health due to its role in normal growth/tissue repair; neural, cognitive and sexual development; immune function, resistance to disease and stress. Estimates indicate that approximately 20.5% of the world’s population might be at risk of zinc deficiency [6]. Zinc affects health, mental/physical function, and survival of more than two billion people worldwide and ranks fifth in the leading risk factors for illness and disease in developing countries with high mortality [7]. Zinc deficiency is estimated to be responsible for 453,207 deaths globally [8]. Of these, 260,502 occur in Africa, 182,546 in Asia and 10,159 in Latin America. Zinc deficiency is considered responsible for 14.4% of diarrhea deaths, 10.4% of malaria deaths and 6.7% of pneumonia deaths among children between 6 months and 5 years of age [8]. A loss of nearly 16 million global disability-adjusted life years (DALYs) is attributed to zinc deficiency [9]. In India, estimated population at risk of inadequate zinc intake is as much as 25.9 % which is considered to be high risk category [7].

28.4

Zinc epidemiology

The epidemiological data on zinc deficiency has lagged behind that for other more well known vitamin and mineral deficiencies because of lack of scientific, practical, and accepted indicators for zinc deficiency. Population-based surveys have not been undertaken, marginal zinc

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deficiency is not characterized by a highly specific deficiency syndrome and severe clinical deficiency in humans is rare. Importance of mild zinc deficiency has been documented in the last decade in clinical trials of zinc supplementation. Risk of zinc deficiency is highest among infants, young children, pregnant and lactating women, when there is an extra demand due to multiplicative cell growth. Risk factors include insufficient dietary intake due to poverty, food taboos, and special diets (i.e. vegetarian diets that are high in phytate and fiber). Dietary zinc intake of young children appears to be inadequate in many developing countries [10, 11]. Women of childbearing age have inadequate dietary zinc intake in many populations [12, 13]. Eighty percent of women globally, and 100% women in developing countries, have inadequate zinc intake during pregnancy [14]. Individuals with malabsorption syndromes, diarrhea and parasitic diseases, acrodermatitis enteropathica, sickle cell disease, and cystic fibrosis are also at higher risk of zinc deficiency.

28.5

Clinical manifestations of zinc deficiency

Clinical manifestations of zinc deficiency are generally non-specific, vary widely, and depend on the severity of deficiency. The clinical manifestations in severe cases of zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males and are fatal if unrecognized and untreated. Moderate zinc deficiency is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, the symptoms include oligospermia, slight weight loss, and hyperammonemia [15].

28.6

Dietary sources, intake, absorption and bioavailability

Zinc content in foods is closely related to their protein content. Richest sources of dietary zinc are animal products such as shellfish, poultry, beef, and other red meats. Nuts and legumes are relatively good plant sources of zinc. Foods from plant sources such as beans, lentils, chickpeas, and peas are relatively rich in zinc. Little zinc is found in white rice or wheat breads, as zinc is contained in the bran and germ portions of whole cereal grains, which are normally lost through milling. Dairy products contain only moderate amounts of zinc. Zinc content of some common foods is shown in Table 28.1. Zinc intake in developing

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countries is commonly sub-optimal due to usual consumption of foods with very poor sources of zinc. Table 28.1 Zinc content of some of the commonly consumed foods Zinc category (mg/1000 kcal)

Foods

Very poor (0-2)

Fats, oils, butter, cream, cheese, sweets, chocolates, soft drinks, alcoholic drinks, preserves Fish, fruits, refined cereal products, pastries, biscuits, cakes, puddings, tubers, plantains, sausages, chips Whole grains, pork, poultry, milk, low fat cheese, yoghurt, eggs, nuts Lamb, leaf, and root vegetables, crustacea, beef, kidney, liver, heart, mollusks

Poor (1-5) Rich (4-12) Very rich (12-882)

Zinc in flesh foods is more bioavailable than the zinc in plant foods because during their digestion certain L-amino acids and cysteine containing peptides are released, which form soluble ligands with zinc. Plant based diets often contain high levels of phytic acid (myoinositol hexaphosphate), dietary fiber, oxalate, tannin and lignin, the components known to inhibit absorption of dietary zinc. Of these, phytic acid, the major storage form of phosphorus in whole grains, legumes, oleaginous seeds and leafy vegetables, is the most potent inhibitor of zinc absorption as it forms insoluble chelates at alkaline pH [16]. However, lower inositol phosphates (i.e. tetra-, tri-, di-, and mono-inositol phosphates), formed by enzymatic or non-enzymatic hydrolysis of phytic acid, do not form insoluble complexes with zinc. The bioavailability of dietary zinc can be predicted from the ratio of phytic acid (Phy) to zinc (Zn) in the diets. The critical (Phy): (Zn) molar ratios associated with the risk of zinc deficiency are equivocal; ratios above 15 having been associated with biochemical, and in some cases, even the clinical signs of zinc deficiency in humans [17]. Soaking and fermentation of plant foods are among some strategies that can be used to reduce intake of phytic acid, as phytate is partially hydrolyzed to other analogous metabolites that have a lower capacity to bind zinc. The enzymatic action of yeast reduces the level of phytic acid in foods. Therefore, leavened whole grain breads have more bioavailable zinc than unleavened whole grain breads.

28.7

Physiology of zinc

28.7.1 Physiology and metabolism of zinc The total body content of zinc is approximately 2 g and it is present in all the tissues/fluids of the body [18]. The skeletal muscle accounts for about 60%, bone for 30% and plasma 0.1% of the total body content of zinc. But

Zinc – an essential micronutrient for health and development

741

plasma zinc has a rapid turnover rate, and its level appears to be under close homeostatic control. High concentration of zinc is found in the choroid of the eye as well as in prostatic fluids, semen ejaculates up to 1 mg and losses in menstruation are small (0.01 mg) [19, 20], other losses like normal daily zinc loss of hair are probably insignificant. Zinc is not stored in the conventional sense. Under conditions of bone resorption and tissue catabolism, it can be released and to some extent reutilized. Experimental studies in humans showed that in low zinc-containing diets (2.6–3.6 mg/day), plasma zinc and the activities of zinc-containing enzymes can be maintained within a normal range over several months indicating some zinc availability from tissues [21]. Zinc is lost from the body via kidneys, skin and the intestine; the endogenous intestinal losses can range between 0.5 and 3.0 mg/day depending on the zinc intake but exercise, diarrhea and fever could lead to large losses [22].

28.7.2 Zinc absorption Zinc is absorbed mainly in the small intestine. Under normal circumstances the gastrointestinal tract adapts effectively to changes in zinc intake and/or nutriture with compensatory changes in the fractional absorption and excretion of endogenous zinc [23]. Pancreatic secretions deliver zinc into the duodenum equivalent to that provided by most meals. The intestine reabsorbs appropriate amounts of zinc from both dietary and endogenous sources to maintain favorable zinc balance. Zinc is absorbed both by passive diffusion and through a carrier-mediated process on the brush border of enterocytes. Zinc absorbed from the intestinal lumen is bound to many different molecules within the enterocytes, and metallothionein and cysteine-rich intestinal protein play a role in transmucosal transport.

28.7.3 Zinc homeostasis Zinc homeostasis is affected by the liver and intestine at adequate and marginally adequate dietary zinc intakes [24]. When the body is at risk of zinc deprivation, intestinal absorption of exogenous zinc increases and there is a reduction in intestinal losses of endogenous zinc arising from intestinal conservation with an up regulation of carrier sites, and from a reduction in the pancreatico-biliary secretion of zinc, and to a lesser extent, increased renal conservation of the element [23]. These mechanisms are important because with the exception of the possible hepatic labile pool, there are no specific systemic stores of zinc and we are dependent on acquiring zinc from external sources [25]. Zinc transporters such as ZIP proteins (zinc importer proteins) and ZnT

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(zinc transporter proteins) have recently been recognized as two families of proteins involved in understanding the mechanisms of zinc-absorption and homeostasis. ZIP proteins transport zinc from the extracellular space and intracellular organelles into the cytoplasm [26]. ZnT proteins are primarily involved in the cellular efflux of zinc and in uptake of zinc by intracellular organelles. Thus, the net effect of these transporters is to decrease cytoplasmic zinc [27].

28.7.4 Zinc requirements Varied estimates of zinc requirements have been proposed by several expert committees [28–32]. In 2004, the International Zinc Consultative Group (IZiNCG) Steering Committee [7] reviewed the methods used by the World Health Organization and Food and Nutrition Board/Institute of Medicine (FNB/IOM) committees to estimate zinc requirements, taking into consideration the methodology used to measure absorption, the types of diets and subjects from whom the data were derived, as well as the models used to summarize these data. Based on the review, this Committee followed the factorial approach used by the FNB/IOM but decided to base intestinal losses of endogenous zinc on the estimates derived by IZiNCG [7], and to use the NCHS/CDC/WHO reference body weights for laying down the zinc requirements. Using this approach for computing the estimated average requirement (EAR) of zinc [EAR of zinc is the amount of zinc that must be absorbed to match the amount of endogenous zinc losses. Both intestinal and non-intestinal sources (urine, surface losses of skin/hair/nail/sweat) contribute to endogenous zinc losses], the requirements for different ages and physiologic groups are laid down (Table 28.2). Table 28.2 Recommended dietary intake of zinc [31] Children Population Age group

Adults

Males Females Population (mg/day) (mg/day) group

Age

Males Females (mg/ day) (mg/day)

Infants Infants

0-6 months 2 (AI) 7-12 months 3

2 (AI) 3

Adolescents 14-18 years Adults 19 years and

Children

1-3 years

3

Pregnancy

older 18 years and

-

12

Pregnancy

younger 19 years and

-

11

Lactation

older 18 years and

-

13

Lactation

younger 19 years and

-

12

Children Children -

4-8 years 9-13 years -

3 5 8 -

5 8 -

older

11 11

9 8

Zinc – an essential micronutrient for health and development

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28.7.5 Interaction of zinc with other trace elements A bi-directional interaction between copper and zinc has been postulated, one reducing the bioavailability of the other [33]. High levels of zinc (120– 240 mg/kg) in the diets of rats have been reported to result in lower copper levels in the serum and liver. Dietary zinc deficiency has also been reported to cause mild increase in tissue copper levels. Conversely copper deficiency has been reported to result in mild increase in zinc absorption. Experimental zinc deficiency in guinea pigs caused significant reductions in plasma sodium (Na), potassium (K) and zinc (Zn) and increase in copper (Cu) and iron (Fe) content(s) of liver and kidney. Conversely, zinc supplementation improved the serum and tissue mineral levels whereas levels of hepatic Cu and Fe remained unchanged [11]. Zinc and vitamin A interact in several ways. Zinc is a component of retinol-binding protein, a protein necessary for transporting vitamin A in the blood. Zinc is also required for the enzyme that converts retinol (vitamin A) to retinal. This latter form of vitamin A is necessary for the synthesis of rhodopsin, a protein in the eye that absorbs light and thus is involved in dark adaptation. Zinc deficiency is associated with decreased release of vitamin A from the liver, which may contribute to symptoms of night blindness that are seen with vitamin A deficiency [34, 35]. I n c h i l d r e n w i t h s e v e r e p r o t e i n e n e rg y m a l n u t r i t i o n , z i n c supplementation improved serum retinol binding protein and retinol concentration [36]. Combined zinc and vitamin A synergistically reduced the prevalence of persistent diarrhea and dysentery. Zinc was associated with a significant increase in acute lower respiratory infection, but this adverse effect was reduced by the interaction between zinc and vitamin A [37]. The zinc to iron ratio in the diet may be of importance for the absorption of the individual trace elements [38]. In thirty-one adult subjects, simultaneous administration of zinc sulphate and ferrous sulphate in a ratio of Fe/Zn of 1:1 slightly inhibited zinc absorption while Fe/Zn ratio 2:1 and 3:1 inhibited zinc uptake [39]. High iron concentrations that are present in some supplements can reduce zinc absorption. The effect of iron on zinc will only occur when the iron to zinc ratio is very high (such as 25:1) and both are administered in solutions. Similarly, iron fortification of food has no adverse effect on zinc absorption and long term use of iron supplements does not impair zinc absorption or status. Thus, under most dietary conditions, Zn–Fe interaction is not likely to have a major influence on zinc requirement. But there is now evidence to suggest that iron supplementation with zinc may increase morbidity of infectious diseases [40] and the risk of adverse events especially in malarious areas [41], and may reduce linear growth in iron replete infants [42, 43].

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There is also evidence that high calcium (2.0 g/d) reduced zinc absorption significantly whereas phosphorus (2.0 g/d) did not change the absorption. However, zinc balance was not significantly different with change in dietary calcium levels. Excess dietary calcium has been shown to decrease zinc absorption in animals, but such an effect is less conclusive in humans. While calcium phosphate decreases zinc absorption, calcium citrate-malate does not. The presence of phytate may also influence the effect of calcium on zinc absorption. Calcium may interact with zinc and phytate to form insoluble complexes, thus rendering zinc unavailable. Nonetheless, available data suggest that a calcium-rich diet has no significant inhibitory effect on zinc absorption, provided intake of zinc is adequate [44]. Studies on zinc-folate interaction have produced conflicting results. Some have shown low zinc intake decreases folate absorption, while others have not found such an adverse effect. Administration of 800 μg of folic acid daily for 2 weeks to a group of adults inhibited zinc absorption when the fractional rate of zinc absorption was higher than 30% [45]. This finding raises concern about pregnant women, who are often given supplemental folic acid to reduce the risk of birth defects. Otherwise, folate supplementation does not appear to have a deleterious effect on zinc status.

28.7.6 Zinc and immune response Zinc is known to play a central role in the immune system, and zincdeficient individuals experience increased susceptibility to a variety of pathogens. The immunologic mechanisms whereby zinc modulates increased susceptibility to infection have been studied for several decades. Zinc affects multiple aspects of the immune system, from the barrier of the skin to gene regulation within lymphocytes. Zinc is crucial for normal development and function of cells mediating nonspecific immunity such as neutrophils and natural killer cells. Zinc deficiency also affects development of acquired immunity by preventing both the outgrowth and certain functions of T lymphocytes such as activation, Th1 cytokine production, and B lymphocyte help. Likewise, B lymphocyte development and antibody production, particularly immunoglobulin G, is compromised. The macrophage, a pivotal cell in many immunologic functions, is adversely affected by zinc deficiency, which can dysregulate intracellular killing, cytokine production, and phagocytosis. The effects of zinc on these key immunologic mediators is rooted in the myriad roles for zinc in basic cellular functions such as DNA replication, RNA transcription, cell division, and cell activation. Apoptosis is potentiated by zinc deficiency. Zinc provides a biological basis for the altered host resistance to infections observed during zinc deficiency and supplementation [46–48].

Zinc – an essential micronutrient for health and development

28.8

745

Evidence from zinc supplementation studies on child health

28.8.1 Zinc supplementation and physical growth Zinc-responsive growth stunting has been identified in many studies from several regions worldwide. A meta-analysis of growth data from zinc intervention trials recently confirmed the widespread occurrence of growthlimiting zinc deficiency in young children, especially in developing countries [49]. The meta-analysis showed a significant positive effect of zinc supplementation (ranging from 0.9 to 21.4 mg of zinc/day) on growth among prepubertal children [50]. Zinc supplementation produced a highly significant, positive impact on children’s linear growth, with effect size of 0.170 (95% CI: 0.075 to 0.264, p = 0.001) and weight gain, with a mean effect size of 0.119 (95% CI: 0.048 to 0.190; p = 0.002). Although the exact mechanism for the growth-limiting effects of zinc deficiency is not known, research indicates that zinc availability affects cell-signaling systems that coordinate the response to the growth-regulating hormone, insulin-like growth factor-1 (IGF-1) [51].

28.8.2 Therapeutic effects of zinc supplementation and morbidity Effects of zinc on diarrhea Diarrhea is still the major cause of childhood mortality estimated to cause 2 million deaths and remains responsible for 18% of all child deaths [52, 53]. The adverse effects of zinc deficiency on immune system function are likely to increase the susceptibility of children to infectious diarrhea, and persistent diarrhea contributes to zinc deficiency and malnutrition. Zinc deficiency may also potentiate the effects of toxins produced by diarrheacausing bacteria like E. coli [54]. Two measures of the effects of zinc supplementation on diarrhea have been reported in the literature. First, the ‘therapeutic effect’ which describes the effect of giving zinc supplementation to the child during an episode of diarrhea. Second, the ‘preventive effect’ which describes the effect of zinc supplementation given over a prolonged period on the occurrence and severity of diarrhea morbidity to all children in a population where there is some indication of zinc deficiency. Therapeutic effects of zinc supplementation on acute and persistent diarrhea The role of zinc supplement (5–45 mg/day) in acute diarrhea (<7 days duration) has been recently updated in a meta-analysis which included 14 randomized controlled trials (Figure 28.1) [55].

28.1 Impact of zinc supplementation on mean duration of acute diarrhea, all age groups, WMD, weighted mean difference [55]

746 Public health nutrition in developing countries

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Current analysis of the adjunctive therapeutic benefit of zinc in acute diarrhea corroborates existing reviews [5] and provides evidence of reduction in duration of diarrhea by half a day. However, zinc supplementation was found to have no beneficial impact in infants under 6 months of age. Studies assessing the impact of zinc supplementation on the clinical outcome of the treated episode demonstrated 32% reduction in episodes of diarrhea lasting more than 7 days and a reduction in the frequency and/or volume of stools [56, 57]. Zinc supplementation given during a diarrheal episode and for a few days following the end of the episode (14 days) [58, 59] provides additional benefits, including decline in diarrheal incidence, and reduction in non-injury deaths. Boxes 28.1 and 28.2 present the experience with introduction of zinc supplementation in treating childhood diarrhea in India and other developing countries. Box 28.1 Experiences with introduction of zinc supplementation in treating childhood diarrhea in developing countries In recent years, three large-scale effectiveness trials using zinc for the treatment of diarrhea have been completed in India, Pakistan, and Bangladesh through both the public and the private sector health systems. Preliminary evidence suggests there was substantial reduction in diarrheal morbidity with zinc usage [60]. In these studies, the strategy was to give 20 mg elemental zinc daily in tablet/syrup form for 14 days along with ORS. In India [59], the study was conducted in rural Haryana and the strategy was to give 1 blister strip containing 14 dispersible zinc tablets (20 mg each) along with 2 ORS packets (to mix in 1 litre of water each) to all of the children aged 1 month to 4 years with diarrhea. Infants aged <6 months were to receive half a tablet in a teaspoonful of breast milk; older children were to receive 1 tablet dissolved in breast milk or clean water. The results demonstrated utilization of zinc supplements in 36.5% ( n = 1,571) and 59.8% ( n = 1,649) of diarrheal episodes occurring in the 4 weeks preceding interviews in the intervention areas [59]. The prevalence rates of diarrhea and pneumonia during the preceding 14 days were lower by 44% and 45% respectively in the intervention communities during the third quarterly survey. The numbers of hospitalizations for any cause, diarrhea, and pneumonia in the preceding 3 months were reduced in the intervention compared with the control areas (survey 3) (odds ratio for diarrhea hospitalizations, 0.69; 95% CI, 0.50 to 0.95; odds ratio for pneumonia hospitalizations, 0.29; 95% CI, 0.15 to 0.54). In a similar large-scale project in Matiari district in Pakistan, zinc supplements delivered by primary care government health workers to children with acute diarrhea produced a reduction in the subsequent incidence rates of diarrhea and mortality. These results have led to the incorporation of oral zinc sulfate for the treatment of diarrhea by the national primary health care programs and policies. In addition, the large effectiveness studies conducted in Bangladesh and in India [61, 62], have shown that when zinc and ORS are promoted together for the treatment of diarrhea, as part of a diarrhea control program, it led to increased ORS prescription rates, increased ORS use rates, decreased irrational antibiotic use rates, decreased anti-diarrheal use rates, and reduction in hospital rates.

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Box 28.2 Experiences with introduction of zinc supplementation in treating childhood diarrhea in Mali [63] Zinc for the treatment of childhood diarrhea was introduced in a pilot area in southern Mali to prepare for a cluster-randomized effectiveness study and to inform policies on how to best introduce and promote zinc at the community level. Dispersible zinc tablets in 14-tablet blister packs were provided through community health centres and drug kits managed by community health workers (CHWs) in two health zones in Bougouni district, Mali. Population-based household surveys with caretakers of children sick in the previous two weeks were carried out before and four months after the introduction of zinc supplementation. Household follow-up visits with children receiving zinc from the health centres and CHWs were conducted on days 3 and 14 after treatment for a subsample of children. A qualitative process evaluation also was conducted to investigate operational issues. Preliminary evidence from this study suggests that the introduction of zinc does not reduce the use of ORS and may reduce inappropriate antibiotic use for childhood diarrhea. Financial access to treatments, management of concurrent diarrhea and fever, and high use of unauthorized drug vendors were identified as factors affecting the effectiveness of the intervention in this setting.

In five studies that evaluated the effect of zinc supplementation on persistent diarrhea (episode that lasts 14 days or more) in children under 5 years of age, zinc-supplementation resulted in a significant reduction of duration of persistent diarrhea by 0.68 day and 21% lower probability of continuation of diarrhea on a given day. The meta-analysis showed a significant mean reduction of 42% (range, 10–63%) in the rate of treatment failure or death in children (<5 years of age) [55]. The benefit appeared to be more marked in children who were aged <12 months, were male, and had wasting or lowered baseline plasma zinc levels. Therapeutic effects of zinc supplementation on other illnesses Evidence of the benefit of zinc supplementation on pneumonia, malaria and tuberculosis in children under 5 years of age is insufficient and needs further evaluation [55].

28.8.3 Preventive effects of zinc supplementation Brown et al [50] recently conducted a series of meta-analyses of the randomized controlled trials to quantify the impact of preventive zinc supplementation on morbidity, mortality and physical growth. A total of 55 individual trials i.e. 7 from Africa, 23 from Asia, 12 from South America, 11 from North America, 1 from Australia, and 1 from Europe were included in the analyses which enrolled 202,692 children. Preventive effects of zinc on diarrhea morbidity Zinc supplementation has been shown to reduce the incidence of diarrhea in several community and hospital based studies. The preventive effects

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of zinc supplementation on diarrhea have recently been updated by Brown et al [50] from 24 randomized controlled trials (Figure 28.2).

28.2 Effect of zinc supplementation on diarrhea incidence from 24 intervention trials with 33 groupwise comparisons in which the supplements differed only bythe presence or absence of zinc [50].

Data from these studies which enrolled 16,339 children aged <4 years were pooled by using random-effect models with significant heterogeneity among

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children. The supplementation periods ranged from 2 weeks to 15 months and the dosage ranged from 1 to 70 mg per dose (median, 10 mg) mainly in the form of zinc sulfate. There was a significant 20% lower incidence of diarrhea among children who received zinc supplementation. The data indicated that the mean initial age of the study subjects was highly significantly associated with the magnitude of the effect of zinc supplementation. Among the subset of studies that enrolled children with the mean initial age greater than 12 months, the relative risk of diarrhea incidence was reduced by 27%. Data on duration of diarrhea from 9 studies which enrolled 1,692 children in the age group of 6 to 29 months indicated no significant effect of preventive zinc supplementation on duration of diarrhea. Preventive effects of zinc on pneumonia Zinc supplementation may also reduce the incidence of lower respiratory infections, such as pneumonia. Recently, Brown et al [50] have updated the meta-analysis, which included 12 randomized controlled trials with 16 group-wise comparisons, to evaluate the efficacy of zinc supplementation in respiratory illnesses among children between the mean initial ages of 0.9 and 49 months (Figure 28.3). Pooled data indicated that children who received a zinc supplement had significantly 15% reduction in lower respiratory tract infection or pneumonia than did those who received a placebo. Zinc supplementation and malarial morbidity In Gambia, using a twice-weekly 70 mg zinc supplementation, Bates et al [64] reported a 32% reduction in clinic visits due to malaria. In Papua New Guinea using daily 10 mg zinc supplementation, Shankar et al [65] reported a reduction of 38% in health center-based episodes of Plasmodium falciparum. Using a 12.5 mg daily zinc supplementation in Burkina Faso, Muller et al [66] found no effect in the incidence of P. falciparum malaria (relative risk of 0.98). Additionally, a randomized controlled trial reported that zinc supplementation did not benefit preschool-aged children with acute, uncomplicated P. falciparum malaria [67]. In a study in the Peruvian Amazon, children who received zinc or zinc plus iron had 15% fewer episodes of Plasmodium vivax infections though the results were not statistically significant [68]. A randomized controlled trial in over 42,000 children aged 1 to 48 months found that zinc supplementation did not significantly reduce mortality associated with malaria and other infections [69]. In a recently completed study in Burkina Faso, children who received zinc daily plus a single dose of vitamin A had 22% lower rate of fever and 30% reduction in malaria incidence [70]. In summary, there is still insufficient evidence to allow definitive conclusions to be drawn regarding the effect of zinc supplementation on

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28.3 Effect of zinc supplementation on the incidence of acute lower respiratory tract infection (ALRI)a from 12 intervention trials with 16 groupwise comparisons in which the supplements differed only by the presence or absence of zinc. (a)

Gray circles indicate studies in which ALRI was diagnosed by fieldworkers or physicians by using objective clinical signs: black circles indicate studies in which the diagnoise was based on caregiver reports of elevated respiratory rate or difficulty breathing [50].

the risk of malaria, although the weight of currently available information suggests that zinc may reduce the incidence of malaria, especially that of more severe cases that result in clinic attendance. Zinc supplementation and mortality Given the effects of zinc supplementation on diarrhea and pneumonia morbidity, which are the main causes of mortality in preschool children, there is a strong case for the impact of zinc supplementation on mortality. To date there are ten studies with information on impact of zinc supplementation, given alone or with iron folic acid, on mortality. However, these studies are heterogeneous in terms of the study population. Seven studies measured the impact on unselected populations of young children (Burkina Faso,

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Bangladesh, India, Nepal, Tanzania and Papua New Guinea) [65, 66, 69, 71–74]. Zinc supplementation had a marginal 6% impact on overall child mortality (Figure 28.4), there was an 18% reduction in deaths among zincsupplemented children older than 12 months of age but it had no effect on younger children. Two studies which measured the impact of zinc supplementation on selected population, low birth weight (LBW) and small for gestational age (SGA) infants (Brazil, India) [75, 76], found 52–68% lower mortality rates among children who received zinc and showed a pooled RR for reducing mortality of 0.35. In these studies the children were followed up for <1 year, therefore the impact of zinc supplementation is not available beyond 1 year. These results are consistent with the analyses by birth weight in Nepal (2006), wherein they reported the relative risk of mortality was reduced by 44% [74]. One study carried out in Bangladesh enrolled ill children with diarrhea, with subsequent home based zinc supplementation for 14 days [61]. There was 51% lower rate of non-injury deaths in the group of children receiving zinc in addition to ORS as a part of diarrhea management than the group of children that was just receiving ORS.

=

a

28.4 Effect of zinc supplementation on childhood mortality from 10 intervention trials (a) is with 13 groupwise comparisons in which the supplements differed only by the presence or absence of zinc. (a)

The figure does not include the study by Bhandari et al. [73] (India, 2002; n = 2,482) because this study had no deaths in the zinc-supplemented group.

These combined sets of results indicate that providing preventive zinc supplementation in settings where there is an increased risk of zinc deficiency would reduce mortality among children greater than 1year of age and possibly among LBW infants. However, additional studies are needed to confirm the results.

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28.8.4 Zinc supplementation and neurological/behavioral, mental and motor development of children Low maternal zinc nutritional status has been associated with diminished attention in newborn infants and poorer motor function at six months of age. Zinc supplementation has been associated with improved motor development in very low-birth-weight infants, more vigorous activity in Indian infants and toddlers, and more functional activity in Guatemalan infants and toddlers [14, 77]. Additionally, zinc supplementation was associated with better neuropsychologic functioning (e.g. attention) in Chinese first grade students, but this was observed only when zinc was provided with other micronutrients [78]. Two other studies failed to find an association between zinc supplementation and measures of attention in children diagnosed with growth retardation. Investigations of zinc supplementation on infants’ development and behavior have yielded inconsistent findings [79]. There are 7 studies (provided nine groupwise comparisons) that reported on children’s developmental outcomes in relation to zinc supplementation [50]. The study duration ranged from 1.9 to 12 months, and just two studies lasted more than 6 months. Two comparisons evaluated the impact of zinc supplementation versus placebo [80, 81], and the others provided additional micronutrients, such as iron [82, 84] or vitamin A [84, 85], to both groups. None of the studies found a significant positive effect of zinc on Mental Development Index (MDI). As with MDI, there was no significant overall impact of zinc supplementation on PDI (Psychomotor Development Index).

28.9

Zinc supplementation in pregnancy

Poor maternal zinc nutritional status has been associated with a number of adverse outcomes of pregnancy, including low birth weight, premature delivery, labor and delivery complications, fetal growth retardation, congenital anomalies and early postnatal infant immune dysfunction [86]. However, the results of maternal zinc supplementation trials in the U.S. and developing countries have been mixed [14]. Although some studies have found maternal zinc supplementation increases birth weight and decreases the likelihood of premature delivery, two placebo-controlled studies in Peruvian and Bangladeshi women found that zinc supplementation did not affect the incidence of low birth weight or premature delivery [87, 88]. Supplementation studies designed to examine the effect of zinc supplementation on labor and delivery complications have also generated mixed results, though few have been conducted in

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zinc-deficient populations [14]. A recent systematic review of 17 randomized controlled trials found that zinc supplementation during pregnancy was associated with a 14% reduction in premature deliveries; the lower incidence of preterm births was observed mainly in low-income women [89]. This analysis, however, did not find zinc supplementation to benefit other indicators of maternal or infant health. However, these results are quite limited, and more studies are needed to confirm these observations.

28.10 Effect of zinc on immune response in the elderly Age-related declines in immune function are similar to those associated with zinc deficiency, and the elderly are vulnerable to mild zinc deficiency. However, the results of zinc supplementation trials on immune function in the elderly have been mixed. A randomized placebocontrolled study in men and women over 65 years of age found that a zinc supplement of 25 mg/day for three months increased levels of some circulating immune cells (i.e., CD4 T-cells and cytotoxic Tlymphocytes) compared to placebo [90]. However, other studies have reported zinc supplementation does not improve parameters of immune function, indicating that more research is required before any recommendations can be made regarding zinc and immune system response in the elderly.

28.11 Zinc toxicity Zinc toxicity can occur in both acute and chronic forms. Acute adverse effects of high zinc intake include nausea, vomiting, loss of appetite, abdominal cramps, diarrhea, and headaches [31]. One case report cited severe nausea and vomiting within 30 minutes of ingesting 4 g of zinc gluconate (570 mg elemental zinc) [91]. Relatively speaking, zinc is nontoxic, non-accumulative compared to other trace elements such as lead, cadmium or arsenic and the proportion absorbed is inversely related to the amount ingested [92, 93]. Intakes of 150–450 mg of zinc per day have been associated with such chronic effects as low copper status, altered iron function, reduced immune function, and reduced levels of high-density lipoproteins [94]. Reductions in a copper-containing enzyme, a marker of copper status, have been reported with even moderately high zinc intakes of approximately 60 mg/day for up to 10 weeks [19]. The doses of zinc used in the Age-Related Eye Disease Study (80 mg per day of zinc in the form of zinc oxide for 6.3 years, on an average) have been associated with a significant increase in

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hospitalizations for genitourinary causes, raising the possibility that chronically high intakes of zinc adversely affect some aspects of urinary physiology [95].

28.12 Assessment of zinc status The diagnosis of zinc deficiency is hampered by the lack of a single, sensitive, and specific low-cost indicator of zinc status. There are no generally accepted methods. Zinc status can be assessed by measurement of zinc in plasma, erythrocytes, leucocytes (lymphocytes/ neutrophils), platelets, urine, skin, sweat, saliva, and/or hair [96, 97].

28.12.1 Plasma/serum zinc concentrations Plasma or serum zinc concentrations are the most widely used indicator for zinc status. In general, during zinc deficiency, plasma or serum zinc concentrations will decrease. The amount of zinc circulating in plasma is <0.2% of the total body zinc content, as most of the total body content of zinc is contained in muscle and liver. There are several confounding factors that may limit the use of plasma or serum zinc concentrations such as infection, inflammation, chronic disease, pregnancy and malnutrition. The cut off for plasma or serum zinc concentrations generally used to assess the risk of zinc deficiency is <10.71 μmol/L (<70 μg/dL) for pre-prandial samples and <9.95 μmol/L (<65 μg/dL) for post prandial samples. Zinc plasma or serum concentrations can be measured by flame atomic absorption spectroscopy and most recent methods include flameless atomic absorption spectroscopy or inductively coupled plasma mass spectrometry. Plasma or serum should be separated as quickly as possible, as zinc concentrations may change if the plasma or serum has not separated from the blood within 1 hour. Hemolyzed samples should not be used, as zinc concentrations are higher in erythrocytes than in plasma. As zinc contamination may occur with use of regular blood-drawing equipments and supplies, trace element-free syringes, pipette tips and storage tubes should be used for the collection of plasma or serum for zinc determination.

28.12.2 Leucocyte and Erythrocyte Zinc Content Leucocyte zinc content may be a useful indicator as leuocytes turnover is rapid but requires large quantity of blood sample (~10 ml), subject to contamination and is difficult to obtain from young children. Polymorphonuclear leucocytes can be collected relatively free from

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contamination with platelets but monocytes which are in themselves a very mixed population are difficult to collect free of contamination with platelets. Leucocyte subsets have different zinc contents e.g. mean (SD): neutrophils 1.26 (0.27); monocytes 2.58 (0.65); lymphocytes 1.85 (0.32) μmol zinc/mg protein. Each has a different biological half-life (e.g. neutrophils 6 hours; monocytes 1–3 days; T lymphocytes 30 hours – 200 days). Pathophysiological changes in the relative proportions of the leucocyte subsets would lead to significant changes in the zinc content of the entire population. These phenomena could seriously limit the interpretation of mixed white cell analyses and the use of selected white cell subsets may seem to be more valuable. Analyses on selected separated subsets may prove to be more useful but are for the moment too impractical for routine or emergency use. In a systematic study of zinc supplemented children, leucocyte zinc concentrations were found to be a useful indicator of zinc deprivation [98]. Though, erythrocytes have a long shelf life (approximately 40 days), their zinc contents cannot be regarded as reliable indicators of recent or acute changes in zinc supply, unless zinc toxicity is suspected, but even so there are no adequate reference ranges to enable data to be evaluated.

28.12.3 Hair zinc concentrations Although hair zinc has been used in literature due to ease of obtaining a sample, the limitations of determining hair zinc concentrations to detect severe zinc deprivation have been shown in animal models in which there is a paradoxical increase in zinc content of hair with severe zinc deprivation. This has been noted in malnourished children. A possible explanation for this is that as zinc supply becomes limiting, hair synthesis in the follicle is reduced such that despite the reduced supply of zinc, it accumulates in the hair root at a normal or increased rate.

28.12.4 Functional indices of zinc Proxy indicators, such as activity of zinc metalloenzymes (alkaline phosphatase, carbonic anhydrase etc.), have been shown to be useful [99]. Serum alkaline phosphatase is low in severe zinc deficiency and returns to normal and a rise in serum alkaline phosphatase after zinc supplementation has been considered as a supportive indicator for the diagnosis of zinc deficiency. Increase in the plasma alkaline phosphatase following zinc supplementation to zinc deficient subjects has been frequently reported [100, 101]. Alkaline phosphatase level in serum responds to zinc depletion through a significant reduction in activity. Since

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the activity of this enzyme decreased before any sign of a lower food intake or reduced growth, it can be considered that the activity of serum alkaline phosphatase returns to the level of the control animals within 3 days of supplementation with zinc [100]. Improvement in serum alkaline phosphatase level was associated with corresponding improvement of clinical signs of zinc deficiency [99]. The metalloenzymes which responded with reduced activities in experimental zinc deficiency are alkaline phosphatase, pancreatic carboxy-peptidase, carbonic anhydrase, glutamic dehydrogenase, lactic and malic dehydrogenate, aldolase, NADH Diaphorase and pyridoxal phosphokinase. Metallothionein, a cytoplasmic metalloprotein, has been implicated in metabolism of zinc [102]. Experiments in rats indicated that metallothionein in hepatic and intestinal mucosal cells responded to altered dietary zinc content and serum zinc was directly related to metallothionein. To assess an acute zinc deficiency state, measurement of zinc metalloenzymes or tissue, which has a rapid turnover rate, may be more practical. Labeled isotopes such as 69zn and 70zn have been used in absorption studies [103]. A good correlation between zinc status and the activity of the ribonuclease (RNase) has been observed.

28.12.5 Zinc pool – size and turnover rates The exchangeable zinc pool (EZP) is the sum of the combined pools that exchange with zinc in the plasma within 48–72 hours and is thought to be critical for zinc dependent biological processes. The estimates of the size of the EZP have been found to be positively related to dietary zinc intake, especially the amount of absorbed zinc and fecal excretion of endogenous zinc. Once links to clinical, biochemical, or molecular effects of zinc deficiency have been achieved, the pool size and turnover measurements may be of value in evaluating the zinc status and zinc homeostasis [104, 105].

28.12.6 Growth faltering Although growth faltering alone is not diagnostic of zinc deficiency, it is along with other factors a possible cause. A falling of height and weight measurements compared with normal standards or previous records of growth velocity may be one of the first clinical observations that suggest zinc deficiency. Growth faltering is a hall mark of severe zinc deficiency, and a rapid decline in growth velocity is the most striking clinical feature of mild zinc deficiency. Both linear and ponderal growth are negatively affected by inadequate zinc intake [106]. In populations where stunting is

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prevalent, growth of stunted children is most often significantly improved following zinc supplementation. Zinc supplementation had a positive impact on linear growth (effect size = 0.46) as well as, though small, but a highly significant impact on weight increments (effect size = 0.26 SD units) among those studies that enrolled stunted children (HAZ <-2SD). Thus the prevalence of growth stunting may be a useful indicator of poor zinc status in the population [107].

28.12.7 Dietary zinc estimates Dietary zinc intake can be assessed quantitatively by a number of different methods, the simplest of which for population assessment is a modified interactive 24-hour dietary recall [108, 109]. Once the daily food intake is known, the total zinc intake can be estimated by multiplying the amount of each of the foods that are consumed by its zinc content, as recorded in local food composition tables or in databases available internationally, such as the US Department of Agriculture (USDA) food composition database [110]. For developing countries the World Food Dietary Assessment Program can be used [111]. The nutrient database associated with this system contains food composition values for 1800 foods from six countries (Egypt, Kenya, Mexico, Senegal, India, and Indonesia) and provides data for 53 nutrients and antinutritional factors that interfere with the absorption of nutrients including zinc, iron, dietary fiber, and phytate. Local databases are theoretically advantageous because the zinc content of foods can vary according to soil conditions, agronomic practices, and local food-processing techniques, although in many cases local food composition tables contain fewer food items and fewer replicate analyses per item. Moreover, these local tables frequently omit analyses of zinc and phytate. To estimate the amount of zinc available for absorption from the diet, the diet can be categorized according to its phytate–zinc molar ratio.

28.13 Scaling up programs to improve zinc nutrition Despite the promising effects of zinc supplementation, public health programs have been slow to embrace zinc-related interventions. Reasons for the lack of large-scale programs to prevent zinc deficiency may include the limited information available on the prevalence of zinc deficiency and need for practical intervention strategies that could be incorporated into ongoing health programs. This section presents an abstracted overview of current public health programs and possible gaps in information needed to design large scale programs which has been reviewed in detail by Brown et al [112].

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28.13.1 Assessment of population zinc status Very few countries have systematically collected information on population zinc status, so the global prevalence of zinc deficiency remains unknown. To address this issue on an interim basis, IZiNCG has proposed using suggestive evidence of zinc deficiency, based on the rates of stunting of under-five children and information on the absorbable zinc content of the national food supply using FAO’s food balance sheets [6]. National surveys of representative samples of the population are needed in high risk areas. Studies are also needed to validate the suggested cutoffs of zinc status indicators in relation to the functional effects of zinc deficiency. Additional field-applicable biomarkers of zinc status need to be developed. Finally, the suggestive evidence for classifying the population risk of zinc deficiency needs to be validated against objective biomarkers of zinc status.

28.13.2 Zinc intervention strategies Three major nutrition-related strategies proposed to control zinc deficiency include supplementation, fortification, and dietary diversification/ modification. The supplementation can further be divided into therapeutic and preventive supplementation. Therapeutic zinc supplementation for treatment of diarrhea This is by and large the most advanced component programmatically. Programs have begun in several countries, testing various approaches to training both health facility staff and community health workers, developing and delivering behavior change communication messages and consumer educational materials, and monitoring program progress. Private sector zinc programs are testing the feasibility of marketing zinc tablets and ORS as standalone products or packaging them together as a Diarrhea Treatment Kit (DTK). Box 28.3 presents the WHO/UNICEF Zinc recommendations for treatment for diarrhea. Box 28.3 Zinc as a treatment for diarrhea – WHO/UNICEF recommendations Based on the updated meta-analyses of randomized, controlled intervention trials on children, the WHO/UNICEF recommended 20 mg zinc/day for 10–14 days for children with acute diarrhea and 10 mg/day for infants under 6 months of age in the form of sulfate, gluconate, or acetate. These updated recommendations take into account new research findings showing the beneficial effects of oral rehydration salts (ORS) containing lower concentrations of glucose and salts as well as of zinc

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supplementation. In combination with prevention and treatment of dehydration with appropriate fluids, breastfeeding, continued feeding and selective use of antibiotics, these two scientific advances – regarding ORS and zinc supplementation can drastically diminish the number of child deaths by reducing the duration and severity of diarrheal episodes and lowering their incidence [113, 114].

Subsequent to global recommendations upon review Indian Academy of Pediatrics (IAP) and Government of India also have revised guidelines for the use of zinc in diarrhea as given below (see Boxes 28.4 and 28.5): Box 28.4 Revised recommendations of the IAP National Task Force for use of zinc in diarrhea, May 2006 1. All cases of diarrhea should receive zinc in addition to ORS. A uniform dose of 20 mg of elemental zinc should be given to all children older than 6 months and should be started as soon as diarrhea starts and continued for a total period of 14 days. Children aged 2 months to 6 months should be advised 10 mg per day of elemental zinc for a total period of 14 days. 2. Based on all the studies the group proposed that zinc salts e.g. sulphate, gluconate or acetate may be recommended. 3. The industry should be encouraged to prepare dispersible tablets that are reasonably priced, can be stored and transported easily. They can be dissolved in breast milk or water before use.

Box 28.5 Recommendations by the Government of India, 2007 Based on the WHO/UNICEF and the IAP recommendations and the data available on the evaluation of addition of zinc to current case management strategy in primary health setting [59] and personal communication of a larger study by Bhandari, et al. The Ministry of Health, Government of India has recommended that 20 mg of elemental zinc should be given to all children with diarrhea, older than 6 months, and should be started as soon as diarrhea starts and continued for a total period of 14 days. Children aged 2 months to 6 months should be advised 10 mg per day of elemental zinc for a total period of 14 days.

As part of global leadership mandate, USAID’s Social Marketing Plus for Diarrheal Disease Control: Point-of-Use Water Disinfection and Zinc Treatment (POUZN) Project, has been implemented in 20 countries [115]. Box 28.6 presents the scaling up efforts of zinc supplementation programme in Nepal. These efforts have focused on involving private companies to produce appropriate preparation for the diarrhea treatment and use social marketing approach to help scaling up its implementation. It is also recommended as part of standard case management in persistent diarrhea and in those with severe malnutrition.

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Box 28.6 Successful zinc supplementation scale-up in Nepal In 2005, the Ministry of Health and Population requested assistance from the United States Agency for International Development (USAID) to support the integration of zinc into the government’s diarrhea management programme. In 2005, the Government of Nepal, through the Ministry of Health and Population’s (MOHP) Child Health Division, is one of the first health ministries in the world to create a Zinc Task Force and prepare stakeholders for the introduction of zinc in line with the new World Health Organization (WHO)/UNICEF recommendations for standard management of childhood diarrhea, which includes ORS/ORT along with a 10–14 day regimen of pediatric zinc. USAID’s Nepal Family Health Project and UNICEF took the lead in providing commodities, training, and technical assistance to strengthen the skills of public sector health care providers in treating childhood diarrheas with both ORS/ ORT and zinc. At the same time, USAID/ Nepal funded the global Social Marketing Plus for Diarrheal Disease Control: Point-of-Use Water Disinfection and Zinc Treatment (POUZN) Project , implemented by Abt Associates in partnership with Population Services International, to introduce pediatric zinc in Nepal through the private sector as a companion piece to the introduction of zinc as the standard pediatric diarrhea treatment at public sector health facilities. Both public and private sector programs have now been implemented in 30 targeted districts encompassing 65% of the population. The POUZN programme in Nepal, although active nationwide for only six months, has already successfully contributed to an increase in zinc use from 0.4% in 2005 to nearly 16% in 2008. Of users, 85% correctly took zinc and ORS together, and 67% correctly took zinc for the full 10 days, demonstrating the positive impact of the communications messages.

Box 28.7 presents the Scaling Up Zinc for Young Children (SUZY) project in Bangladesh. Box 28.7 Scaling Up Zinc for Young Children (SUZY) Project in Bangladesh The Scaling Up of Zinc for Young Children (SUZY) Project was established in 2003 with the aim of setting Bangladesh on the path to covering all under-five children with zinc treatment of any diarrheal illness episode. ICDDR, B is the implementing and coordinating agency of the SUZY Project. Ministry of Health and Family Welfare (MoHFW) in collaboration with the SUZY team has developed two committees: (1) a National Advisory Committee, headed by the Health Secretary and (2) a Planning and Implementation Committee, headed by the Joint Secretary, Public Health and WHO. These two committees have been formed to have effective effort on policy decision. The National Advisory Committee of MoHFW approved the policy on using zinc in addition to ORS for under-five children suffering from diarrhea on 13 September 2006 and revised the National Diarrhea Treatment Guideline to incorporate zinc treatment in it. A partnership was also created that included public, private, nongovernmental organization, and multinational sector agencies. Over a period of 3 years activities in support of preparing for the national scale up included formative and operational research, product registration and technology transfer, awareness building and orientation of health professionals, and preparation of mass media messages. In December, 2006 a national mass media campaign to promote a dispersible tablet zinc formulation, “Baby Zinc,” for the treatment of childhood diarrhea was launched. All media messages linked zinc treatment to the continued use of oral rehydration salts (ORS). The scale-up of zinc treatment of childhood diarrhea rapidly attained widespread awareness, but actual use has lagged behind. Disparities in zinc coverage favoring higher income, urban households were

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identified, but these were gradually diminished over the two years of follow-up monitoring. The scale up campaign has not had any adverse effect on the use of ORS.

Preventive zinc supplementation The evidence for preventive zinc supplementation on the functional outcomes of morbidity and mortality and physical growth, have been presented earlier. There has not been progress in scaling up preventive zinc supplementation. For scale up information is needed on the optimal safe and effective dose of preventive zinc supplements for children of different ages and the appropriate frequency and duration of supplementation, with and without other micronutrients. Information from effectiveness studies combining zinc supplementation with other routine health/nutrition contacts, such as growth monitoring, EPI, or periodic vitamin A supplementation activities is needed. Finally, the best way of integrating preventive and therapeutic supplementation programs would contribute a big step. Zinc fortification Several studies have evaluated the effects of fortifying different food products with multiple micronutrients, including zinc. Serum zinc concentrations of older infants did not respond to zinc-containing, multimicronutrient fortified, cereal-based complementary foods in the four studies that measured this outcome [116–120]. Also there were no effects of the interventions on growth. In contrast serum zinc concentrations increased significantly among school children who received a multimicronutrient fortified beverage between meals [121] or a multimicronutrient fortified seasoning powder with meals [122]. Very little information is available from large-scale, programmatic interventions. Studies investigating the impact of home-based fortification using a mixture of vitamins and minerals packaged in small sachets containing a daily dose of micronutrients have focused mainly on the prevention of anemia and iron deficiency [123, 124]. Little is known about the impact of other micronutrients included in the multi-micronutrients mixture. In particular, there is limited information regarding their impact on zinc status. In general the health benefits of zinc included in “Sprinkles” have not yet been proven. Information is needed on the efficacy of zinc fortification programs (with and without other micronutrients), including their impact on biochemical indicators of zinc status and related functional outcomes. Similar information is needed for home fortification programs with zinc-containing micronutrient mixtures.

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Dietary diversification Diets in low income countries are predominantly plant-based and consumption of animal-source foods, such as meat, poultry, and fish, is often limited because of economic, cultural, and/or religious constraints. As a result, the zinc content of such diets is low and the efficiency of absorption is limited. Dietary inadequacy is probably the primary cause of zinc deficiency. To increase the zinc content in the diets, promotion of small-livestock husbandry, aquaculture, and production of other indigenous zinc-rich food has been proposed. At the household level, reduction of phytate content of the diet by using simple techniques to activate phytase, which is present naturally in cereals and legumes has been suggested. Such strategies have the added advantage of simultaneously improving the content and bioavailability of iron, vitamin B12, vitamin A, and calcium while enhancing protein quality and digestibility [125]. However there is little experience from large-scale programs to promote increased intake of zinc-rich foods. Practical information is needed on how best to identify locally available, low-cost, culturally acceptable zinc-rich foods and promote their consumption by those at risk of zinc deficiency. Information is also needed on best ways of implementing both large-scale and homebased food processing interventions to enhance zinc absorption from the usual diet [126, 127]. Agricultural interventions to increase dietary zinc content through improved agronomic practices and/or plant breeding need to be implemented and assessed.

28.14 Conclusion Zinc is a crucial micronutrient because it affects few hundred enzyme systems, DNA replication and various immune mechanisms and modulates host resistance to several pathogens. Zinc nutrition is necessary for optimal child health, physical growth, and normal pregnancy outcomes. In recent years, global recognition of the importance of zinc nutrition in public health has been recognized and there is some understanding for the design and implementation of zinc intervention programs. Zinc supplementation reduces morbidity from diarrhea and pneumonia in high risk populations. A large body of evidence shows important therapeutic benefits with zinc administration during and after diarrhea and some studies also reported reduction in diarrhea morbidity in the subsequent 2–3 months without further supplementation. Zinc supplementation is also shown to have positive impact on growth in terms of height and weight gain in pre-pubertal children. In the interim, the present WHO strategy to focus on introduction of zinc for treatment of diarrhea is an important step forward. The administration of zinc with oral rehydration salts for diarrhea in the program

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settings resulted in increased use of these salts, decreased use of antimicrobials and harmful anti-diarrheal drugs, and also reduced hospital admissions. Further evidence is required for qualifying its use in treatment of other infectious diseases like pneumonia. In view of the available data on effect of zinc supplementation in reducing the diarrheal and pneumonia morbidity and child mortality, preventive zinc supplementation has a potential to contribute to achievement of the MDG 4 (reduction in child mortality) by 2015 [128]. In the long-term, measures to improve zinc intake of children, improvement of the overall diet, supplementation, food fortification, and sub-selection of crops with improved zinc content need to be explored and assessed. However, the challenges of delivery of zinc as a preventive intervention in a population like India where centralized food processing is not existent need to be sorted out before any program recommendation can be made. Effectiveness studies for novel ways to deliver zinc need to be undertaken to inform policy. More data and may be studies starting in pre-conception period are needed to make any firm conclusion about maternal supplementation during pregnancy.

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complementary foods on growth and micronutrient status of Ghanaian infants from 6 to 12 mo of age. Am J Clin Nutr, 70, pp. 391–404. OELOFSE A , VAN RAAIJ JM, BENADE AJ , DHANSAY MA , TOLBOOM JJ and HAUTVAST JG (2003). The effect of a micronutrient fortified complementary food on micronutrient status, growth and development of 6- to 12-month-old disadvantaged urban South African infants. Internatl J Food Sci Nutr, 54, pp. 399–407. FABER M, KVALSVIG JD , LOMBARD CJ and BENADE AJ (2005). Effect of a fortified maize-meal porridge on anemia, micronutrient status, and motor development of infants. Am J Clin Nutr, 82, pp. 1032–1039. LUTTER CK , SEMPERTEGUI F, RODRIGUEZ A , FUENMAYOR G , AVILA L and MADERO J (2006). Evaluacion e impacto del programa nacional de alimentacion nutricion PANN 2000. Washington DC: Organizacion Panamericana de la Salud. BROWN KH , LÓPEZ DE ROMAÑA G , ARSENAULT JE , PEERSON JM and PENNY ME . Effect of mode of delivery of zinc (provided in a fortified food or as a liquid supplement) on the growth, morbidity and plasma zinc concentration of young Peruvian children. Am J Clin Nutr, in press. ABRAMS SA , MUSHI A , HILMERS DC , GRIFFIN IJ , AVILA P and ALLEN L (2003). A multinutrient-fortified beverage enhances the nutritional status of children in Botswana. J Nutr, 13(3), pp. 1834–1840. WINICHAGOON P , MCKENZIE JE , CHAVASIT V , PONGCHAROEN T , GOWACHIRAPANT S , BOONPRADERM A , MANGER MS , BAILEY KB , WASANTWISUT E and GIBSON RS (2006). A multimicronutrient-fortified seasoning powder enhances the hemoglobin, zinc, and iodine status of primary school children in North East Thailand: a randomized controlled trial of efficacy. J Nutr, 13(6), pp. 1617–1623. ZLOTKIN S , ARTHUR P, SCHAUER C, ANTWI KY , YEUNG G and PIEKARZ A (2003). Homefortification with iron and zinc sprinkles or iron sprinkles alone successfully treats anemia in infants and young children. J Nutr, 13(3), pp. 1075–1080. GIOVANNINI M, SALA D , USUELLI M , LIVIO L , FRANCESCATO G , BRAGA M , RADAELLI F and RIVA E (2006). Double-blind, placebo-controlled trial comparing effects of supplementation with two different combinations of micronutrients delivered as sprinkles on growth, anemia, and iron deficiency in Cambodian infants. J Ped Gastroenterol Nutr, 42, pp. 306–312. GIBSON RS , YEUDALL F, DROST N , MTITIMUNI BM and CULLINAN TR (2003). Experiences of a community-based dietary intervention to enhance micronutrient adequacy of diets low in animal source foods and high in phytate: a case study in rural Malawian children. J Nutr, 13(3), pp. 3992S–3999S. BROWN KH , ENGLE -STONE R , KREBS NF, PEERSON JM (2009). Dietary intervention strategies to enhance zinc nutrition: promotion and support of breastfeeding for infants and young children. Food Nutr Bull. 30(1), pp. S144–171. GIBSON RS and ANDERSON VP (2009). A review of interventions based on dietary diversification or modification strategies with the potential to enhance intakes of total and absorbable zinc. Food Nutr Bull. 30(1), pp. S108–143. BRYCE J and VICTORIA CG (2005). Child survival: countdown to 2015. The Lancet, 365 (9478), pp. 2153–2154.

29 Vitamin A and zinc supplements for child survival – experiences and challenges ahead Anand Lakshman

Anand Lakshman, a medical doctor with a Masters in Health Administration, has worked on tribal health issues in Karnataka and on the Revised National Tuberculosis Control Programme in West Bengal. Dr Lakshman, Coordinator Planning & Knowledge Management at the Micronutrient Initiative’s (MI) Asia office, spearheaded MI’s support to national programs in India, including vitamin A supplementation and therapeutic zinc supplementation.

29.1

Introduction

In 2008, a group of world-renowned economists in an exercise known as the Copenhagen Consensus [1], ranked micronutrient supplements as the top development priority out of more than 40 interventions, such as The Doha Development Agenda, Expanded Immunization Coverage for Children, Malaria Prevention and Treatment and Peace-keeping in postconflict situations. The criteria used included the benefit–cost ratio, as well as feasibility and sustainability of the interventions. Specifically, it identified vitamin A supplementation for children (every 4–6 months, from age 6 months to 5 years) and therapeutic zinc supplementation along with oral rehydration therapy for diarrhea (10–14 days of supplementation, up to the age of 5) as interventions which can contribute significantly to reducing child mortality world wide with relatively modest investments. Global evidence summaries have suggested that vitamin A supplementation can reduce all-cause mortality for children 6–59 months by 23%, and several studies have indicated that therapeutic zinc supplements for diarrhea can reduce diarrheal mortality below the age of five by 50%.

29.2

Magnitude of the problem

Undernutrition remains a major issue in developing countries, being an

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underlying cause of 3.5 million deaths each year [2]. It is estimated that up to 219 million children are deficient in vitamin A [3] and over 1 billion people are susceptible to zinc deficiency [2]. Children with these deficiencies are significantly more likely to experience morbidity and mortality. Vitamin A deficiency in newborn babies, infants, and children accounts for about 6% of under-5 deaths, 5% of under-5 DALYs (disabilityadjusted life years), and 1.7% of total DALYs lost. Zinc deficiency accounts for about 4% of under-5 deaths and DALYs and 1% of total DALYs lost. Vitamin A deficiency annually claims the lives of almost 670,000 children under five and zinc deficiency claims more than 450,000 lives [2]. Table 29.1 Global deaths and DALYs in children under 5 years attributable to micronutrient deficiencies – 2004 Deficiency

Deaths

Percentage of deaths in children under 5 years

Disease Burden in 1000 Disability Adjusted Life Years (DALYs)

Percentage of DALYs in children under 5 years

Vitamin A Zinc

667771 453207

6.5% 4.4%

22668 16342

5.3% 3.8%

Category of public health significance (prevalence of serum retinol <0.70 μ mol/l) None (<2%) Mild (>2% – <10%) Moderate (>10% – <20%) Severe (>20%) GDP > US$ 15 000 (countries assumed to be free of vitamin A deficiency of public health signifcance) No data

29.1 Global Prevalence of Vitamin A Deficiency (retinol) as a public health problem by country 1995–2005. Source: WHO global prevalence of Vitamin A deficiency in population at risk 1995– 2005. WHO global database on Vitamin A deficiency. Geneva, WHO, 2009.

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29.2 National risk of zinc deficiency in children under 5 years [4]

29.3

The challenge

The diets of poor households in developing countries are lacking in many of the key vitamins and minerals, which are essential to keep people strong, healthy and productive. Dietary diversification, including consumption of animal products or more fruits and vegetables, can help satisfy human vitamin and mineral requirements. Though animal products are very good sources of the most bio-available forms of vitamin A, iron and of absorbable zinc; they are also costly food items which cannot be afforded by most poor people who have limited opportunities to diversify their meals. In addition, during periods of increased needs or acute vulnerability, everyday foods with high bulk and low density of vitamins and minerals do not contribute to the required nutrients in critical phases of life. Children are particularly vulnerable to deficiency of vitamin and zinc because of their physiological needs and vulnerability to infections. In regions where vitamin A deficiency (VAD) is a public health problem and the under-five mortality rate is high, children under the age of five are at particular risk of further increased morbidity and mortality. They are born with negligible vitamin A stores, are exposed to frequent infections, and do not receive much vitamin A through breast milk in the first six months (particularly if their mother is malnourished). As they get older, even if some vitamin A rich foods are available in the household, young children cannot eat enough to prevent the effects of deficiency without being supplemented. To overcome deficiency in these children

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by eating fruits and vegetables alone, they would have to increase their intake many fold. Zinc deficiency may occur due to diets inadequate in bio-available zinc, certain diseases like diarrhea, loss of zinc in processing foods, and poor soil deprived of zinc with reduced zinc content in agricultural products. Zinc deficiency is also caused due to infections that decrease appetite and food intake (e.g. respiratory infections) and increase zinc loss. The prevalence of zinc deficiency has not been adequately investigated, partly due to lack of suitable biomarkers. Based on the food balance data, it is estimated that a large section of the world population is at risk of developing zinc deficiency. The risk of deficiency is highest in populations, which consume predominantly cereal-based diets with little or no meat consumption. Zinc occurs in a wide variety of food sources, but is found in highest concentrations in animal-source foods. Zinc content is also relatively high in nuts, seeds, legumes, and whole-grain cereals, and is lower in tubers, refined cereals, fruits, and vegetables. The absorption of zinc is inhibited by phytates and dietary calcium, and enhanced by protein. Thus predominantly plant-based diets with high phytate content and low consumption of animal-source foods contribute to low zinc consumption and limited absorption.

29.4

Vitamin A and zinc deficiencies – implications on child mortality

Both vitamin A and zinc have important roles in the immune system. The role of clinical vitamin A deficiency in measles mortality has been well understood for some decades, and a series of meta-analyses of the role of vitamin A in the early 1990s led to the consensus that vitamin A deficiency is associated with increased risk of mortality in children [5]. Evidence shows that in children 6–59 months, there is 47% higher chance of mortality due to diarrhea and a 35% higher chance of measles mortality associated with vitamin A deficiency in unsupplemented children. The scientific evidence of the impact of zinc deficiency and those of zinc supplementation interventions are also quite recent and the metaanalyses mostly date after 2000. The increased risk of mortality associated with zinc deficiency is estimated to be 27% for diarrheal deaths, 18% for pneumonia related deaths, and 11% for malarial deaths. Similar effects of zinc deficiency on morbidity have been observed in trials of preventive zinc supplements in children aged 1–59 months [2]. Zinc deficiency is also associated with stunting, which has significant adverse effects on health and productivity. Studies suggest that therapeutic zinc for diarrhea can decrease mortality by 50%.

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A series of large-scale trials of zinc supplementation among children suffering from diarrhea revealed that zinc-supplemented children had a significantly lower probability of continuing diarrhea (acute and persistent). In addition, zinc supplemented children had 26% faster recovery [6]. Zinc treatment also resulted in a 20% reduction in the chances of an episode lasting more than seven days. In a large trial in Bangladesh, mortality rates (excluding deaths from injury) were 51% lower in the cluster with therapeutic zinc supplementation for diarrhea, than the control [7]. Zinc-supplemented children had a 15% lower probability of continuing diarrhea on a given day in the acute-diarrhea trials and a 24% lower probability of continuing diarrhea and a 42% lower rate of treatment failure or death in the persistent diarrhea trials [6]. Appropriately, the Lancet journal series on child survival identified vitamin A supplementation and therapeutic zinc supplementation in childhood diarrhea as key proven interventions to reduce child mortality [8]. Table 29.2 Under-5 deaths that could be prevented in 42 high-burden countries accounting for 90% of all child deaths if coverage of individual interventions were to be scaled up to 100% from estimated coverage in 2003 [8] Mean estimated coverage of Target population (range among countries) Preventive Interventions Breastfeeding (6–11 months) Measles vaccine Vitamin A Clean delivery (skilled attendant at birth) Tetanus toxoid Water, sanitation, hygiene Exclusive breastfeeding (<6 months) Newborn temperature management Antibiotics for premature rupture of membranes Antenatal steroids Nevirapine and replacement feeding Insecticide-treated materials Hib vaccine Antimalarial intermittent preventive treatment in pregnancy Zinc Complementary feeding Treatment Interventions Vitamin A Antibiotics for pneumonia Antibiotics for dysentery Antimalarials Oral rehydration therapy Antibiotics for sepsis Newborn resuscitation Zinc

90% (42–100) 68% (39–99) 55% (11–99) 54% (6–89) 49% (13–90) 47% (8–98) 39% (1–84) 20% 10% 5% 5% 2% (0–16) 1% 1% 0% † 55% (11–99) 40% 30% 29% (3–65) 20% (4–50) 10% 3% 0%

Vitamin A and zinc supplements for child survival

29.5

777

Approaches to address vitamin A deficiency

29.5.1 Food-based approaches Ideally for children to be fully protected from VAD, they need to consume sufficient vitamin A to meet their physiological requirements. VAD can be controlled if dietary source and intake of vitamin A can be improved sufficiently and sustainably. Commercial marketing, community-based distribution, subsidized provision and/or social marketing of affordable vitamin A rich foods, and/or the development and increased cultivation of vitamin A rich foods, all can potentially help improving intake of vitamin A. However there is no comprehensive comparative assessment available of the extent and effectiveness of food-based approaches for VAD reduction vis-à-vis the health systems approach of providing periodic high dose vitamin A supplements (VAS). Poverty is associated with poor quality diets which lack many micronutrients; poor diets lack protein and energy; diets low in animal products lack retinol. Improving diets could in principle tackle VAD and other issues simultaneously. This could involve increased production and consumption of micronutrient-rich foods, from commercial or home gardening sources, small livestock or aquaculture; nutrition education, mass media and programs aimed at changing food choices; steps to improve nutrient bioavailability by food processing or biotechnological measures. Increased intake of vitamin A from good plant sources such as red palm oil, orange flesh sweet potatoes etc, integrated with behaviour change support, can have a significant impact on nutritional status: giving red palm oil to children has been reported as having a small impact on reducing the prevalence of clinical VAD; providing it to mothers has been shown to increase maternal serum and breast milk retinol as well as infant serum retinol. However, much work remains to be done on resolving the logistics and costs of implementing such programs on wide scale. Results from countries such as Nicaragua have shown that the widespread fortification of a commonly consumed food (sugar) in some settings can contribute to reducing VAD. Other countries are enriching other foods with vitamin A (South Africa: cereal flours; Bangladesh: edible oils); and World Food Program (WFP) policy requires international procured or donated vegetable oil to be fortified with vitamins A and D. However there is generally too little data to be able to assess the extent of the effectiveness of these approaches in reducing VAD in young children. The only evidence of large scale effectiveness relates to sugar fortification [9]. Prospects for achieving sustained improved widespread intake through food based approaches in the short term appear to be limited in countries with high child mortality rates and sub-optimal access to centrally processed foods. Such foods are often not accessible to the poorest and most deficient

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and this section of population may be the last to benefit from any enriched foods available other than through targeted feeding programs.

29.5.2 Health-systems-based provision of VAS Where VAD is a public health problem, twice yearly provision of vitamin A supplements (VAS) to all children aged 6–59 months is accepted as a highly cost-effective way of improving intake. In addition, all cases needing therapeutic doses of vitamin A must be treated promptly in primary health care settings.

29.3 The relationship between vitamin A and child survival

Thus, vitamin A is a critical nutrient which can promote child survival and help achieve the Millennium Development Goal No. 4.

29.5.3 Brief history of the VAS program for preschool children India was one of the first countries in the world to launch a high dose vitamin A Supplementation program which was initiated in 1970 under the name “The National Prophylaxis Programme for Prevention of Blindness Due to Vitamin A Deficiency.” Renewed focus on vitamin A supplementation at large scale began in the late 1990s when the World Health Organization (WHO), recognizing its impact on child survival

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recommended delivering VA supplements along with polio vaccination during immunization campaigns, called National Immunization Days (NIDs) and integrating its provision with other health services. As polio NIDs became widespread, increasing numbers of children under five received at least one high-dose of VAS each year. The scope of these immunization campaigns provided an opportunity for countries to achieve very high coverage of children under five every 6 months, however the strategy of linking vitamin A supplementation with polio NIDs was always recognized as being time-limited. As polio NIDs continue to be phased out, countries are faced with the challenge of maintaining the necessary high coverage twice a year, without the well-funded, vertical program of polio NIDs. Countries which achieved polio eradication or had only one NID in a year moved towards holding micronutrients days or integrated child health events to provide VAS and other complementary services to communities. This approach has been described as the ‘REACH’ (Regular Events to Advance Child Health). Many countries are now working to institutionalize twice yearly distribution using the existing health system infrastructure without the risk of drop in coverage. A series of assessments of supplementation programs in 20 countries with high under five mortality rates revealed that in many countries, vitamin A supplements are being distributed successfully through the routine, primary health care system when combined with regular, twice-yearly outreach of services targeting all children under five, such as Child Health Days [10]. Thus in many countries, national guidelines now define routine for vitamin A supplementation as a mix of facility-based, outreach and community-based interventions, though some countries continue to use polio NIDS for delivering at least one dose a year. Until routine health services can reach all targeted children on a regular basis, outreach and biannual events such as Child Health Days will be critical to ensure full protection of children 6–59 months of age, not just with vitamin A supplements, but with other essential, preventive health services. Outreach entails not only extending the reach of the health services to all children who are live far from the health facility, but also to those older than 12 months who no longer receive regular immunizations. For example, in Bangladesh, the strategy for vitamin A supplementation is two-fold: for children 6–11 months of age it is through the routine health services (Expanded Program of Immunization, 9 months of age measles booster) contact points, and to for children 12– 59 months the twice-yearly Child Health Day approach is relied on, often called the National Vitamin A Plus Campaign. Conversely, in Kenya, twice-yearly coverage of children 6–59 months of age with vitamin A was over 80% when linked with immunization campaigns. However, in 2007 when the country decided to stop using campaigns and instead

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support increased delivery of routine services using fixed health facilities only (with no outreach), coverage for the full 6–59 month old age group dropped to approximately 20%. This drastic drop in coverage was not due as much to the 6–11 month old age group, whose coverage remained above 65% due to regular immunization contact points, but mainly due to the 12–59 month old age group whose coverage was less than 14% [11]. A similar problem is observed in India in those states that rely only on routine health services such as immunization contact points to deliver vitamin A supplementation, and which are only reaching children up to 18 months of age successfully. Child Health Days/Weeks or the Biannual Child Health & Nutrition promotion months as they are referred to in India, are a combination of fixed-site, outreach and community-based health days, offer the opportunity to strengthen the existing health system and deliver a package of essential child survival interventions. An example is in Ghana where their Child Health Days provide a package of services twice a year to over 80% of children 6–59 months, including vitamin A supplementation, immunization, deworming, re-treatment of insecticide-treated bed nets, issuing of child health cards and undertaking birth registration [10]. Another example is in Chattisgarh, India where a child protection month is celebrated twice a year (April and October) and delivers a package of services to over 85% of children. The services include vitamin A supplementation, deworming, growth monitoring, immunization focused on children never or partially vaccinated and salt testing for iodine content in households and community feeding centers. In Indonesia, the months of February and August are designated “Vitamin A Months”, where intensified communication and social mobilization encourages mothers to bring their children 6–59 months to their nearest health post for vitamin A supplementation, nutrition counseling, immunization and growth monitoring. In the Democratic Republic of Congo, the joint delivery of vitamin A and deworming is reported to boost the attendance of immunization and vitamin A supplementation programs [10]. Although such events require a significant amount of planning, strong logistical support and coordination among different departments of the Ministry of Health (EPI, Nutrition, Maternal Health for instance), the stakeholders and donors, they are very efficient in increasing coverage of several services at once. The delivery two VA doses has became a key indicator of progress towards improved child health, and is reported annually in UNICEF’s State of the World’s Children report and has been adopted as an indicator of progress toward the MDG of reducing child mortality [11]. VAS provision is recognized as a key part of the ‘arsenal of effective interventions against childhood killers.

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Box 29.1 Initiatives for VAS distribution in India In the late 1990s and early 2000s, States in India adopted various implementation strategies for VAS, as health falls under the State’s mandate. Some States conducted vitamin A supplementation campaigns or distributed vitamin A along with pulse polio initiatives for achieving high coverage. However, these distribution mechanisms were halted by the Central Government in late 2001 due to reported side effects (vomiting and diarrhea) and 12 children dying after a vitamin A campaign in Assam (November 2001). Although a Government investigation found no evidence of a link between the vitamin A and the child deaths, the incidents were widely reported in Indian media and globally. The incident prompted the Government of India (GOI) to issue instructions to the States that they halt standalone vitamin A campaigns or vitamin A linked to polio National Immunization Days. This resulted in many States linking vitamin A with routine immunization, considerably lowering coverage. Since 2004, VAS coverage has improved dramatically in most states. In part, this is because of increased advocacy for the program, increasing partner support, and movement toward a biannual approach. While most states include the first dose at the 9-month contact for measles, most also expand services to include older children during the biannual child health and nutrition promotion months. The VAS program has been supported by a number of partners, including UNICEF, MI and A2Z, a USAID project and a variety of Indian NGOs including CARE and the Child in Need Institute (CINI) and the MI India trust (MII). These partners have helped in a variety of ways including help with procurement, training and capacity building, supervision and monitoring. The degree of support from partners varies considerably from state to state with most support focused on the states with higher child mortality.

29.5.4 Bottlenecks in achieving universal twice yearly VAS coverage Assessments by MI and UNICEF in 2004, of the VAS programme in more than twenty countries, revealed several common findings with much still needed to be done to institutionalize ways of providing full and sustained protection against VAD to all children under five. Integration with routine health system efforts Many countries are working towards integrating VAS with routine immunization contacts at fixed sites and via outreach services. However the coverage currently achieved by these services is often sub-optimal. Second, this approach alone offers little scope to provide protection for children over a year old where immunization contacts focus on younger children. In a few cases, VAD control continues to be understood exclusively as a blindness prevention program; and the importance of VAS to child survival is not acknowledged. Resource commitments VAS in most countries is not included in government budgets; this weakens

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Public health nutrition in developing countries

VAS as a policy priority. Internationally, only a few donor agencies are actively funding vitamin A supplementation and investments in capacity and system strengthening approaches is inadequate and distribution costs are often not factored in adequately in donor contributions or in government budgets. Coordination issues Policy confusion and ineffective co-ordination at national level are exacerbated by mixed messages from the international community about primary health care (PHC) and child survival priorities and about the best strategies for controlling VAD. Insufficient collaboration and communication between many global initiatives makes it worse. VAD control programs end up fragmented between different units or departments, with gaps in policy and leadership, limited strategic choices, sub-optimal guidelines and poor co-ordination. Capacity issues Limited capacity and imperfect training in key operational areas, including supervision and monitoring, contribute to low rates of coverage. Monitoring performance Coverage estimation and denominators of children to be reached are not always reliable; and the emphasis placed on measuring percentage (%) coverage tends to obscure the importance of action at all levels to assure the provision of full and sustained protection for each child under five from VAD. Availability of sufficient supplies and other logistics and preparation of detailed micro-plans are not well monitored. Demand generation Following years of social mobilization alongside OPV, VAS does however seem reasonably well accepted by mothers and helps with their motivation to attend outreach or other contact points. However awareness of the benefits of VA is low with impact on night blindness being only consistent message that is known across communities. Supplies Supply chain, storage, inventory and logistics management are often weak with expiry of stocks and wastage being problems which are not effectively addressed.

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In summary it appears from the analyses, that the factors critical to achieving universal coverage of twice yearly VA supplements among children under five are the existence and quality of policy guidelines, plans and strategies for delivering VAS; effectiveness of local championship and co-ordination of efforts to ensure that VAS is delivered to all children under five twice yearly; adequate state of the Primary Health Care infrastructure, availability of both financial, and appropriately trained human, resources; extent of advocacy about VAS and of public awareness about the benefits of VAS; quality and timeliness of monitoring, reporting and information exchange; availability and quality of operational support & training; and the efficiency of local supply chains & logistics.

29.5.5 Reaching the unreached children with VAS In addition, well monitored programs are necessary to track progress, improve program delivery, and ensure that those intended to be reached are in fact being reached. Most countries will need complementary strategies to reach all children: the mainstream strategy to reach perhaps the first 80%, then the specialized, hard-to-reach strategy for the last 20%. The cost per child reached will vary between these two strategies, the “last 20%” expected to be the most costly to reach, but expected to yield a higher benefit. Although there is a strong belief that children who are currently not reached by vitamin A supplementation program are the most vulnerable and those arguably most in need, there is yet no clear picture of who are the unreached. Two studies from Indonesia suggest that children who are not supplemented come from lower socioeconomic status households, with lower immunization rates and lower parental education than children receiving supplements [12, 13]. Although it is assumed that the unreached live in geographically inaccessible areas, weak urban health infrastructure in poor urban areas makes health services such as vitamin A supplementation a challenge. Therefore in many cases, the unreached may also live in or around big cities such as Nairobi and Delhi. Ongoing operations research and pilot programs comparing alternative strategies to reach hard-to-reach populations will yield cost data and a better understanding of who are the unreached. Working with local and community-based organizations or using community extenders is one way to identify and reach the hard to reach. Box 29.2 Reaching the unreached – The Bangladesh experience A successful program in rural Bangladesh initiated in 2007 provides a good model for the rest of Asia, and the world, on how to reach the unreached. It was estimated

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that around 600,000 children in Bangladesh, primarily from socio-economically vulnerable households were not being reached with vitamin A supplementation. Building on an already successful two-district pilot project to reach hard-to reach children, local resource persons were trained and deployed as Vitamin A Extenders in more than 12 districts, who then coordinated with government health staff and trained special community volunteers. The volunteers collected data, conducted house-to-house visits, made follow-up visits and monitored distribution. Through this outreach, not only did 360,000 formerly unreached rural children receive vitamin A, but also essential information was collected about the needs of those children so they can receive additional health and social services. Key to this success was the use of active involvement of community groups and special volunteers, including women, active in the community in monitoring, collecting data and mobilizing families with previously unreached children. It cost about three times as much to reach this group of children as compared to those reached by regular distribution in 2007, although it is hoped that the differential could be reduced such that the “hard-to-reach” group would only cost 50% more than the regular distribution in future. [14]

29.5.6 Post-partum maternal and neonatal VAS Post-partum vitamin A supplementation for breastfeeding mothers, which is recommended to ensure that all infants receive the immune-boosting protection of vitamin A in the first six months of life, lags behind supplementation for children 6–59 months of age. Programs exist in only two thirds of priority countries, and most are limited in scope. International recommendations also allow for low-dose supplementation of pregnant women with xerophthalmia, but coverage is not widespread. Supplementing mothers – missed opportunities Opportunities exist to administer supplements to mothers at delivery in health facilities or more commonly at home. In Nepal, community health volunteers, many of them illiterate, administer vitamin A supplements to mothers soon after birth. Alternatively, mothers can receive their postpartum dose at the time of the newborn’s first immunization contact for BCG. While BCG coverage is quite high in most countries (approximately 80%), not many countries actually use this opportunity to supplement new mothers with vitamin A, which clearly represents a missed opportunity. Emerging research – neonatal high dose VA supplementation Review of recent evidence suggests that supplementing newborns with a single large dose (50,000 IU) within a couple of days of birth reduces neonatal mortality [15]. It appears that providing a vitamin A supplement to newborns in South Asia in the first 48 hours can reduce the risk of infant death by approximately 20% [15, 16]. As some other studies have not demonstrated similar benefits [17], the WHO is currently

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commissioning a set of studies to facilitate the generation of further scientific evidence in different geographical contexts. Further confusion exists as it has been shown in several studies that vitamin A supplementation of children 1–5 months of age has no effect on child morbidity or mortality rates.

29.6

Addressing zinc deficiency

It is clear from the results of numerous zinc supplementation trials that a wide range of health benefits can be realized by increasing the intake of zinc where intakes were previously insufficient [4]. The approaches to increase zinc intake can be classified under:

29.6.1 Food-based approaches Strategies to diversify or modify the diet aim to enhance the access to, and utilization of, foods with a high content of absorbable zinc throughout the year. These strategies can involve changes in food production practices, food selection patterns, and traditional household methods for preparing and processing indigenous foods. Agricultural strategies to increase total and/or absorbable zinc content in staple foods include the use of fertilizers and improved plant breeding and genetic modification while strategies to increase production and/or intake of zinc-rich foods include promoting small live stock production or aquaculture. Household processing methods such as soaking, germination and fermentation can help increase the absorbable zinc in the diet [4]. Fortification of both staples and snacks with zinc has been attempted but no evidence of impact is available at large scale.

29.6.2 Zinc supplementation Research trials have indicated reduction of morbidities as well as impact on mortality with both preventive as well as therapeutic zinc supplementation. However the evidence for preventive zinc supplementation, especially with regards to reduction of mortality is not conclusive. Two large studies on the impact on zinc on mortality conducted in Nepal and in Tanzania [18, 19] reported a modest non-significant reduction in overall mortality in children under five years of age. When all of the prevention trials examining the impact on mortality of zinc supplementation in young children (excluding trials that only included selected specific groups such as low birth weight or malnourished children) are viewed together, a 9% reduction in mortality is observed [20].

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There is however compelling evidence regarding the benefits of therapeutic zinc along oral rehydration therapy for childhood diarrhea which has built scientific consensus supporting low osmolarity oral rehydration salts and zinc for diarrhea management. This led to the joint WHO/UNICEF recommendation of administering 10–14 days of therapeutic zinc for children under 5 years of age along with oral rehydration. Zinc supplementation paired with low osmolarity oral rehydration solution (ORS) were recognized as important approaches to tackle childhood diarrhea which would be critical for achieving the Millennium Development Goal 4 on reduction of child mortality by two thirds of 1990 levels.

29.6.3 Global developments to introduce and scale up the new recommendations on use of zinc and change in guidelines for use of low osmolarity ORS The new WHO/UNICEF recommendations on the clinical management of acute diarrhea, including the provision of zinc to all children with diarrhea treated in health facilities and at home, with ORS or recommended home fluids, were published in May 2004 [21]. Following this recommendation all WHO diarrhea management guidelines, including the Integrated Management of Childhood Illness (IMCI) treatment charts, were revised to incorporate these new recommendations. In March 2005, zinc was added to the WHO Model List of Essential Medicines [22]. New documents were developed by the WHO in collaboration with the Zinc Task Force to facilitate the adoption and implementation of the new diarrhea recommendations at country level, and to assist program managers and pharmaceutical manufacturers in choosing or producing zinc products adequate for use in the management of diarrhea.

29.6.4 Moving from efficacy to effectiveness to full scale programs: need for traction In order to assist countries in including zinc supplementation in the management of diarrhea, three introduction studies were conducted in India, Mali and Pakistan. The aims were to assess potential constraints when implementing this new recommendation together with the administration of lower osmolarity ORS solution, as well as to determine the best possible delivery channels for zinc supplements. The preliminary results from these three large effectiveness studies clearly show that zinc encourages greater uptake of ORS and reduces inappropriate drug use. One study showed that an intervention that included caregiver education

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on the use of zinc and ORS during childhood diarrhea, and provision of both zinc and ORS by public and private health care providers to caregivers, was associated with reduction in the prevalence of diarrhea and pneumonia, and in all-cause, diarrhea, and pneumonia hospitalizations. The intervention also resulted in reduction in the use of unwarranted oral and injectable drugs during diarrhea, reduction in the out-of-pocket costs for care of diarrhea to the family, and substantial increase in the ORS use rates. [23] Nevertheless, delays in moving from knowledge to action are being currently experienced. Policy initiatives, such as the joint WHO/UNICEF statement, have not yet acquired enough momentum to ensure widespread introduction of low osmolarity ORS and zinc across the world. Only about 53 countries have included therapeutic zinc in the diarrhea management policy, and fewer than 30 countries have initiated pilot programs so far [24]. Bangladesh is the only country to attempt a national scale-up, and Nepal is the first country to engage in large-scale social marketing, which now covers half its population [25]. Several other countries such as India, Guatemala and Bolivia have issued policy guidelines and are in the process of rolling out their programs. The private sector is very critical in improving access to appropriate diarrhea treatment. The USAID supported POUZN (Point of Use Water Disinfection) project has supported the marketing of zinc products in India, Indonesia, and Tanzania by the private sector and raised awareness regarding the intervention and availability of product among health providers of both the formal and non-formal sectors. A diarrhea treatment kit (DTK), created by packaging together zinc tablets and ORS and delivered through both commercial retail outlets and NGOs, has been piloted successfully in Cambodia [25]. Box 29.3 Steps in scaling up of the Zinc and ORS Program for childhood diarrhea ● ● ● ● ● ●

●

Awareness of the policy at all levels including states and districts. Defining roles and responsibilities of all stakeholders. Devising program strategy and its adaptation in different settings. Procuring supplies of zinc and ORS and logistics. Developing training material and program for training different cadres. Developing monitoring and evaluation systems that will include measurement of coverage and costs. Provide for mid-course corrections and continuing innovation.

Box 29.4 The Bangladesh experiences of scale up Zinc and ORS Programme [26] Building upon the success of small-scale introduction through effectiveness trial activities in Matlab, the Gates-funded SUZY project was implemented in Bangladesh with the objective of nationally scaling up zinc. This is the first such

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example of efforts to nationally introduce zinc. Zinc, like ORS was listed as an over the counter (OTC) drug which was distributed through all possible channels, including the informal private sector. The development of a local brand of zinc dispersible tablets was a key element of the strategy with an attractive tag line rhyming with a bicycle’s ring “Cring… Cring… Baby Zinc” along with a logo of a playful boy and girl being used in all forms of advertising across the country. Demand for this new product was created through two mechanisms: ● ●

Provider promotion, and Mass media marketing once the product was well known from providers and the strategy was in place.

From what little has been reported it is known that while efforts to promote zinc through intensive provider engagement, mass media campaigns, and other strategies, corresponded to increased awareness, zinc coverage rates remained low with the Demographic Health Survey, 2007 reporting a 23% overall use rate with a 33% urban use rate and a 20% rural use rate.

29.6.5 Challenges of scale up of zinc use in childhood diarrhea in India In India, the apex professional organization, the Indian Academy of Pediatrics (IAP) approved zinc as an adjunct therapy to ORS in the management of diarrhea in the year 2004 and the revised guidelines were endorsed in September 2007. The revised national policy for the treatment of childhood diarrhea announced by the Government of India in November 2006 include zinc as an adjunct to ORS in the management of acute diarrhea in the national program. The recommendation is that all cases of diarrhea receive a 20 mg zinc sulphate dispersible tablet; ½ tablet for infants aged 2 months to 6 months and 1 tablet for older children, for 14 days in addition to ORS. The policy emphasizes that (i) zinc tablets should be available in all parts of the country including at child care centres of ICDS or Anganwadi centres, (ii) that zinc be made an over-the-counter (OTC) formulation, (iii) an effective communication strategy be put in place and that (iv) health care providers are oriented and trained in the use of zinc along with ORS. Zinc dispersible tablets are a part of the new treatment guidelines and the Government of India has already accepted zinc dispersible tablets (20 mg) as a part of supply kit A of the Reproductive Child Health Programme (RCH). The following challenges are recognized to be critical for the successful scaling up the new diarrhea case management package in the Indian context: ORS use rates ORS use rates in India continue to remain low for the last 25 years. The strategy for scaling up zinc treatment should be a package along with ORS.

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Recent programmatic trials have shown that when zinc is packaged with ORS, the ORS use rates go up dramatically. In addition to health facilities, community depot holders for zinc and ORS need to be created. Creating awareness in stakeholders All stakeholders including those at the state level need to be sensitized to the new diarrhea policy. This would include state and district level planners. Communications strategy A strong communications strategy with regional focus is essential for promotion of usage of ORS and Zinc. Although mass media would help boost the use rates the involvement of mass media should only occur once all the providers are sensitized and supplies are in place. Involvement of the private sector Data from various surveys show at large majority of diarrhea is treated by the private sector (formal and informal). Pediatricians and other formal providers will need to be sensitized through the provider associations. The new strategy should effectively reach networks of the informal private sector and sensitize them on the use of ORS and zinc as well. Formulations, pricing and supplies ORS and zinc are OTC products with a unique safety profile and therefore should be easily accessible and readily available to families close to their homes. Dispersible tablets of zinc and ORS should be dispensed free of cost through the government system i.e. from the PHC and community based outreach workers such as Anganwadi workers and health community volunteers such as ASHA. The private sector would have several options for dispersible tablets and syrups available in the market to choose from. However, keeping in mind the competition with antibiotics and anti-diarrheals, the pricing of these formulations should be such that the profit margin for the providers does not reduce substantially. Monitoring and evaluation systems Follow up action will need to be ensured at all levels and once the programs are in place, monitoring and evaluation systems need to be designed which are integrated with the existing systems and are able to guide decision making for improving the program reach and quality.

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Box 29.5 Zinc and ORS distribution in an emergency situation in Bihar In October 2008, large parts of the state of Bihar were ravaged by floods due to breach in the embankments of the river Kosi near the Indo-Nepal border, leading to a change in the course of the river which affected more than 4 million people living in 5 districts of the state (Araria, Purnea, Supaul, Madhepura and Saharsa) which are downstream from the breach in the river near the Nepal border. The Government of Bihar as part of the flood relief measures planned to advance the biannual round of VAS distribution by 1 month in these 5 districts. They included the distribution of zinc and Low osmolarity ORS for children with diarrhea as part of the package of services. The Government of Bihar with assistance from UNICEF and MI distributed 58,000 Diarrhea Treatment Kits (DTKs) (consisting of a 10 day course of zinc (in accordance with WHO guidelines) and 2 packets of low osmolarity ORS) to children suffering from diarrhea in five flood affected districts as part of a special child health package along with vitamin A supplementation (VAS) which is delivered twice a year, through a special biannual approach in Bihar. The use of biannual VAS rounds to promote the use of zinc and ORS for the treatment of diarrhea was unique as it allowed multiple synergistic child health services to be provided at the same time. As part of the flood relief operations, it offered humanitarian aid in the time of crisis. Since zinc had not been distributed in the state along with ORS, the introduction of zinc during this period provided an opportunity to demonstrate positive attributes of zinc as a package of health services. It also provided an opportunity to check the effectiveness of the use of VAS biannual rounds as a means to promote the use and the knowledge of the use of zinc for treatment of diarrhea. There were logistical difficulties in ensuring the availability of supplies at field level, given the nature of the emergency, with the process evaluation survey reporting that 14% of sites reporting not having received the DTKs and only 59% of sites reporting that the quantities supplied were adequate. As it was a new intervention, the level of preparedness of frontline workers was not optimum, as only 74% of workers said that they recommended that zinc tablets be taken for 10–14 days.

29.7

Economic analysis of cost and benefit of vitamin A and zinc supplementation

The cost per child for achieving different levels of coverage of vitamin A supplementation and therapeutic zinc supplementation has been estimated for different parts of the world (see Table 29.3). It is generally accepted that it would cost more and be increasingly difficult to scale up coverage to reach the last 20% of the population who are likely to be the ‘hard to reach’. These interventions are highly cost effective at these costs given the likely impact in terms of lives saved.

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Table 29.3 Estimates of total cost of supplementation per child per year, by region and level of coverage [27] Region(s)

Vitamin A, coverage 20–80%

Vitamin A, coverage 80–90%

Zinc, coverage 0–40%

South Asia, Sub-Saharan Africa, East Asia Central Asia Latin America and the Caribbean

$1.20

$2.40

$1.00

$1.60 $2.60

$3.20 $5.20

$1.35 $2.20

29.7.1 Vitamin A supplementation VAS is relatively inexpensive on a per-child basis. Costs vary widely by region, tend to be lower in large-scale government programs than smaller nongovernment-organization programs, and are lower when vitamin A supplement delivery is combined with other health interventions. Reported costs are often substantially underestimated if personnel time is not included since the cost of capsule /VA syrup may be only 5–10% of costs. Other program costs include expenditure on training, logistics, promotional material etc. Cost-effectiveness studies have estimated the per death-averted costs are less than US$ 500 as estimated in different contexts and regions, usually ranging from about US$228 through the Enhanced Outreach Strategy of using Child Health days in Ethiopia [28] to about US$ 327 in Nepal where community health workers are used for VA supplement distribution [29]. Costs per death averted vary depending on the number and proportion of the child population reached, number of doses received per child, and child mortality rates and the actual distribution costs involved [30]. This makes vitamin A supplementation among the most cost effective public health interventions in the world. As there are no current zinc and ORS programs at significant scale, operational research is needed to develop and test varying delivery mechanisms in the public and private sectors (formal and informal), including comparative cost analysis. Estimates of cost-effectiveness by Robberstad et al [31] suggest that the incremental cost of zinc as part of case management is $0.47 per course of treatment, leading to an average cost of $73 per DALY gained, and $2,100 per death-averted. The cost of tablets range from $0.01 to 0.02 each, hence a course of the tablets costs about $0.10–0.19, with the additional costs representing distribution and administration. A broad cost analysis for a micronutrient investment plan for India estimated that it would cost US$0.35 per child per episode of diarrhea including programmatic costs such as training, communication material and monitoring, for a scale up of therapeutic zinc for childhood diarrhea [32]. Preliminary results from the economic evaluations performed in India and Pakistan based on the large-scale effectiveness trials have shown that zinc is cost effective in treating diarrhea in patients under 5 years as

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compared to ORS alone in this setting. The introduction of zinc led to a decrease in out of pocket payments for medicine/ consultation fees of over USD$1.00 per patient per episode.

29.8

Implications and conclusions

Vitamin A supplementation for young children and therapeutic zinc supplements for management of diarrhea in young children should be treated as priority interventions. Although, twice yearly vitamin A supplementation is now occurring in many countries as part of a minimum package of health services, the challenge is to ensure that the remaining 30% of children, who are not covered, are being reached to ensure and sustain universal supplementation for child survival. This requires additional resources to “do that last mile” and commitment from governments to mobilize and efficiently use supplementary resources. Countries which are lagging behind need to adopt best practices including twice yearly events like Child Health Days to extend the outreach of the primary health care system, identifying those who are regularly unreached, and using of vitamin A coverage as a health performance indicator. Experience with zinc supplementation as an adjunct treatment for diarrhea is more recent. In spite of strong evidence of efficacy of zinc supplementation and more recently on effectiveness, very few countries have shown encouraging progress by revising their diarrhea management policy to include zinc, encouraging local production, ensuring sufficient supplies, and creating demand through social mobilization and marketing. It is essential that therapeutic zinc supplementation is integrated into the primary health care system at the community level. Such a strategy has been demonstrated to synergistically help boost ORS coverage as well. Twice yearly vitamin A supplementation through the REACH strategy and provision of ORS and zinc by community level providers to children with diarrhea will help achieve universal coverage with these essential child health interventions, which is a must for developing nations to reduce child mortality significantly and the world to achieve the Millennium Development Goals and move beyond.

References 1.

CONSENSUS (2008). Available at http:// www.copenhagenconsensus.com/home.aspx (Accessed on 07.11.2009). 2. BLACK RE, ALLEN LH, BHUTTA ZA , CAULFIELD LE , DE ONIS M, EZZATI M , MATHERS C, RIVERA J (2008). The Maternal and Child Undernutrition Study Group, Maternal and Child Undernutrition: Global and Regional Exposures and Health Consequences, The Lancet, 371(9608), p. 253. COPENHAGEN

Vitamin A and zinc supplements for child survival 3.

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(2005). Recent trends in malnutrition in developing regions: vitamin A deficiency, anemia, iodine deficiency and child underweight. Food and Nutrition Bulletin, 26, pp. 57–162. HOTZ C and BROWN KH (eds) (2004). IZINCG Technical Document No 1. Assessment of the risk of zinc deficiency in populations and options for its control. Food Nutr Bull, p. 25. BEATON GH et al. (1993). Effectiveness of vitamin A supplementation in the control of young child morbidity and mortality in developing countries. Nutrition Policy Discussion Paper 13: Administrative Committee on Coordination— Subcommittee on Nutrition (ACC/SCN). Geneva, Switzerland: World Health Organization. BHUTTA ZA , BIRD SM , BLACK RE , BROWN KH , GARDNER JM , HIDAYAT A , KHATUN F , MARTORELL R, NINH NX , PENNY ME , ROSADO JL , ROY SK , RUEL M, SAZAWAL S, SHANKAR A (2000). The Zinc Investigators’ Collaborative Group. Am J Clin Nutr, 72, pp. 1516–1522. BAQUI AH , BLACK RE, ARIFEEN SE , YUNUS M , CHAKRABORTY J , AHMED S, VAUGHAN JP (2002). Effect of Zinc Supplementation Started During Diarrhoea on Morbidity and Mortality in Bangladeshi Children: Community Randomised Trial, BMJ, 32(5), p. 1059. Downloaded from http://www.bmj.com on 25 September 2008. JONES G , STEKETEE RW , BLACK RE, BHUTTA ZA , MORRIS SS and the Bellagio Child Survival Study Group (2003). How Many Child Deaths Can We Prevent This Year. The Lancet, p. 362, http://www.thelancet.com. ARROYAVE G , MEJIA LA and AGUILAR JR (1981). The Effect of Vitamin A Fortification of Sugar on the Serum Vitamin A Levels of Preschool Guatemalan Children: A Longitudinal Evaluation. Am. J. Clin. Nutr, 34, pp. 41–49. A G U AY O V M , G A R N I E R D , B A K E R S K (2007). Drops of Life: Vitamin A Supplementation for Child Survival. Progress and Lessons Learned in West and Central Africa. UNICEF Regional Office for West and Central Africa. WAGSTAFF A and CLEASON M (2004). The Millennium Development Goals for Health: Rising to the Challenges. Washington DC: World Bank. PANGARIBUAN R, ERHARDT JG, SCHERBAUM V , BIESALSKI HK (2003). Vitamin A Capsule Distribution to Control Vitamin A Deficiency in Indonesia: Effect of Supplementation in Pre-School Children and Compliance with the Programme. Public Health Nutr, 6(2), pp. 209–216. BERGER SG, DE PEE S, BLOEM MW , HALATI S , SEMBA RD (2008). Malnutrition and Morbidity are higher in children who are missed by periodic vitamin A capsule distribution for child survival in rural Indonesia, Public Health, 122(4), pp. 371–378. MICRONUTRIENT INITIATIVE . Annual Report 2008-09. HAIDER BA and BHUTTA ZA (2008). Review of Vitamin A Supplementation in the Neonatal Period, Webappendix 11, Lancet Series on Maternal and Child Undernutrition, http://www.globalnutritionseries.org (accessed on June 18, 2008). KLEMM RD , LABRIQUE AB , CHRISTIAN P , RASHID M , SHAMIM AA , KATZ J , SOMMER A, WEST KP , JR (2008). Newborn Vitamin A Supplementation Reduced Infant Mortality in Rural Bangladesh, Pediatrics, 122(1), pp. E242–E250. MALABA LC et al. (2005). Effect of postpartum maternal or neonatal vitamin A supplementation on infant mortality among infants born to HIV-negative mothers in Zimbabwe. Am J Clin Nutr, 81, pp. 454–460.

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(2007). Effect of Zinc Supplementation on Mortality in Children Aged 1–48 Months: A Community-Based Randomised Placebo Controlled Trial, p. 369. TIELSCH JM , KHATRY SK , STOLZFUS RJ, KATZ J , LECLERQ SC , ADHIKARI R , MULLANY LC, BLACK R , SHRESTA S (2007). Effect of Daily Zinc Supplementation on Child Mortality in Southern Nepal: A Community-Based, Cluster Randomized PlaceboControlled Trial, vol. 370, http://www.thelancet.com. Report of Workshop to Review the Results of Studies Evaluating the Impact of Zinc Supplementation on Childhood Mortality and Severe Morbidity (Geneva, Switzerland, 15–16 September, 2006). WHO / UNICEF (2004). Joint Statement on The Clinical Management of Acute Diarrhoea. http://whqlibdoc.who.int/hq/2005/a87017eng.pdf (accessed on 09.02.2010). BHANDARI N , MAZUMDAR S , TANEJA S, DUBE B , AGARWAL RC, MAHALANABIS D , FONTAINE O , BLACK RE , BHAN MK (2008). Effectiveness of Zinc Supplementation Plus Oral Rehydration Salts Compared with Oral Rehydration Salts Alone as a Treatment for Acute Diarrhoea in a Primary Care Setting: A Cluster Randomized Trial. Pediatrics, 12(1), pp. E1279–E1285. FISCHER CLW, FONTAINE O , YOUNG MW , BLACK RE. Zinc and Low-Osmolarity Ors for Diarrhoea: A Call to Action Four Years After the WHO/UNICEF Global Recommendation. Unpublished. DARY O , HARVEY P, HOUSTON R, RAH J (2008). The Evidence on Micronutrient Programs: A Selected Review, Micronutrient Forum. KOEHLMOOS T (2009). Scaling Up Zinc For The Treatment Of Young Children With Diarrhoea. ICDDR, B: Dhaka, Bangladesh. HORTON S, BEGIN F , GREIG A , LAKSHMAN A (2008). Best Practice Paper, Micronutrient Supplements For Child Survival (Vitamin A And Zinc), Copenhagen Consensus Center, Working Paper. FIEDLER JL and CHUKO T (2008). The Cost of Child Health Days: A Case Study of The Ethiopian EOS Program. Health Policy and Planning, 23, pp. 222–233. FIEDLER JL (2000). The Nepal National Vitamin A Program: Prototype to Emulate or Donor Enclave? Health Policy and Planning, 15(2), pp. 145–156. CHING P , BIRMINGHAM M , GOODMAN T , SUTTER R, LOEVINSOHN B (2000). Childhood Mortality Impact and Costs of Integrating Vitamin A Supplementation into Immunization Campaigns. Am J Pub Health, 90(10), pp. 1526–1529. ROBBERSTAD B , STRAND T , BLACK RE, SOMMERFELT H (2004). Bulletin of the World Health Organization, 82(7). MICRONUTRIENT INITIATIVE (2007). India Micronutrient Investment Plan.

30 Addressing micronutrient malnutrition through food fortification Saraswati Bulusu and Annie S. Wesley

Saraswati Bulusu, PhD, in Biochemistry from Calcutta University, with specialization in Nutritional Toxicology, has undertaken special trainings in Program Monitoring and Evaluation at Tufts University, Boston, and Project & Financial Management at IIM Bangalore. Dr. Bulusu was a National Program Manager and the Managing Trustee of the Micronutrient Initiative, India, for more than 10 years and was responsible for developing various fortified low cost products and introduction of such products in the public and private systems. She is currently a nutrition specialist with UNICEF, Hyderabad office, India. She is a recipient of the Junior Scientist Award of the Indian Science Congress Association, Government of India. Annie S. Wesley is a Senior Program Specialist at the Micronutrient Initiative, Ottawa, Canada since 1999. Dr. Wesley completed PhD in Food Science from the Central Food Technological Research Institute, Mysore, India and obtained post-doctoral experience in cereal chemistry and food technology from the Department of Grain Science and Industry, Kansas State University, USA and the Cereal Research Centre, Winnipeg, Canada. Currently she provides technical support in the area of food fortification to MI programs in Asia, Africa and the Middle East.

!.1

Introduction

Malnutrition is broadly categorized as macro malnutrition caused primarily due to deficiency of proteins and calories and micronutrient malnutrition caused due to deficiency of micronutrients such as vitamin A, vitamin B1, vitamin B 2, vitamin B3, folic acid, iodine, iron, calcium, zinc, selenium, etc. Data from developing country such as India show that percentage of children and adults with intake of major micronutrients below 50% recommended dietary allowances (RDA) is rather high (Table 30.1) [1]. Intake of iron is less than 50% of the RDA in all age groups, with the proportions varying from 70% to 80%. Similarly, vitamin A intake is less than 50% of the RDA in all age groups, with the proportions varying from

795

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80% to 90%. There is increasing evidence to show that lack of micronutrients cause devastating damage to health and well being of the population [2]. Table 30.1 Percentage of adults and children with nutrient intake below 50% of the RDA in rural areas of India in 2001 Adults (% <50% RDA)

Children (% <50% RDA)

Age (year Proteins Calories Iron Vitamin A Age (year Proteins Calories Iron Vitamin A and sex) and sex) =18 F(L) =18 F(P) =18 F (NPL) =18 M 16–17 F 16–17M

13.9 15.4 4.7

1.3 1.6 1.4

71.1 86.7 68.1 82.4 67.9 85.7

1–3 4–6 7–9

17.4 6.3 11.2

38.0 24.1 19.0

72.1 87.5 70.7 87.3 76.2 90.0

5.4 22.7 24.7

3.0 5.9 6.6

50.1 83.5 71.2 87.8 73.3 87.8

10–12 M 10–12 F 13–15 M 13–15 F

19.2 23.8 24.4 24.9

16.8 8.5 10.3 5.8

80.7 77.5 79.6 68.0

87.8 87.8 86.3 87.7

M – Male; F – female; L – lactating; P – pregnant; NPL – neither pregnant nor lactating.

Micronutrient malnutrition is commonly referred to as “hidden hunger”, since micronutrient deficiencies often go unnoticed but cause individuals and families to suffer serious consequences including learning disabilities, impaired work capacity and illness, ultimately leading to death. Though micronutrients are required only in milligrams or micrograms, these nutrients are necessary for efficient metabolic activities and for functions such as growth, cognition, immune system and reproduction. It is therefore important to address micronutrient malnutrition right from the early childhood to reduce long-term effects on growth and development. The implications of micronutrient deficiencies on the millennium development goals are presented in Table 30.2 [3].

30.2

Micronutrient malnutrition – an overview

Nearly one-third of people, especially in the developing world, are affected by one or more micronutrient deficiencies, principally iron, iodine, vitamin A, folic acid or zinc [2]. The critical role of vitamins and minerals in the health and well being is demonstrated by the fact that iron, zinc and vitamin A deficiencies are among the first 15 of 26 major risk factors of the global burden of disease (Figure 30.1) [4]. A recent global progress report states that 35 percent of people in the world lack adequate iodine, 40 percent in the developing world suffer

On children: decreased school attendance

Education and literacy impact (MDG2)

On children: Increased risk of death for >1 million young children yearly

Major infectious disease impact (MDG6) On children: 40% of under-fives immunocompromised by VAD with reduced protection against diarrhoea, measles, and other infections

Child mortality impact (MDG4) Maternal health impact (MDG5)

Gender equality impact On women and girl children: caring for (MDG3) sick young children affects earning a livelihood

On caregivers: care for the sick/dying On families: cost of funerals On families: loss of future earnings

Impact of iodine deficiency disorders(IDD)

On people: Impact of malaria exacerbated by iron deficiency On children: anemia is linked to most malaria related deaths in young children

On countries: In iodine deficient population mean IQ lowered by 10– 15% On adults: reduces productivity On adults: negatively affects On caregivers: care for the sick livelihoods On children: impairs learning On caregivers: care for the sick On children: impaired mental On children: impaired mental development for 50% of 6–24 monthdevelopment for 18 million children old children in developing world: hard to globally: 60,000 severely mentally learn and keep jobs retarded On adults: impaired productivity On women and girl children: caring increases risks to livelihood. Greater for sick young children affects health impact on women. earning a livelihood and school attendance On children: 15,000 infants at greater On children: increased risk of still risk of death due to maternal anemia. births On mothers: Death of 50,000 women/year during pregnancy and childbirth

Impact of iron deficiency anemia (IDA)

On countries: higher burden of death and On countries: economic loss in disease to be managed affected countries = 1% of GDP

Impact of vitamin A deficiency (VAD)

Poverty and hunger impact (MDG1)

Goal

Table 30.2 Linkages between micronutrient deficiencies and Millennium Development Goals (MDGs) [3]

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30.1 Global disease burden.

from iron deficiency, and more than 40 percent of children are vitamin A deficient [2]. The situation in India is presented in Box 30.1. Box 30.1 Micronutrient Deficiency – Magnitude of Problem in India According to the National Family Health Survey (NFHS)-3 India report [5], anemia prevalence is more than 79% in children 6–35 months of age, 56.2% in ever married women of 15–49 years, 57.9% in pregnant women 15–49 years and 24.3 % in men. In a study of pregnant women, anemia is reported to be over 80 percent in various regions of India [6]. As per National Nutrition Monitoring Bureau (NNMB) Report [1], the prevalence of conjunctival xerosis and Bitot spots, the signs of vitamin A deficiency was reported in 0.9% and 0.6% of pre-school children and 1.9% and 1.6% in school age children and 1.3% in adolescents. The prevalence of Bitot spots, the objective sign of vitamin A deficiency was more than the WHO cut-off level (0.5%) in several States. The prevalence of total goitre ranged between 3.3% and 13.7% in various states. As discussed earlier (Table 30.1), data from National Nutrition Monitoring Bureau 2002 shows that in India, the intake of iron and vitamin A is less than 50% of the Recommended Dietary Allowance in all age groups. For iron, apart from a low dietary intake, there is also poor absorption due to a largely vegetarian diet. Such poor intakes are reflected in the nutritional status of the population in all age groups [7]. Added to these are other factors including lack of awareness, availability, accessibility, acceptability and affordability of micronutrient rich foods. Though the extent of the micronutrient deficiencies are quite staggering these deficiencies can be prevented and even eliminated if populations consume small quantities of bio-available forms of required vitamins and minerals on a continuous and ongoing basis. According to a recent landmark document by the World Bank [8], the control of vitamin and mineral deficiencies is one of the most extraordinary

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development-related scientific advances of recent years. Probably no other technology available today offers as large an opportunity to improve lives and accelerate development at such a low cost and in such a short time [9]. The Government of India in 1993 adopted the National Nutrition Policy (NNP) and committed itself to achieve by 2000: ● ● ●

● ●

Virtual elimination of iodine and vitamin A deficiency. Reduction of IDA in women by 1/3 rd by the year 2000. Elimination of blindness due to VAD and reduction in prevalence of Bitot’s Spots to less than 0.5%. Reduction in IDA among pregnant woman to 25% and Universal iodization of salt for reduction of IDD (Total Goitre Prevalence <10%).

India has come a long way in understanding the nature, magnitude and range of solutions to micronutrient malnutrition. Given the size and diversity of the nation, and the enormity and complexity of the problems of micronutrient deficiencies, the population’s vitamin mineral requirements can be met only through a combination of strategies which have a synergistic effect as they can address multiple nutrient deficiencies simultaneously, foster the development of sustainable food production system, build partnerships among Government, consumer groups, food industry and other organizations and also promote self reliance and community participation. This concept is well reflected in the National Nutrition Policy, 1993. Fortification of foods with appropriate nutrients is recommended as one of the important priority actions.

30.3

Complementary strategies to overcome micronutrient malnutrition

Since neither the macro nor micro nutrient malnutrition occurs in isolation, there is a need to combine interventions for improving macro and micronutrients status in various development programs. As a consequence of the World Summit for Children, New York, 1990 [10], Ending Hidden Hunger Conference (1991) [11] and International Conference on Nutrition (Rome, 1992) [12], a number of developing countries intensified efforts to address the problem of micronutrient deficiencies. The awareness on the micronutrient malnutrition has greatly increased in the past two to three decades. Most of the countries today are making efforts to approach the problem with real determination both at the national and community level [13]. For successful and sustainable micronutrient interventions, food fortification is recognised to be very essential. Food fortification is a medium term approach to improve micronutrient intakes across the population on a consistent basis. Complementary to fortification, a short term approach during severe deficiency situations to ensure relief to vulnerable groups is being addressed through ‘supplementation’. This involves administering high doses of the micronutrient in a concentrated supplement form to overcome the severe deficiency. An example is the six monthly high dose vitamin A supplementation being administered to children under 5 years of age in a

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number of developing countries. A longer term approach to ensure sustained outcome is through dietary diversification and involves ensuring access and encouraging population to consume foods rich in micronutrients including fruits and vegetables. This chapter presents the various aspects of food fortification to meet the vitamin mineral needs of general population as well as specific target groups like women and children who are more susceptible to the deficiencies.

30.4

Food fortification

Food fortification can be described as a method of adding essential vitamins and minerals to foods to increase their nutritional value. According to Codex Alimentarius, fortification or enrichment is the addition of one or more essential nutrients to a food, whether or not it is normally contained in the food, for the purpose of preventing or correcting a demonstrated deficiency of one or more nutrients in the population or specific population groups [14]. The food to which the nutrients are added is called ‘vehicle’ for fortification and the added nutrients are called as ‘fortificants’. Fortification is the cheapest, most efficient and effective way to reach large populations with essential micronutrients. However, it is also important to recognize that food fortification is one part of a range of measures that influence the quality of food including improved agricultural practices, improved food processing and storage and consumer education to adopt good food preparation practices. Food fortification can be regarded as the best food based approach for solving the nutritional problems in developing countries.

30.5

History of food fortification

Food fortification is a public health initiative with a long history of being used effectively to remedy nutritional deficiencies that were causing widespread national public health problems. The earliest known nutrient supplementation of food was in 400 BC, when the physician Melanpus added iron filings to wine to increase Persian soldiers’ strength. In 1833, the French agricultural chemist Jean Baptiste Boussingault urged his government to add iodine to salt to prevent goitre. It took until 1920 for his suggestion to be implemented. In the early 1920s, medical researchers announced that iodine could prevent goitre, which was widespread at that time. Fortification of salt with iodine proved to be an effective strategy in decreasing goitre incidence by 74–90% in the areas surveyed. It was so successful in reducing goitre and cretinism in affected populations that it prepared the way for future fortification of foods in the United States of America in 1922.

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Between 1924 and 1944, iodine was added to salt, vitamins A and D to margarine, vitamin D to milk, and vitamins B1, B 2, niacin and iron to flour and bread. The major impetus to fortification was World War II. Both the United Kingdom and the United States governments recommended voluntary fortification of flour and bread. By 1943, the US Army purchased only fortified flour or bread. In the UK, calcium, thiamine, niacin and iron were added to bread. These countries have added iron and vitamins to flour, bread and other foodstuffs with the intent of preventing or alleviating nutritional deficiencies in their population. Current efforts include enrichment of cereal grain-based foods with folate since such fortification has been demonstrated to reduce the annual incidence of neural tube birth defects by 25% [15].

30.6

Technical considerations

Food fortification has several advantages over other interventions as it does not necessitate a change in dietary patterns of the population, delivers a significant proportion of the recommended dietary allowances for a number of micronutrients on a continuous basis and does not call for individual compliance. It could often be dovetailed into the existing food production and distribution system, and therefore, can be sustained over a long period of time. The technical considerations in food fortification include selection of appropriate food vehicles that are consumed by a sizable proportion of the population and lend themselves to centralized processing on an economical scale. The product needs to be distributed through a wide network so that it reaches all parts of the country. When there is no single universally consumed vehicle in a country, fortification of a number of foods may be considered. The choice of food vehicle depends on local availability and consumption patterns. A technical consultation by the Food and Agriculture Organization [14] agreed that, ideally, a fortified food should: ●

●

Be commonly consumed by the target population – the food vehicle selected for fortification should be commonly consumed and needs to be identified as per the region. For example, in China soya sauce was identified as the choice for fortification because of the high consumption by the target population. Similarly, in India because of varied consumption patterns, wheat flour is regarded as the ideal food vehicle in North India, while rice is considered more suitable for the southern states of India. Have a constant consumption pattern with a low risk of excess consumption – salt is a good example here since its consumption is fairly constant, varying between 7 to 10 g per person per day.

802

●

●

●

●

●

Public health nutrition in developing countries

Moreover, the unacceptable taste of additional salt prevents accidental excess consumption of the nutrients being carried through salt as the vehicle of fortification. Have good stability during storage – for example, vitamin A and D are the recommended nutrients for oil fortification because these two nutrients are fat soluble and have been demonstrated to have high stability during storage. Be relatively low in cost – commonly consumed foods like wheat flour and salt can be fortified at a very low additional cost. In India the additional cost of fortification of wheat flour with iron, folic acid and vitamin A in the state of West Bengal is approximately Rs. 1.50 (US$0.03) per beneficiary per year at a consumption profile of 100 grams per day. Be centrally processed, with minimal stratification of the fortificant – wheat that is centrally processed in large roller mills is being targeted for fortification in many developing countries. The particle size of the micronutrient premix used is close to that of wheat flour which minimizes separation or stratification of the nutrient in the flour. Have no interaction between the fortificant and the food vehicle – for double fortification of salt with iron and iodine, encapsulated form of iron is used to prevent interaction of the iron with salt as well as with iodine. Be linked to energy intake – while determining the levels of nutrients for fortification, the quantity of a specific food item consumed as well as the energy derived from the specific quantity is taken into consideration. This is essential since food intake, especially staple foods consumed by different age groups is generally proportional to their energy requirements. Taking into consideration both food and energy intakes helps in identifying the appropriate levels of micronutrients to be added to the food being fortified and ensuring that no single age group is getting either too low or too high levels of the micronutrients.

It is evident that selection of an appropriate vehicle is critical for a successful fortification programme. Staple foods and condiments are the obvious choice for fortification given their consistent consumption by large sections of the population. Commonly consumed foods used for fortification in different countries since early 1930s include wheat and corn flour, rice, oil, margarine, dairy products, salt, sugar and sauces (Table 30.3).

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803

Technology for food fortification

The actual mechanics of adding the nutrients to the food is technically simple. It involves the use of a ‘pre-mix’ containing the required nutrients in a concentrated form and adding it to the selected food during processing and ensuring proper blending of the premix with the food. Depending on the food processing technologies, different addition methods have been developed [18]. Common examples include: ●

●

●

●

●

Dry mixing for cereal flours and their products, powder milk, powder beverages Dissolution in water for liquid milk, drinks, fruit juices and in the water to be used for making bread, pastas, cookies etc. Dissolution in oil for adding lipid soluble vitamins to oily products like margarine. Spraying technique as for iodization of salt and some types of corn flakes – this process involves preparation of a solution containing the nutrients and spraying through a nozzle as the food to be fortified moves along the processing line. Adhesion as in sugar fortification where the vitamin A in powder form is adhered to the crystals surface by a vegetable oil.

Table 30.3 Food fortification in developed countries [14, 16, 17] Year of initiation

Country

Nutrients/ Vehicles

Deficiency Current status – current statusdisorders to be country policy controlled

19th to 20th century

France/ USA

Iodine in salt Control of IDD (Cretinism, mental retardation)

1918

Denmark Vitamin A in Nutritional margarine blindness

As per the current Danish food additive regulations, vitamin A is a permitted nutrient additive in margarine

1930s

USA

Vitamin D in Rickets milk

The U.S. Food and Drug Administration (FDA) standards are available for optional addition of vitamins A and D to milk. Evaporated milk must contain added vitamin D. Non-fat dry milk that is labeled “fortified with vitamins A and D” must be fortified with those vitamins.

1940s

USA

Iron and B vitamins in wheat flour

FDA has set standards of identity for both wheat flour and enriched (fortified) wheat flour. Sale of nonfortified flour is not prohibited as

Beri-beri, pellagra

Legislation in place to ensure that fortificant levels are defined and iodized and non-iodized salt are labeled

804 Year of initiation

Public health nutrition in developing countries Country

Nutrients/ Vehicles

Deficiency Current status – current statusdisorders to be country policy controlled long as the product meets the labeling requirement. Nevertheless, given consumer interest in nutrition and value enhanced products most flour currently sold for household use is enriched with B vitamins, iron and folate.

1980s

USA

Calcium in flour, dairy products and other foods

Osteoporosis Calcium fortification by the industry (largely market is allowed as an option. FDA driven) permits a health claim regarding calcium and osteoporosis on foods that contain at least 20 percent of the reference daily intake (RDI)

1998

USA

Folic acid in Neural tube wheat flour defects

FDA mandates that all enriched (fortified) wheat flour contains folic acid

The technology of food fortification therefore involves careful consideration regarding selection of appropriate food vehicle and nutrients, levels of fortification, safety index, feasibility and sensory acceptability, bio-availability, storage and stability, methods of blending, efficacy and, last but not the least, the cost [19].

30.8

Fortificants

Clearer understanding of the interaction of fortificants with other dietary factors needs to be achieved if one is to optimize fortification programs. In cases where there is more than one demonstrated micronutrient deficiency in a target population, addition of more than one micronutrient to a single vehicle (multiple fortification) could be advantageous. With the expanding range of fortificant compounds available, and the need to use various food vehicles according to the designated target groups, it is important to consider the technologies best suited to achieve a fortified product with the desired properties. In many cases identification of suitable vehicles is made difficult due to absence of reliable information on dietary habits of the target population. Fortificants must meet quality criteria specifications explicitly established for each application. Selection of an appropriate vehicle is a critical step in successful fortification to ensure stability, appearance, bioavailability and homogeneity. It is essential to undertake field testing of fortified food at several locations in the country in differing environmental conditions. This is important for understanding problems potentiated by scaling up production activities from pilot to industrial

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scale. The various fortificants and food vehicles which are commonly in use are presented below: (a) Iodine – Salt is the most suitable vehicle for iodine fortification. Two chemical forms of iodine are currently used for iodization; these are iodates and iodides. The Codex Alimentarius standard for food grade salt [20] permits the use of both the sodium and potassium salts of iodides and iodates in the iodization of salt. According to international recommendations, the iodine concentration in salt at the point of production should be within the range of 20–40 mg of iodine per kg of salt (i.e. 20–40 ppm of iodine). Considering iodine losses from production site to households, adequately iodized salt at household level is recommended to contain 15 ppm of iodine [21]. The levels for iodization are, however, established by national authorities in light of the prevailing iodine deficiency. For example, Europe-wide uniform minimum and maximum levels (20 and 40 mg/kg salt) is adopted by all EU member states. The two forms of iodine also need to be harmonized in terms of equivalence to avoid trade barriers. There are four major technologies that are used for addition of iodine to salt—dry mixing, drip feed addition, spray mixing and submersion. Program monitoring is important to ensure access to population of adequately iodised salt for elimination of iodine deficiency. Moreover, proper monitoring is critical for avoiding sporadic reports of thyrotoxicosis [22]. Prevalence of such side effect can be reduced by close monitoring of iodine levels in salt which can be adjusted based on monitoring of human urinary iodine excretion. (b) Iron – Cereals are the most widely used vehicles for iron fortification although many others, such as milk products, sugar, curry powder, soya sauce, salt and cookies have been successfully used. Ferrous sulphate, Ferrous fumarate, elemental iron (particularly electrolytic form) and Sodium Iron Ethylene Diamine Tetra Acetate (NaFeEDTA) are examples of preferred iron fortificants. Selection of the iron fortificant is dependent on the food vehicle. The color of iron compounds is often a critical factor when fortifying lightly colored foods. The use of more soluble iron compounds (e.g. Ferrous sulphate) often leads to the development of offcolors and off-flavors due to reactions with other components of the food material, but they have the advantage of being highly bioavailable (Table 30.4). Vitamin C is known to increase the bioavailability of nonheme iron forms (iron from plant foods). In some countries bovine hemoglobin concentrate, which has an exceptionally high bioavailability, is being used as a heme-iron fortificant in local feeding programs. The presence of phytates, polyphenols and calcium are known to adversely affect the bioavailability of non-heme iron fortificants. Increasing evidence indicates that in such cases sodium iron-EDTA may prove to be a better choice of fortificant in the future as iron from the EDTA-complex

806

Public health nutrition in developing countries

remains bioavailable even in the presence of iron absorption inhibitors. Given the wide variability of iron bioavailability, influenced by physical and chemical properties of the fortificant as well as the presence of substances which either inhibit or improve iron absorption, there is a need to develop convenient models for the evaluation of iron bioavailability. This is particularly important as an increasing range of iron fortificants with different physico-chemical properties, is being developed and marketed. It is also essential that surveillance data of iron status is interpreted with caution because of the known alteration of serum ferritin levels and other indicators of iron status in the presence of recent infection. Furthermore, it must be recognised that not all anemia is due to iron deficiency, although the latter is most common. Several aspects of the interaction between iron and other nutrients, such as vitamin A, iodine, zinc and calcium, need to be investigated in relation to the possibility of multiple fortification. The stability and the cost of fortificant compounds as well as the bioavailability of the nutrients need to be considered. (c) Vitamin A – Foods which have been successfully fortified with vitamin A include margarine, fats and oils, milk, sugar, breakfast cereals, and instant noodles with spice mix. Moisture contents in excess of about 7–8% in a food are known to adversely affect the stability of vitamin A. Beyond the critical moisture content there is a rapid increase in water activity which permits various deteriorative reactions to occur. Vitamin A is also shown to be very sensitive to light exposure and repeated heating, as may be experienced with vegetable oils used for frying, is known to significantly degrade vitamin A. Retinol palmitate (also called as vitamin A palmitate) is the frequently used form of vitamin A for fortification. Carotenoids can also be used as a source of vitamin A but its conversion and bioavailability is known to be affected by the vitamin A status of the individual and by dietary composition. A conversion factor of 6:1 (six milligrams of beta carotene equivalent to one milligram of retinol) is currently being applied in calculating intake [26], though a recent recommendation by US Institute of Medicine suggest a conversion of 12:1 [27]. The cost factor in using carotenoids as the source of vitamin A activity in fortification is generally considered prohibitive. (d) Vitamin D – There are a limited number of food vehicles suitable for vitamin D fortification. These include margarine, vegetable oils and dairy products. Vitamin D metabolism is linked to calcium absorption and parathyroid hormone. Susceptible populations for marginal vitamin D status include children under three years of age, the elderly and any population where cultural practices or climatic conditions prevent exposure to sunlight. It is very important that a reliable, accurate, simple and rapid methodology

NaFeEDTA

Chelated iron compounds

Slight risk of colour changes

(a) Colour changes (b) Fat oxidation (c) Metallic taste (d) Precipitation

Undesirable characteristics

Fat oxidation Unwanted color reaction 2–3 times better absorbed than Low absorption FeSO4 from high phytate meals

Ferrous orthophosphate No colour change Ferric ammonium No flavour change orthophosphate Ferric pyrophosphate Elemental iron powders (Electrolytic carbonyl reduced and H-reduced)

Water insoluble/ poorly soluble in dilute acid

Ferrous Sulphate Water solubility

Freely water soluble Ferrous Gluconate Ferrous Ammonium citrate

Ferrous fumarate Ferrous succinate Ferrous saccharate

Desirable characteristics

Iron salts

Soluble in dilute acid

Groups

Table 30.4 Characteristics of iron salts commonly used to fortify foods [23–25]

Man

High extraction flours Infant cereals

Wheat flour Infant cereals Powdered drinks Breakfast cereals

more than 100

25–32 45–58 21–74 – 5–100

Infant 100 cereals, salt 92 Maize flour 74 Powdered drinks

No data available

4.0 times Same Same – –

Same Same Same

Same Same 12.9 times

Vitamin C

Average relative bioavailability (%)

cereal flours 100 Infant 89 formulas –

Uses

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808

Public health nutrition in developing countries

for the assessment of vitamin D status is carried out linked to the process of fortification. Without such assessment, it is difficult to make required adjustments to fortification practices based on feedback from comprehensive monitoring of the impact of fortification on vitamin D status. (e) Vitamin E – Vitamin E, as tocopherol acetate, is added to fats and oils including margarine and fat spreads and breakfast cereals. Vitamin E intake is known to be related to the total dietary intake of fat and it has been shown to enhance absorption and bio-conversion of dietary carotenoids to vitamin A. Emerging evidence indicates that daily intake of vitamin E greater than 30 IU may afford protection against the development of degenerative diseases. Optimal levels of fortification of vitamin E should be reassessed based on such scientific evidence. (f) Vitamin C – There are technologies available for vitamin C fortification of fruit juices, fruit juice drinks, other related beverages, dairy products and some breakfast cereals. High moisture content (greater than 7%) in the presence of oxygen is known to adversely affect the stability of vitamin C in cereals. There is a need to develop more stable vitamin C compounds and evaluate their use in the fortification of a range of vehicles. There is much ongoing investigation on the role of vitamin C in the prevention of anemia, chronic diseases such as cardiovascular disease, cancer and cataracts. Based on the outcome of such research it may be desirable to revise fortification practices for this vitamin. (g) B-Complex vitamins – There are not many problems related to the technology of the addition of B vitamins to cereals and grains. The development of off-flavors due to the thermal instability of thiamine is easily circumvented by adding this vitamin following all heat treatments. The status of B complex vitamins is known to be marginal in populations with low consumption of animal foods (milk, meat, liver) and/or those which use low extraction (highly refined) products of cereals and grains such as flour as well as in populations in transition from rural to urban settlements [28]. Food fortification with B complex vitamins may be appropriate for such populations. The development of improved methodologies for the evaluation of B-vitamin status would be a valuable tool in establishing the need for fortification in target populations and in the monitoring of these programs. A confirmed association between dietary folic acid intake and neural tube defects has been reported. Based on this finding, addition of folic acid to wheat flour has been mandated in several countries [29]. Populations with marginal or low folic acid intake may therefore benefit from fortification of staples with folic acid. Furthermore, folic acid together with vitamin B6 and vitamin B12 has been reported to decrease plasma homocysteine levels; the latter is reported to be inversely

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associated with the development of ischemic heart disease [30]. Further investigation of these relationships is relevant to the evaluation of the adequacy of current fortification practices.

30.9

Planning food fortification intervention

Planning of food fortification begins by identifying the commonly eaten foods that can act as vehicles for one or more micronutrients. Food fortification aims to provide meaningful levels of the nutrient (usually 30% to 50% of the daily adult requirements) at normal consumption pattern of the selected food vehicle. The levels also need to take into account variations in food consumption by different age groups so that the safety of those at the higher end of the scale and impact for those at the lower end are ensured [31]. Ensuring an effective fortification program involves several components and stages that can be considered as part of a “food fortification cycle” (Figure 30.2). The sections of the cycle include: (a) Situation analysis – Collect, review and analyze a range of information related to the problem of vitamin–mineral deficiencies and food vehicles with potential for fortification. (b) Determining feasibility – Explore and confirm technical and economic feasibility of food fortification. The feasibility of any fortification program needs to be ascertained once its efficacy is established, as many a times an extremely efficacious program may not be feasible for implementation or scaling up. Similarly, identifying a feasible vehicle for fortification is equally important for the program to become successful. (c) Enabling partnerships – Bring together a variety of sectors and organizations (most important the food industry and government) to pursue the common goal of reducing vitamin mineral deficiencies through food fortification. Success of partnership building in a fortification program has been depicted in details under wheat flour fortification. (d) Implementing program – Developing an implementation plan with criteria and guidelines; identifying resource inputs; designing the support measures including advocacy and communications, ensuring that legislation is in place, steps to be followed towards formulating standards, ensuring regulation and assuring quality. (e) Monitoring and evaluation – Collect, analyze and interpret data (quantitative and qualitative) and use of the information to identify problems for correction, or to help sustain successful activities. Monitoring and evaluation leads to re-assessment of the situation for further refinement of the program and so the cycle goes on. The cycle could be conceived as a sequential process where the development of one phase follows the

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previous stage. However, the different stages in the cycle are not necessarily sequential and often overlap. Also, it may not always be necessary to start at the beginning of the first phase and each phase may be of varying duration and timing.

30.2 The Food Fortification Cycle.

30.10 Global experiences with food fortification Food fortification has played a major positive role in the health of the populations in several developed and developing countries over the last 70 years. As a result many nutritional deficiencies have been eliminated. More than 25 countries worldwide currently have mandatory fortification while several other countries practice voluntary food fortification. Food fortification in the US was started with salt iodization in Michigan in 1922. In the 1930s and 1940s USA adopted fortification of flour and bread with niacin followed by multiple nutrients including iron. Flour fortification has been instrumental in reducing deaths attributed to pellagra, a condition caused due to niacin deficiency (Figure 30.3) [32]. The current low levels of iron deficiency in the USA are attributable to the wide consumption of fortified foods. Similarly, in Canada, flour fortification with B vitamins began in Newfoundland in 1944. Within four years, deficiencies reduced from 20% to negligible levels. The introduction of mandatory folic acid fortification of cereal-grain products after 1998 in the USA, Canada and Chile has resulted in 30 to 70% reduction of neural tube defects in newborns. It has been documented that even the voluntary fortification of foods, especially breakfast cereals, has contributed to the improvement in micronutrient intakes in many of the developed countries including France, Ireland, the United Kingdom and Spain [33]. The evidence from developed countries suggests that where the food industry is mature with effective quality assurance procedures and where

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commercially processed foods are widely consumed, fortification has played an important role in combating micronutrient malnutrition.

30.3 Deaths from niacin deficiency in United States [32].

In the developing world also, there has been a rapid growth in fortifying a wide range of foods during the last two decades. The most successful global fortification experience is the fortification of salt with iodine. As of 2006 nearly two thirds of the salt consumed in the developing world is being iodized, protecting nearly 70 million newborns each year from the threat of mental impairment and other sub-clinical deficiency disorders [34]. Fortification of staple foods such as flour, oils, sugar, condiments, dairy products and a range of processed foods with micronutrients is also growing [35]. A successful program in Venezuela, started in 1993, enriched precooked corn flour with iron (50 mg), vitamin A (9500 IU), thiamine (3.1 mg), niacin (51 mg) and riboflavin (2.5 mg) per kilogram. The

30.4 Anemia and iron deficiency in Venezuela after fortification. * Fortification of precooked maize flour with iron (50 mg), vitamin A (9500 IU), thiamine (3.1 mg), niacin (51 mg) and riboflavin (2.5 mg) per kilogram

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Public health nutrition in developing countries

prevalence of iron deficiency in school children dropped from 37 to 16% in just two years after the implementation of fortification program (Figure 30.4) [36]. Currently nineteen countries in Latin America and Caribbean have a national food fortification program in which iron and other micronutrients are added to at least one widely consumed food which is often wheat and/or corn flour. In the Middle East and North Africa several countries introduced fortification with iron and folic acid to cereal flour. A program review by the Micronutrient Initiative (MI) in 2006 reported that while prior to 1998 only one country (Saudi Arabia) was fortifying flour, by 2005 a total of 13 countries in the region produced and consumed fortified flour containing at least iron and folic acid (in some instances vitamin A and other B complex vitamins also) on a national or sub-national scale - reaching more than 81 million consumers [37]. There is also growing interest and action on wheat flour fortification in Asia. Flour fortification at the national level is under implementation in Indonesia, Philippines, Pakistan and Nepal while several states in India have initiated or are planning to introduce it. The status of flour fortification in various countries across the world, along with the fortificants being used is presented in Table 30.5 [38]. It has also been demonstrated that choosing a food vehicle that is very specific to the country but consumed by large segments of the population could be effective. For example, soy and fish sauces fortified with iron are emerging as a major vehicle in China, Vietnam and Thailand because more than 80% of the population consumes these sauces regularly with a network of sauce factories operating under government supervision. Table 30.5 Fortification of staple food Staple cereal Maize Rice Wheat

No of countries

Primary micronutrients

9

Thiamin, riboflavin, folic acid, niacin, zinc, iron. At some places calcium, vitamin B12, vitamin B6 and vitamin a were also added

2

Thiamin, riboflavin, folic acid, niacin, zinc, iron

78

Thiamin, riboflavin, folic acid, niacin, zinc, iron. At some places calcium, vitamin B12, vitamin B6 and vitamin a were also added

The World Food Program (WFP) which provides food to displaced populations and in emergency situations has a long history of distributing fortified foods procured from industrialized countries. More recently the WFP is moving towards on-site milling and fortification of locally produced grains. WFP has established a capacity to produce fortified blended foods in 13 of the world’s poorest countries including Nepal, Madagascar, Ethiopia and Malawi.

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A national program to provide fortified milk to infants up to 18 months of age has helped reduce anemia in Chilean infants from 21% to around 1%. Fortified complementary foods provided through public feeding programs and commercial channels in Mexico, Ecuador and Chile had significant health and developmental impacts on children. In a number of situations where fortified foods are not accessible to children between 6 months to two years of age, multiple ways to deliver micronutrients to this age group has been experimented to enable mothers to either add them into the cooking pot or to mix them into the food they feed their infants. Such efforts have been successful in Bolivia, Guatemala, Sudan and Kenya as well as in several other countries. This approach is referred to as “Home Fortification” [39].

30.11 Food fortification in a developing country— experiences from India To translate the National Nutrition Policy [40, 13] adopted by Government of India in 1993, into forceful, viable and sustained efforts, the National Plan of Action on Nutrition [ 41], was released by Government of India in 1995, which recommended a combination of interventions such as promotion of dietary diversification, nutrient supplementation, food fortification and public health measures to be implemented. The Department of Women and Child Development, Ministry of Human Resource Development, India along with the United Nations World Food Program in 2000, prepared a white paper on prevention of micronutrient malnutrition through the national programme of Integrated Child Development Services or ICDS [42]. The strategies for overcoming micronutrient malnutrition as mentioned in the white paper are as follows: ● ● ● ● ●

Dietary diversification through behavior modification Fortification of foods with nutrients Horticulture interventions for adequate supply of nutrient rich foods Supplementation with specific micronutrients Sensitization of policy on issues related to prevention of micronutrient malnutrition

Government of India policy and the plan accepts food fortification as one of the most effective food based approach to address micronutrient deficiencies. The focus in planning a fortification program takes into consideration the fact that the prevention of malnutrition must address the problem at various stages of the life cycle. In developing countries like India, many of the staple foods are processed at the community level and

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Public health nutrition in developing countries

they are often consumed in the areas where they are grown. However, the consumption of centrally processed foods is steadily increasing. Moreover, it is recognised that in situations like this where there is no single universally consumed and centrally processed food, fortification of a number of foods needs to be considered. The choice of the food vehicle depends on local availability and consumption patterns. In view of the diverse food consumption patterns and food processing situation in India, it is obvious that a single approach is not the answer. With the expanding range of fortificant compounds available and the need to use a combination of vehicles, it is essential to consider the technologies that are best suited to achieve a fortified product with the desired properties. In India food fortification has evolved over the past few decades through a number of trials which has resulted in the availability of several fortified foods and also led to increased interest in future potential for further expansion.

30.11.1 Initial efforts of food fortification in India Initial efforts on food fortification in India were focused on improving the protein and energy levels of the diet and gradually progressed to fortification with vitamins and minerals. Fortification of tapioca flour with a high protein source like edible peanut flour and blending of 75 per cent edible peanut flour with 25 per cent of Bengal gram (Cicer arietinum) to produce Indian Multi-purpose Food (IMPF) were successfully tried at the Central Food Technological Research Institute (CFTRI) as early as 1950s [43, 44]. Though these products had significant nutritive value and established consumer acceptance, they were neither widely marketed through commercial channels nor promoted through government programs [45]. On the other hand, fortification of whole wheat flour (atta) with edible peanut flour introduced problems of consumer acceptability as confirmed by studies by the Protein Foods and Nutritional Development Association of India. Fortification of bread with lysine, vitamins and minerals tried by Modern Bakeries, a public sector organization of the Government of India showed significant improvement in the weight and height of children [46]. Elwood et al [47], using labeled iron in chapati , reported poor absorption of both iron in the wheat and from the iron salt used for fortification. Based on this finding, it was stressed that there was a need to discover or develop an iron salt that can be added to flour in relatively high concentration without adverse impact on the keeping quality or baking quality of wheat. Fortification of salt (with iron), consumed by all groups irrespective of age, economic status, and rural or urban setting was taken up by the Food and Nutrition Board of the Government of India in collaboration with the National Institute of Nutrition (NIN), wherein

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parameters like bio-availability, storage, and utilization of iron in Indian culinary practices were studied [48]. Fortification with iron of other foods like sugar [49] and tea [50] were also tried out.

30.11.2 Fortification of industrially processed foods Many processed foods, infant foods and weaning foods (complementary feeding foods), manufactured by multinational companies are currently being fortified with vitamins, calcium, and iron, and in some cases with amino acids as per the specifications of the Indian Standards Institution (ISI) [51], with labels presenting specific amount of vitamins that a child of six months would derive from these foods in a normal day in comparison with his/her actual nutrient requirements. The micronutrient content in well known commercial baby foods shown in Table 30.6 indicates that all of the formulations are fortified with one or more essential vitamins and minerals. The level of micronutrients consumed through the baby foods is at least 100% of the child’s actual requirement, many times more than the requirement (Table 30.7 and 30.8). Table 30.6 Micronutrient levels in samples of commercial baby foods (per 100 g) Nutrients

Amul

Calories 450 Calcium (mg) 1.0 Iron (mg) 4.0 Vitamin A (IU) 1,500 Vitamin D (IU) 400 Vitamin B1 (mg) 0.6 1.0 Vitamin B2 (mg) Vitamin B6 (mg) 0.3 Vitamin B12 (ng) – Folic acid (ng) – Niacinamide (mg) 6.0 Calcium pantothenate (mg) – Vitamin E (ng) – Vitamin C (mg) 30

Glaxo spray

Lactogen

Sapan

Bal amul

574 – 4.0 1,500 400 – – – – – – – – –

474 – 4.0 1,500 400 0.4 0.6 1.0 2.0 – 6.0 – – 40

454 1.0 4.0 1,500 500 0.6 1.0 0.3 1.2 – 6.0 – – 40

391 1.0 6.0 1,500 300 0.5 0.6 – – – 5.0 – – 50

Farex Nestum 375 366 0.75 0.69 20 0 15.6 – 1,875 300 500 – 0.6 – 0.7 – 0.4 – – – 25 – 6.0 – 4.6 – 6.0 – 45

Another industrially processed food which is being fortified is hydrogenated vegetable fat – referred as vanaspati in India. It is mandatory for vanaspati to be fortified with 25 International unit (IU) of vitamin A per gram (4% RDA). There has been substantial decrease in consumption of vanaspati in the pasty two decades and it is estimated that the consumption this type of fat is as low as 0.3 to 1.1 g/day/person. On the other hand, since 1993–94 the per capita consumption of edible oil has risen over a period of eleven years by as much as 30% in rural India and

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Public health nutrition in developing countries

about 18% in urban India. In both rural and urban India, per capita consumption of oil other than groundnut oil, mustard oil, vanaspati and coconut oil has more than doubled. The oil varieties which have increased remarkably include sunflower oil, soyabean oil, other vegetable oil and rice bran oil. Fortification of oil, rather than any vanaspati is therefore considered important. There is however no mandatory fortification for any of these oils [52]. Table 30.7 Vitamin and mineral intake of children—fortified commercial baby foods compared to actual requirements

Vitamin A (IU) Vitamin D (IU) Vitamin B1 (mg) Vitamin B2 (mg) Vitamin B6 (mg) Niacinamide (mg) Calcium (mg) Iron (mg)

Intake/day

Requirement

Percentage requirement

2,430 590 0.91 1.39 0.62 9.14 1.62 7.64

1,333 200 0.6 0.8 – 8.0 0.4 7.0

182. 3 295. 0 151.7 173.8 – 114.2 405.0 109.0

Table 30.8 Suggested fortification of commercial baby foods Recommended dietary intake of a child of six months Calories

708

Vitamin A (IU) 1,333 Vitamin D (IU) 200 Vitamin C (mg) 20 Thiamine (mg) 0.35 Riboflavin (mg) 0.43 Niacinamide (mg) 4.68 Pyridoxine (mg) 0.3 Folic acid (ng) 25.0 Vitamin B12 (ng) 0.2 Iron (mg) 6.0

Fortification of baby foods as at present per 100 g

450 (as at present) 1,500 400 30 0.6 1.0 6.0 0.3 – – 4.0

Fortification Percentage ISI on calorie basis of excess standards (plus 10% extra) fortification per 100 g 450 938 140 14 0.25 0.30 3.29 0.21 17.6 0.14 4.2

– 160 286 214 240 334 182 142 – – –

– 1,500 200–300 30 0.5 10 5.0 0.3 50.0 1.0 4.0

Other products like fortified breakfast cereals, noodles, milk, edible oils, fruit juices, breads, biscuits etc. are also flooding the Indian markets. However, most of these products are out of reach of the poor. The need for developing fortified products which are affordable, acceptable, scalable and sustainable is recognised. Moreover, it is also appreciated that a system needs to be introduced to ensure sustainability of these products to reach the entire population.

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30.11.3 Fortification of food supplied under the government supported programmes In India, several public programs such as the Integrated Child Development Services (ICDS), Mid Day Meal (MDM) and Targeted Public Distribution System (TPDS) provide supplementary food to various age groups. ICDS has a life cycle approach of reaching children 6 months to 6 years of age, as well as adolescent girls and pregnant and lactating mothers. Too often they meet only the macro level requirements of energy and protein and do not address micronutrient deficiencies sufficiently. However, the Ministry of Human Resource Development, Dept of Women and Child Development, Government of India wide their circular No. 5-17/2004ND/Tech.FF dt. 12 July, 2005, issued a notification to all the State Governments to fortify the supplementary nutrition component with multiple micronutrients providing 50% of RDA of selected nutrients to the children and women beneficiaries, as presented in Table 30.9 below. Table 30.9 Micronutrient levels in ICDS as per the Government of India guidelines Micronutrients

Per child per day

Iron Vitamin A Folic acid Iodine Zinc Thiamin Riboflavin Ascorbic acid Calcium

15 mg 400 μg 35 μg 100 μg 10 mg 0.8 mg 0.8 mg 40 mg 400 mg

Recently with efforts by Government of India and several State Governments and support from various international agencies, like WFP, CARE, MI and GAIN, fortified supplementary foods are being distributed through these public programs with encouraging results. Some of the success stories are highlighted below: (i) Point of use fortification of ICDS supplementary cooked food “Point of Use Fortification” is a term used to include both home fortification as well as fortification at the point of institutional or large cooking. In West Bengal, India, such point of use fortification is undertaken through the large Integrated Child Development Services (ICDS) programme. A local food item Khichdi (rice, lentils and oil mixture cooked to a soft semi-solid consistency), a supplementary food distributed through ICDS, is fortified with a multiple micronutrient premix “vita shakti” which

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provides 500 IU of vitamin A, 14mg of microencapsulated iron (ferrous fumarate) and 0.05mg folic acid per day. Initially in 2006, fortified food reached 4.8 million beneficiaries .The strategy being cost-effective was scaled up by the State Government of West Bengal at their own cost (additional cost of fortification being Rs.9/- per annum) in the year 2006-07. This concept of addition of micronutrient mix such as “vita shakti” has been adopted in Africa where “Rahama” is added to food at home to overcome micronutrient deficiency problems among population. The fortificant ‘vita shakti’ is in the form of a powder and is recommended to be added to the prepared khichdi at the level of 0.25 mg at the ICDS village centre (referred as Anganwadi center or AWC ) using a measured spoon, calibrated to serve five beneficiaries. The addition of ‘vita shakti’, the MI produced fortified premix, to the ICDS khichdi program is unique as it is community based with the micronutrient premix added at the child centre of ICDS (AWC) level. Fortification at the community level is advantageous as it instills ownership of the fortification program in the village community and demystifies the fortification process to local mothers, while ensuring that the fortified food is consumed at the proper levels by the targeted population. Community based programs also have the added benefit of using locally produced and consumed food vehicle which increases the acceptability, sustainability, and adherence to the fortification program. The findings of the khichdi fortification programme revealed that the strategy was feasible and the product was acceptable as was indicated by the high program compliance by both ICDS workers who prepared the fortified Khichdi and by the enrolled children, who consumed it. Monitoring records showed no problems with the storage and preparation of the Khichdi at the Anganwadi center. In focus group discussions, ICDS workers reported no problems with the addition of the premix to the cooked Khichdi. A study was undertaken on children in the Fortified Khichdi (FK) and Non Fortified Group(NFK) group .The study showed that Khichdi fortified with a microencapsulated ferrous fumarate and vitamin A premix was efficacious in improving iron status (Fig. 30.5 and reducing the prevalence of anemia, iron deficiency (ID) and iron deficiency Anemia (IDA) in preschool aged children in West Bengal. The premix was also efficacious in increasing the serum retinol (SR) concentration of females in the targeted population [53]. The significant change in hemoglobin (Hb) concentration in children who received the fortified Khichdi (FK) was evident. (Fig. 30.6). Over a period of six months, the incidence of anemia was reduced from 19.1% in the FK at week 0 to 4.1% at week 24 against 32.6% in NFK at week 0 to 20.7% for week 24. Of the children in the FK who were still anemic after 24 weeks of intervention, 50% had hemoglobin concentration of 109.5g/L

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which further showed the ability of the fortified Khichdi to remove preschool aged children from an anemic state and maintain their nutrient stores at a sufficient level.

30.5 Prevalence (%) iron deficiency for NFK and FK at 0 and 24 weeks.

Prevalence of iron deficiency Anemia was low in both FK and NFK at baseline, but the provision of fortified Khichdi almost eliminated IDA during the 6 month intervention (4.9% to 0.4%) while there was very little change in the prevalence of iron deficiency anemia (IDA) in children in NFK (9.6% to 9.3%). The fortified Khichdi was very effective in increasing ferritin level (Fig. 30.7) and in eliminating IDA in the target population during the relatively short intervention time.

30.6 Prevalence (%) iron deficiency anemia in children consuming for NFK and FK at 0 and 24 weeks.

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30.7 Serum ferritin concentration in anemic NFK and FK at 0 and 24 weeks .

Serum Retinol increased in both FK and NFK during the 6 month intervention (Fig. 30.8) Serum retinol concentration was significantly different at baseline between the fortified (1.098 ±0.437) and NFK (1.226±0.505). (ii) Fortifification of factory produced Ready-to-Eat (RTE) foods Fortification of RTE food has been reported to be cost-effective strategy. RTE food , supplied as supplementary food in the ICDS programme, is produced at factory level using wheat and chick pea flour. RTE product which reached 0.35 million beneficiaries in four districts of Gujarat State was fortified with 50% of RDA levels of iron, vitamin A and folic acid.

30.8 Serum retinol concentration in NFK and FK at 0 and 24 weeks.

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Unlike ‘vita shakti’, the product was centrally fortified at production level. The impact assessment on the nutritional status of the beneficiaries consuming fortified ready-to-eat food showed a significant reduction in the prevalence of micronutrient deficiencies. In children the prevalence of vitamin A deficiency (serum retinol <0.7 μmol/1) decreased from 33% to 9% in the intervention district as compared to the control district. The prevalence of night blindness in children decreased from 2.0% to 0.1% in the intervention district (Panchmahal), and from 0.9% to 0.7% in the control district (Vadodra). There was no significant change in the anemia prevalence in children in intervention and control areas at endline—anemia in women decreased from 83% to 73.5% in the intervention district, whereas the anemia prevalence in the control area remained more or less the same [54]. The reason for non-response in children was attributed to possible prevalence of worm infestation and other infections contributing to anemia which were not addressed. Following the initial trials, the project was scaled up to reach fortified complementary food distribution state wide in the state of Gujarat for under 3 year children. (iii) Fortification of food for the school feeding programme Improving the health and nutritional status of school-age children is important for improving school concentration, productivity and school performance. A good example of school feeding programme is the provision of supplementary food under the National Program of Nutritional Support for Primary Education, popularly called the MidDay Meal Scheme (MDM). The National Advisory Council of India (28 th August 2004) recommended that “From 1 July 2005, all mid-day meal schemes should include a component of “micronutrient supplementation”, covering essential micronutrients such as Vitamin A, iron and iodine. Central assistance should be available for this component of the midday meal schemes and the necessary financial allocations should be made in the 2005-6 budget.” MDM program has recently begun to focus on a cooked food supplementation provided to school children five days a week, with a specified menu for each day of the week. Recipes prepared from rice / wheat, vegetable / dal are prepared for MDM and provide 450 calories and 12 grams of protein per day. The cooked food often lacked adequate micronutrient. In the State of Uttaranchal [55], a multiple micronutrient premix “Sampoorna” having 14 different micronutrients developed by WFP was used to fortify the mid day meal in all the schools in Tehri district. The premix was added at the rate of 0.25 g per child per day. Micronutrient levels provided per 0.25 g is presented below (Table 30.10).

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Public health nutrition in developing countries Table 30.10 Pre-mix composition per 0.25 g Vitamin A Vitamin D Vitamin E Vitamin C Vitamin B1 Vitamin B2 Vitamin B3 Vitamin B6 Vitamin B12 Folic Acid Iron Zinc Copper Iodine

(Sampoorna) 375 3.75 5.25 26.25 0.68 0.68 9 0.75 1.35 225 10 4.2 0.45 90

µg µg mg mg mg mg mg mg µg µg mg mg mg µg

A cross-sectional randomized controlled study assessed the social acceptability of micronutrient fortified lunch meals cooked at schools. Subjects were randomly assigned to treatment and control groups. The treatment group consumed a weighed amount of cooked lunch meals fortified with locally produced multi-micronutrient premix and the control group consumed a weighed amount of the same meals but without added micronutrient premix. After having eaten, subjects were asked to rate, on a 3-point Likert scale using “smiley” faces, the pleasantness of smell, taste, and overall satisfaction with the food. The mean age of study children was 7.96 ± 1.64 y. The average amounts of food consumed by the treatment and control groups were 345 ± 114 and 360 ± 102.4 g, respectively. Addition of the multi-micronutrient premix to school meals did not significantly affect the mean amount of food consumed by the schoolchildren (P > 0.05; independent sample t-test). No significant differences were seen between treatment and control groups in terms of ratings for taste, smell, and the general acceptance of the micronutrient fortified or the unfortified school meals. In conclusion, the addition of a multiple micronutrient premix to school meals was well liked by schoolchildren and did not adversely affect their food consumption [56]. The study showed that, micronutrient fortification of cooked school meals by trained school authorities was effective in improving vitamin A, folate, iron and vitamin B12 status of school children. The results are encouraging since such addition of micronutrient premix to meals at the school has advantages of being locally acceptable, sustainable and has low implementation cost since it is built on the already existing government school feeding program. However, for adoption of this fortification strategy in other regions may require adjustment to the micronutrient levels in the premix based on the micronutrient status and/

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or consumption profile of the population in context, to avoid excessive intake of the vitamins and minerals. There is also the need for careful post fortification monitoring to ensure safety and potential effectiveness for the target populations. (iv) Fortification of wheat flour supplied through Targeted Public Distribution System (TPDS) The Planning Commission of India in its 10th Five Year Plan document has recommended ‘food fortification’ as an important strategy for prevention and control of micronutrient deficiencies. Iron fortification of wheat flour (locally referred as atta ) is specifically referred in the Planning Commission document. A pilot project was implemented to test the operational effectiveness of fortified wheat flour in improving the iron and vitamin A status of the population in West Bengal (the Sadar subdivision of Darjeeling district) in India [54]. In this area, the government distributes high extraction wheat flour (atta), 200 g/person/day to about 0.6 million beneficiaries below poverty line through the TPDS. Distribution of 200 g of wheat flour fortified with iron, folic acid and vitamin A, as per the composition of pre mix and wheat flour (Table 30.11) was undertaken through the public distribution system to four different target groups viz. pregnant and lactating women, pre school children, school age children and adolescent girls in the population. A ‘Pre-post analysis’ with two crosssectional surveys at baseline and 18 months after intervention was conducted . Kalimpong served as the control area for the same. Table 30.11 Composition of pre-mix and fortified wheat flour Micronutrient

Per 200 g of pre-mix

Per Kg of wheat flour

ICMR RDI

Per 200 g of wheat flour

Vit A Folic Acid Iron

3.33 IU 1.5 g 60 g

3300 IU 1.5 mg 60 mg

2000 IU 100 μg 30 mg

660 IU 300 μg 12 mg

IEC (Information, education and communications) was undertaken to inform community of the benefits of the fortified product and for creating demand. Emphasis was on their benefits, consequences of deficiencies and significance of using the fortified atta. A workshop for the millers and PDS shop owners was organized. Additional teaching aids like wall writings, tableaux, posters, leaflets, danglers and street plays in the local language were also used for IEC activities. From the endline survey conducted after 24 months of intervention, a significant reduction in anemia prevalence was observed in all the target groups in the intervention area (Figure 30.9).

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30.9 Impact of fortified wheat flour* on prevalence of anemia. * Wheat flour fortification details presented in Table 30.11

Though the quantity of flour distributed in the PDS is same for all age groups, the differences in the impact could be attributed to the consumption profile and needs in the respective physiological conditions. Process evaluation during the period of the study also revealed that there was no technical difficulty faced by the miller. Also, it was found that fortified wheat flour was acceptable to the population in terms of appearance, taste or storage quality of the flour. As the cost of fortification was nominal, (an additional 6 to 10 paise, one fifth of one US cent, per kg of fortified atta) which in fact is less than the seasonal fluctuation that occurs with wheat price, therefore it was not passed on to the consumer. However, the process did require one time investment by the miller towards installation and commissioning of a micro feeder to deliver the premix at a fixed flow rate, costing approximately INR 70,000/-(about US $ 1750), provided that the miller has all other infrastructure needed for wheat milling in place. Based on the positive outcome, the fortification programme was scaled up in the entire state of West Bengal. By 2009, the fortified atta (called Enriched Atta) was being sold in the PDS outlets in 750 g poly pack bags at a cost of Rs 5/- which in fact is now being passed on to the consumer thereby demonstrating a sustainable, successful collaboration of the government and industry. As a result of the success in one West Bengal, the supply of fortified wheat flour through the Public Distribution System has been introduced in many other states of the country such as Andhra Pradesh and Gujarat. The Roller Flour Millers Association of Gujarat has played an active role and have also launched a flour fortification program through the open market route [57]. Unlike in West Bengal, the premix formulation being used in Gujarat, as per the international recommendation, consists of two nutrients – ferrous sulphate 30ppm and folic acid 1.5 ppm i.e. (30mg of

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iron and 150μg of folic acid per kg of atta), [58]. The Government ensured political commitment at the highest level and also created an enabling environment to the millers by lending a logo, which helped in creating demand among the population. Recognizing, wheat milling is commonly done at local village level using traditional hand milling technique or chakkies, a small scale chakki fortification programme was experimented in Sundernagar district of Gujarat. Small sachets containing 1.5 g of premix (equivalent to international recommendations of 30mg of iron and 150 μg of folic acid per kg of atta) have been developed with instructions of adding and mixing the contents to 10 kg of flour. Pioneering efforts in food fortification by the state government of Gujarat of about two years has resulted in overcoming the initial resistance and convincing the industry partners including roller flour millers, organized chakki operators and small chakki owners for fortifying flour. Encouraged by initial success, the state now extended the fortification program to include the distribution and utilization of fortified flour through the government feeding programmes such as the Public Distribution System, ICDS and the Mid Day Meal programs. The flour fortification programme has been adopted in many states of India such as the Union Territory of Chandigarh, Governments of Tamilnadu, Kerala, Haryana, Punjab. The flour fortification programme is at different stages of implementation, with either a voluntary or a mandatory approach. The program is being implemented through the creation of an alliance among all stakeholders under the India Flour Fortification Network (IFFN). Government supports in monitoring the implementation of the fortification programme. The main lesson learnt from India wheat fortification process is that the government support and commitment is an essential component for a sustainable fortification program. This support needs to be particularly in terms of a political will, lending a government logo, providing support for awareness generation and demand creation, and monitoring the program. Following ten years of implementation, the Ministry of Consumer Affairs, Food & Public Distribution of Government of India on January 24, 2008 issued a revised policy on the distribution of wheat flour to beneficaries of targeted public distribution system TPDS.

30.12 Fortification of selected food items (i) Fortification of salt Salt iodization has been in existence for over 70 years. In 1994 UNICEF and WHO recommended universal salt iodization (USI) as the prime approach to correcting iodine deficiency. Iodine is fortified with either

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potassium iodate (KIO3) or Potassium iodide (KI). Compared to iodides, iodates are less soluble in water, more resistant to oxidation and evaporation, and do not require the co-addition of stabilizers being more stable under adverse climatic conditions. Potassium iodate (KIO3) is thus preferred to potassium iodide (KI), especially in hot and humid climates, and is recommended for salt iodization. Most countries with tropical climates currently use potassium iodate though some countries are still using potassium iodide. Iodine is usually added to salt after the salt has been refined and dried. The common method is where a solution of KIO 3 is either dripped or sprayed at a uniform rate onto salt passing by on a conveyor belt. For the quality control purposes, the iodine content of salt can be determined quantitatively with the titration method, and qualitatively using rapid test kits [21]. The Government of India launched USI efforts in 1992. In India, the fortificant used is potassium iodate. The sustainability of the USI program is critical since IDD prevalence will raise if salt iodization effort weakens [59]. Building on the success of salt iodization, options for double fortifying salt with iron and iodine (commonly referred as Double fortified Salt or DFS) have been explored. Research on DFS over the decades have involved finding ways to prevent iron and iodine interactions through one of several ways including use of stabilizers , encapsulating/coating the iron or iodine with a non-reactive digestible material and identifying iron compounds with high degree of bio-availability but least reactivity with iodine. Scientists at the National Institute of Nutrition (NIN) of India developed DFS by blending iodized refined common salt with ferrous sulphate as the iron source at 1000 ppm iron and sodium hexametaphosphate (SHMP) as a stabilizer at 1%. During the course of the past two decades, NIN successfully conducted production, sensory acceptability and efficacy trials of the product. The stability of the nutrients under laboratory conditions along with their bioavailability were found to be good but varied with the quality of salt used [60], therefore high quality dry refined salt is recommended to maintain the stability. A randomized double-blind study was carried out in 1996 for a period of two years among children belonging to backward communities attending four residential schools in and around Hyderabad, India. The study reported a generalized decrease in hemoglobin levels in both the groups. This decrease was attributed to an increase in physiological requirement for iron during the growth phase and the additional amount of iron supplemented through DFS (about 8±10 mg per day) perhaps being not adequate to increase the mean levels overall of hemoglobin [61]. However, in case of children with mild anemia (100–120 g/L Hb), a

Addressing micronutrient malnutrition through food fortification

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significantly greater increments in hemoglobin levels were noted in those receiving DFS (6.8 g/L) both at the end of 1 year and 2 years demonstrating significant association between improved hemoglobin and consumption of DFS. The studies confirmed that the DFS formulation by NIN is a viable option for salt which is refined and dry. The product has been field tested and commercialized to a limited extent. The Micronutrient Initiative (MI) in collaboration with the University of Toronto identified ferrous fumarate as the iron compound suitable for DFS [62]. The process involves agglomeration of ferrous fumarate (to bring the particle size close to that of salt) and encapsulation or coating (to create a protective barrier around the iron particles). Use of small quantities of stabilizing and color masking compounds improved the product performance. The resulting ‘iron premix’ can be blended with iodized salt at the salt factory through a simple dry blending equipment. After a decade of research and pilot scale trials, the MI has transferred the technology to India in 2003 where the iron premix is being produced in Mumbai and blended with iodized salt at Tamil Nadu Salt Corporation (TNSC). The resulting double fortified salt containing iodine and iron is being used since then in the State Government sponsored mid day meal scheme in Tamil Nadu. Field studies confirmed iodine stability even under hot humid climates [63]. Micronized form of ferric pyrophosphate is another iron compound which has been tested by the research team at the Swiss Federal Institute, Zurich and has been shown to be an additional option for DFS [64]. In a controlled trial in rural areas around Bangalore, India in 2005, a double-blind, household-based intervention was conducted where 5–15 year old children receive iodized salt (IS) or two types of DFS with either encapsulated ferrous fumarate (EFF) or micronized ground ferric pyrophosphate (MGFePP), an alternate iron compound for comparison [65]. After 10 months the prevalence of anemia decreased from 16.8% to 7.7% in the MGFePP group and from 15.1% to 5.0% in the EFF group and the prevalence of iron deficiency dropped from 56.6% to 32.8% in the MGFePP group and from 52.4% to 34.6% in the EFF group demonstrating that both DFSs were efficacious in reducing the prevalence of anemia and iron deficiency in school-age children. In addition to improving the iron status, the EFF formulation showed better iodine stability relative to MGFePP in the presence of moisture confirming that the encapsulated ferrous fumarate is a useful option for producing DFS not only in refined dry salt but as well as lower grade salt with relatively higher moisture content since the encapsulation acts as a barrier preventing iodine losses. The light grey specs in DFS due to the iron premix were acceptable in most of the food preparations while consumer education was found to be important.

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The DFS formulations by both NIN and MI target 1000 ppm of elemental iron (Table 30.12). At an average salt consumption of 10g/day these formulations provide 10 mg of iron per person per day meeting approximately 30% of the dietary requirements. Table 30.12 Characteristics of DFS formulations developed and tested by NIN and MI

Main Characteristics

NIN Formulation [60]

MI Formulation [65]

Iodine (ppm), source Iron (ppm), source Stabilization of iodine

30-40 as KIO3 or KI 1000 as Ferrous Sulphate SHMP and use of high quality dry salt

30-40 as KIO3 or KI 1000 Ferrous Fumarate Encapsulation and stabilization by Soy Stearine and SHMP

For quality control of DFS, it is recommended to check both iodine and iron levels at the production site. For field monitoring purposes, qualitative and semi-quantitative tests for DFS containing encapsulated iron has been developed by the University of Toronto [66]. (ii) Fortification of sugar Sugar fortification with vitamin A in the form of retinyl palmitate at a concentration of 15 mg retinol per kg of sugar has been effective in reducing the prevalence of subclinical vitamin A deficiency in Central America [67]. Box 30.2 Success of sugar fortification at the global level During the 1970s, the Institute of Nutrition of Central America and Panama (INCAP), which is associated with the Pan American Health Organization (PAHO), developed fortification technology and implemented sugar fortification programs in various Central American countries, with the first program launched in 1975 in Guatemala. The vitamin A compound in the form of beadlets is bound to the sugar crystal through a layer of vegetable oil to avoid segregation and stability was established to be 40–70% even after 9 months. Population based studies showed that the prevalence of vitamin A deficiency decreased from 22 to 5 percent over a one-year period, and retinol levels in breast milk and in hepatic reserves increased significantly. Mandatory sugar fortification has been established through a variety of legal instruments, with regulations prepared by the Ministries of Health.

In India, following review of Guatemala sugar fortification successful efforts, Vasantdada Sugar Research Institute (Pune) in collaboration with MI , National Federation of Cooperative Sugar Factories (New Delhi) and the Ministry of Food, Consumer Affairs and Public Distribution System developed a technology for fortifying large crystalline sugar available in India. A series of stability and segregation studies were also conducted with vitamin A in the form of retinyl palmitate at a concentration of 15 mg retinol per kg of sugar. With the financial support from the Government of India, MI installed and commissioned a pilot plant for fortifying sugar at

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Shirpur, Maharashtra [68]. However, sugar fortification was not approved under the Prevention of Food Adulteration Act, 1955 by the government as sugar was not accepted as a very useful vehicle for fortification in India (neither with iron nor with vitamin A), as many of the lower economic groups were found to be using very little sugar. (iii) Fortification of edible oils Countries such as Nigeria, Morocco, Yemen, Bangladesh and Pakistan are implementing national programs to fortify cooking oils with vitamin A. Vitamin A is readily absorbed in the presence of oils and fats. The evidence for the biological effect of fortified oils and fats was reviewed in a report commissioned by SUSTAIN [69]. The review summarized studies before and after the fortification of margarine. In 1944, in Newfoundland it was reported that the percent of subjects with serum vitamin A below 20 μg/dl declined from 48% to 2% in a period of over four years. In Philippines, more recently, a shelf stable margarine was fortified with vitamin A. After consuming the margarine for six months, the percentage of children with serum retinol levels below 20 μg/dl fell from 25.6% to 10.1%. It was also demonstrated that soybean oil fortified with vitamin A in the form of retinol palmitate was well absorbed in humans who were fed fortified oil along with a rice-based diet. Significant increases in plasma retinol were reported. Differences in plasma retinol for subjects receiving uncooked versus cooked soybean oil were not statistically significant. Box 30.3 Success of oil fortification in India MI in collaboration with Central Food Technological Research Institute conducted studies on the stability of vitamin A in oils under different temperatures, varied cooking methods and for preparation of different products to suggest the levels of fortification under Indian culinary practices. In consultation with MI, Government of Gujarat was the first state to initiate edible oils fortification with vitamin A and D at the rate of 25 IU of vitamin A and 2 IU of vitamin D per gram of oil, and has also made it mandatory within the state [70]. All oil millers, packers and processors are fortifying the oil in the State. Fortified edible oils are also being procured and distributed under all government welfare programs like PDS, ICDS, MDM, at an additional cost of 3 paise per kilogram of oil. The quality control is being monitored through government approved laboratories under the Department of Food & Civil Supplies, Government of Gujarat.

(iv) Fortification of rice For fortifying whole grain cereals like rice, a technology to produce simulated rice-shaped premix has been explored. Since rice grains are washed before cooking in many countries including India, rice fortification methods like addition of powder form of micronutrients or external coating methods practiced in North America were not considered suitable. During the past 10

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years, extrusion methods were tried as a practical option where an iron compound with or without other micronutrients can be blended with rice flour and formed into rice shaped premix granules through the extrusion process. The target iron concentration of the premix is recommended to be set at 0.5 g or 1 g Fe/100 g of the premix so that when the premix (in shape of rice grains) is blended with natural rice grains at respective ratios of 1:100 or 1:200 the resulting fortified rice contains 5 mg iron per 100 g of rice. This fortification level would provide 15 mg of additional iron to a person consuming 300 g of rice per day. The premix composition and blending ratio can be adjusted based on rice consumption and targeted level of fortification. Selection of an iron compound for fortification that is bioavailable but at the same time does not cause negative sensory characteristics has been a challenge. Color and sensory acceptability tests, using different iron compounds, conducted in Bangalore, India by St. John’s National Academy of Health Sciences in collaboration with Rutgers University, USA and Institute of Food Science and Nutrition, Zurich, showed that extruded rice premix with excellent sensory characteristics and potential high bioavailability can be produced using micronized ferric pyrophosphate. The fortified rice produced using this premix closely resembled unfortified rice, showed less than 3% iron losses during rinsing and achieved a consistent texture when the fortified rice was cooked [71]. With support from the MI, an efficacy study was conducted in 2004 at St. John’s National Academy of Health Sciences, Bangalore, India in schools located in urban slums around Bangalore where a Government subsidized lunch feeding program provided the students with a 200 to 300g meal of cooked rice daily. In a double-blind, 7 month school-based feeding trial, iron-depleted, 6 to 13 year old children were randomly assigned to receive either a rice-based lunch meal fortified with 20 mg Fe as Micronized Ground Ferric Pyrophosphate or an identical but unfortified control meal. Both the groups received deworming treatment. After 7months of feeding, there was a significant increase in body iron stores in both study groups, with a greater increase in the iron group than in the control group. Iron deficiency fell from 78% to 25% in the dewormed iron group and from 79% to 49% in the dewormed control group. Iron deficiency anemia decreased from 30% to 15% in the iron group but remained virtually unchanged in the control group (28% and 27%) [72]. In addition to the micro-nutrient iron, fortification of rice with vitamins A and B complex vitamins have also been tried by PATH. Efficacy studies on PATH technology, known as Ultra Rice, were conducted in India by the National Institute of Nutrition (NIN). The data from a recently concluded study [73] in school children revealed that consumption of rice fortified with iron Ultra Rice had positive impact on the iron stores as

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evidenced by significant increase in the serum Ferritin levels in the experimental group. It was also observed that the intervention led to a significant reduction in the incidence of morbidities among children in the experimental group as evidenced by a positive trend of lower proportion of children falling sick with increasing duration of intervention observed in the experimental group (31.7%) compared to control group (44.6%). Pilot testing indicated a price increase of 5 to 10% over the non-fortified rice depending on the nutrients included. For rice fortification, premix production can be centralized at a large production facility as being done in China by DSM/Buhler collaboration or as a smaller scale production using pasta making equipment being established by PATH in India.

30.13 Innovative experiments with fortification Innovative approaches to reach specific target groups with micronutrients have been explored in the past decaded (Table 30.13). (i) Hard-boiled sugar lozenges (nutri-candies) are being increasingly used as a vehicle to provide essential micronutrients to young children through targeted programs along with food. The lozenges contain less than 3 g of sugar, center filled along with a number of micronutrients like, vitamin A, Iron, Folic Acid and vitamin C, at 50% of RDA levels for children. Vitamin C not only adds a citric flavor to make the candy more palatable but further enhance iron absorption. A pilot project on distribution of nutri-candies in collaboration with the Government of West Bengal( Howrah district), was undertaken.The evaluation of the effectiveness of the fortified candies showed a 15% reduction in the prevalence of anemia among pre-school children over a span of 18 months (Figure 30.10a). However, no such change was observed in pregnant and lactating mothers as the level of fortification was only 25% of their RDA and not 50% as in the case of pre school children, and possibly not adequate to meet with the additional requirements of pregnancy. In case of adolescent girls, there was a reduction in anemia prevalence by 11% (Figure 30.10b) when paired samples were compared after a period of 18 months [74]. Efficacy trials conducted by the All India Institute of Medical Sciences showed a reduction by nearly 50% within a span of 12 weeks of candies administration [75]. The distribution of the nutri-candies at the ICDS Centre also had an impact on the percentage of children enrolled and attendance [76]. The principal advantages of supplying fortified candies through a programme like the ICDS was that the delivery could be targeted to a specific at-risk groups; distribution was simple and delivery of measured quantity of micronutrients could be ensured unlike in case

6–24 mth old

2–6 years old, Adolescent girls, Pregnant and lactating woman

Entire Population

Entire Population

Children 2-6 & Pregnant & Lactating Women in India & Entire Population in Africa

Anuka/Sprinkles*

Fortified Lozenges/ Candies

Fortified Staples- Maize Meal and Wheat Flour

Double Fortified Salt

Vita-Shakti/Rahma

To be mixed to staple food after cooking

Recommended for use in cooking and as table salt

Consumed as such

Consumed as such after food is consumed at the AWC

Powder to be mixed with complementary food before consumption

Administration Iron, Zinc, Vitamin A, Folic acid, Vitamin C – All 100% RDA except vit A) Vitamin A, Folic acid, Vitamin C and Iron 50% RDA for the children and 25% for pregnant and lactating women Iron, Zinc, Vitamin A, Folic acid, B complex Vitamins – 25 to 50% RDA’s for children & adults Iodine and Iron targeting about 100% RDA for iodine and 30% RDA for iron Iron, Vitamin A, Folic acid 50% RDA for the children and 25% for pregnant and

Fortified Nutrients

35–45 cents per person per year

20 cents per person per year

$0.5 and $5 per metric ton

$1.20 per beneficiary for a one year supply

40 cents per child for 2 months intervention

Cost

Sprinkles*—Two different formulations are available—one with 5 micronutrients as in case of Anuka, and the other with 15 micronutrients, covering all the B complex vitamins.

Target group

Product

Table 30.13 Compiled information on various fortified products developed and/or implemented by MI

832 Public health nutrition in developing countries

Addressing micronutrient malnutrition through food fortification

833

of fortification of staple food wherein, the variation in intake between individuals is large and difficult to control. (ii) Home fortificant–Anuka and Sprinkles A formulation for home fortification of complementary food, called Anuka developed in India with MI support, contains iron, vitamin A, folic acid, zinc and vitamin C (Table 30.13). Anuka, available in sachets, can be added to food just before feeding. It can therefore be regarded as complementary food supplement (CFS) for home fortification. The sachets are easy to use and provide the required dose of micronutrients to children regardless of the quantity of complementary food consumed. CFS provide 100% recommended daily allowances of nutrients in single-serve sachet form, which is added to and mixed with any semi-solid complementary food after it has been cooked and immediately prior to being fed to the child. The vitamin-C component provides a citric flavor and helps in the absorption of iron. Anuka can be distributed to the mothers of target children (6–24 month olds), dispensed as dry powder in sachets. This product has undergone sensory trials, stability tests and acceptability studies. The tasteless dry powder has been tested at both room temperature and normal relative humidity as well as accelerated conditions and found to be stable for more than six months. When added to complementary foods, there is no appreciable change in taste or consistency of food and well accepted both by the service providers and receivers. An acceptability and feasibility study, supported by MI, was conducted in 14 blocks of Howrah District of West Bengal where sachets were distributed to mothers of children through the ICDS (Integrated Child Development Services) or Anganwadi Centers (AWCs) for 70,000 children. Positive results were

30.10a Effectiveness trials on anemia prevalence.

834

Public health nutrition in developing countries

30.10 b Effectiveness trials on anemia prevalence.

noted with 80% to 85% compliance of usage by ICDS workers and mothers [77]. Another Anuka project was implemented by the state Government of Rajasthan. The impact on growth velocity of children (6–12 months), rate of weight and height increase, over a 6 th month period demonstrated very positive results. There was an increase in compliance of the utilization of Anuka–multiple micronutrient sachets along with the complementary feeding, from 58% to 91% over a period of 6 months. The programme implementation involved technical consultations and standardization of recipes, partnerships and alliance building, developing state level master trainers, capacity building of functionaries as well as mothers. Weekly Distribution Day was designated wherein all children along with mothers/ caretakers assembled at the ICDS centre (AWC) and were distributed five sachets of Anuka along with complementary food mix. Presence of mothers at the AWC was ensured b y t h e f r o n t l i n e I C D S w o r k e r o r AW W. D e m o n s t r a t i o n o f complementary food preparation was done by AWWs and grassroots health worker (ASHA) for mothers and caregivers on this day, along with enhancing capacities of mothers regarding usage of Anuka in complementary food. First dose of Anuka was given to each child by their mother, under supervision at the AWC during weekly distribution day. A total of 60 sachets were provided and consumed over a maximum period of 120 days. During home visit, the frontline workers (AWW and ASHA) were responsible to ensure the usage of Anuka. On the week following the distribution, AWW the empty sachets of Anuka were collected by these workers to confirm the compliance. Such close monitoring ensured high compliance. Over a span of 6 months intervention, under weight, stunting and wasting reduced by 3%, 21% and 1% respectively [78].

Addressing micronutrient malnutrition through food fortification

835

Sprinkles a multiple micronutrient premix developed by University of Toronto, Canada comprising iron, vitamin A, zinc, vitamin C and several other micronutrients and tested in several countries, when distributed to children in Mongolia [79] and China [80], reported high levels of feasibility, acceptability, compliance and efficacy, because of perceived benefits and ease of use. (Details on sprinkles are presented in the chapter on Childhood Anemia).

30.14 Public–private partnerships Effective and sustainable fortification program is possible only if the public sector (which has the mandate and responsibility to improve the health of the population), the private sector (which has the experience and expertise in food production and marketing), and the social sector (which has grass-roots contact with the consumer) collaborate to develop, produce and promote micronutrient fortified foods [81]. The key players include (i) the Governments; (ii) Research and academic institutions; (iii) Food and premix manufacturing companies; (iv) Consumer organizations; (v) Development assistance agencies (vi) NGOs, and (vii) Media. Food fortification serves the need of the public sector to reduce malnutrition and sustain economic growth. National governments play an equally important role by providing administrative support and prescribing the framework within which solutions are regulated and implemented. The private food industry contributes not only undertaking production of fortified foods but also in creating demand. Raising product quality through fortification stimulates demand for regional products, and intensifies competition and trade. The consumer once aware of the benefits of food fortification demands the product resulting in mobilizing industry to respond. International agencies provide technical, funding and advocacy support for development of intervention strategies. The wheat flour fortification project in West Bengal, India summarizes the partnerships involved which played an important role in the success of the project (Figure 30.11). The role of each key player was as follows: implementation, monitoring and demand creation was done by the West Bengal Micronutrient Initiative Project (WBMIP) of unit office under the Department of Social Welfare (SW), Government of West Bengal; the Department of Food & Civil Supplies, Government of West Bengal issued the government notification about the policy/legislation of fortified atta and also increased the quota distributed through the PDS; the premix industry provided quality premix, the miller agreed to not only to install

836

Public health nutrition in developing countries

the micro-feeder at their own cost, along with the production of the quality product (fortified atta), but also imposed voluntary regulation at the factory; the local media viz. local newspapers, televisions etc assisted in increasing awareness and demand creation and last but not the least the well reputed non government organization, Child In Need Institute (CINI) conducted an impact assessment study, making it a successful pilot project. Another good example of public–private partnership is IDD elimination through Universal Salt Iodization. The global experience of past years has demonstrated that coordinated action by all sectors of society is the key to eliminating iodine deficiency in any given country: the government authorities pursue policies that protect newborns from preventable brain damage by supporting and sustaining salt iodization as well as by monitoring progress; salt industry and vendors produce and sell adequately iodized salt at a fair price in cities and villages every day while civil society assists in public education regarding the dangers of iodine deficiency and ensuring that iodized salt is available. The Sangkap Pinoy Seal program in the Philippines also is a good example of public–private collaboration. Since the program was launched in 1995, over thirty products from sixteen companies have attained the seal from the Department of Health. In Guatemala, the national program of sugar fortification with vitamin A is

30.11 Public–private partnership in food fortification–West Bengal case study.

Addressing micronutrient malnutrition through food fortification

837

implementedwith full cooperation of the sugar industry. In Vietnam, an alliance of private companies, research institutes, NGOs and donor organizations have jointly developed an iron-fortified fish sauce as well as vitamin-A fortified sugar. A private company provided the required technical expertise and developed a fortified drink called Nutri-Delight, and in partnerships with the governments, NGOs and universities who confirmed the efficacy of the product. The significance of such partnership is evident. Table 30.14 defines the roles of each of the various partners in a Multi Sectoral Collaboration to build Public–Private Partnership model. Table 30.14 Multi-sectoral collaboration Sector

Role

Scientific Community Government Industry Consumer Organizations International/bilateral agencies

Identify problems and solutions, undertake efficacy trials Advocacy, resources and program support Technical inputs, resources and marketing Consumer education to create demand Advocacy, technical input, training, resources

30.15 Monitoring and evaluation Any fortification program needs to be accompanied with a good monitoring and evaluation system in place at production as well as at consumption level. Monitoring quality control at the production level is critical to ensure that the fortified food is produced according to the required procedures and contains adequate levels of the micronutrients. At consumption level, monitoring and evaluation comprises both product monitoring and its impact on the population.The latter includes anthropometric as well as clinical and biochemical measurements.

30.16 Regulations and standards In order to undertake effective food fortification activities, it is important to ensure that laws and regulations provide legal authority and an adequate regulatory framework. Effective regulatory controls through established fortification standards protect consumers against the risk of purchasing and consuming nutritionally inadequate, deceptively mislabelled or misbranded, impure or unsafe foods. Regulations also create a ‘level playing field’ for food manufacturers and sellers. For example, the Prevention of Food Adulteration (PFA) of India defines standards for food items with micronutrients under the prevention of food adulteration rules of 1955 under appendix B. The standards of food items, as prescribed

Iron fortified common salt

Iron

Vitamin A

Iodized salt

Iodine

850 ppm

30ppm 15ppm

Minimum

25 I.U

30 I.U

Bakery shortening

Bakery and industrial margarine

None

None

None None

110ppm

none

maximum

A.18.01.01 A.18.02.01

A. 15. 01

A.15.01

Specific conditions of packing and labeling apply

Specific conditions of packing and labeling apply

Specific conditions of packing and labeling apply

Item no. in the Other conditions, appendix B if any

Synthetic vitamin A per gram at the time A.19.01 of packing and shall show positive test for vitamin A, when tested with Antimony trichloride(Carr price reagent as per I.S 886-1970 Synthetic vitamin A per gram at the time A.12.01 of packing and shall show positive test for vitamin A, when tested with Antimony trichloride(Carr price reagent as per I.S 886-1970

As Fe

On dry weight basis

Specific provisions

Prescribed level of added nutrients

Fortified atta None Fortified maida None

Name of the food

Name of the micronutrient

Table 30.15 Standards for food items as prescribed under the Prevention of Food Adulteration Rules, 1955 under Appendix B

14/8/97

10/10/1983

4/4/1960 4/4/1960

4/1/1985

10/2/1988

Effective date

838 Public health nutrition in developing countries

Addressing micronutrient malnutrition through food fortification

839

under PFA, is presented in Table 30.15 and is being revised to be called “Integrated Food Laws”.

30.17 Conclusion Food fortification is a feasible and cost effective method to address the micronutrient deficiencies, along with other strategies like food diversification, supplementation as well as public health measures like immunization, deworming, safe water and sanitation. Experience gained in developed countries as well as developing countries clearly demonstrates that it is possible to select an appropriate fortification intervention based on the target population and suitable food vehicle. Partnership approach to end ‘hidden hunger’ between the governments, social sector organizations, private sector, academicians, civil societies and last but not the least the consumers need to play pivotal role in creating a demand for quality food and sharing the risks and rewards of combating micronutrient deficiencies.

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31 Agriculture, food and nutrition security Deeksha Kapur

Deeksha Kapur is Professor, Nutritional Sciences, School of Continuing Education, Indira Gandhi National Open University (IGNOU), New Delhi. She has been involved in designing and developing various professional and need-based programmes for distance learners since the past 20 years. She has extensive experience in imparting education and knowledge through various multimedia suited to open and distance education mode.

!.

Introduction

The first Millennium Development Goal (MDG) is not simply about reducing poverty – there is a distinct focus on reducing hunger. Far from achieving the MDG goal of reducing hunger by half by 2015, some 75 million more persons were in fact added to the hunger trap during 2007, principally due to the rise in food prices [1]. The fact remains that 823 million people in developing countries are food insecure and undernourished. These chronically undernourished millions are caught in a vicious cycle – not getting adequate food regularly and therefore, not being able to lead a healthy and active life and without such a life, not being able to either produce or procure required food. Undernutrition has significant economic consequences, leading to estimated individual productivity losses equivalent to 10 percent of lifetime earnings and gross domestic product (GDP) losses of 2–3 percent in the worst-affected countries [4]. Undernutrition is not merely a consequence of limited access to calories. Food must not only be available and accessible, but also be of the right quality and diversity (in terms of energy and micronutrients), be safely prepared, and be consumed by a healthy body, as disease hinders the body’s ability to turn food consumption into adequate nutrition. Lack of dietary diversity and poor diet quality has led to micronutrient malnutrition or hidden hunger, even when energy intakes

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are sufficient. Hidden hunger can cause illness, blindness, and premature death as well as impair the cognitive development of survivors. Overcoming undernutrition requires effective and targeted attention to food (macro and micronutrients, clean drinking water) and non-food factors (such as agricultural production, trade, income, sanitation, governance and political stability). This chapter focuses on the concept of food and nutrition security, the global and the Indian perspective to food and nutrition security, the factors that influence food and nutrition security and finally a review on the policies and programmes for reducing food insecurity and vulnerability, particularly in the Indian context.

!.2

Food and nutrition security: understanding the basic concepts

Some key concepts related to food and nutrition security are defined in Box 31.1. As highlighted in Box 31.1, the commonly accepted definition of food security is “when all people, at all times, have physical, social and economic access to sufficient, safe and nutritious food to meet their dietary needs and food preferences for an active and healthy life”. Food is here defined as any substance that people eat and drink to maintain life and growth. As a result, safe and clean water is an essential part of food commodities. Box 31.1 Food and nutrition security: some basic concepts [5] Hunger is a general concept to describe the sensation of not having enough to eat. FAO’s indicator of hunger is ‘undernourishment’ – a measure of energy deficiency or food deprivation. Vulnerability is defined as a function of ‘exposure to risk and ability to cope’. Food insecurity is defined as the lack of access to enough food for a healthy, active life style. Food security is commonly defined as “when all people, at all times, have physical and economic access to sufficient, safe and nutritious food to meet their dietary needs and food preferences for an active and healthy life”. Nutrition security is defined as “physical, economic, environmental and social access to balanced diet and clean drinking water for every child, woman and man”. Food systems encompass activities related to production, processing, distribution, preparation and consumption of food; and the outcomes of these activities that contribute to food security, such as food availability, food access (including affordability, allocation and preferences) and food use (including nutritional value, social value and food safety).

It is interesting to note that food security as a concept evolved over time. Food security historically referred to the overall regional, national,

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Public health nutrition in developing countries

or even global food supply and shortfalls in supply compared to requirements. But, with increased observation of insufficient food intake by certain groups (despite overall adequacy of food supply), the term has more recently been applied mostly at a community level, local, household or individual level [6].

At the household level, food security is defined as “access to food that is adequate in terms of quality, quantity, safety and cultural acceptability for all household members”. A food-secure household is one in which all household members must be well nourished. In other terms they enjoy nutrition security. “Nutrition Security”, therein, may be considered as adequate nutritional status in terms of protein, energy, vitamins, and minerals for all household members at all times [7] and thus in principle is more than food security as highlighted in Figure 31.1. Nutrition security is achieved for a household when secure access to food is coupled with a sanitary environment, adequate health services, and adequate care to ensure a healthy life for all household members. Nutrition security requires the following inputs: ●

●

● ●

Physical – production and advocacy (communication and information). Economic – purchasing power — one must have the money to buy commodities for a balanced diet, for example, cereals, pulses, fruits and vegetables. Environmental – hygiene, sanitation and safe drinking water. Social – equity in gender terms, social factors including intra- and inter-family distribution of balanced diet.

The necessity to include nutrition into food security evolved over time (Figure 31.1). The nutrition focus includes the aspects of caring practices and health services and healthy environments to the definition and concept of food security (Figure 31.2). Achieving food security therefore has the following three essential dimensions: ●

●

●

Ensure a safe and nutritionally adequate food supply both at the national level and at the household level. A reasonable degree of stability in the supply of food, both from one year to the other and during the year. Ensure that each household has physical, social and economic access to enough food to meet its needs. This means that each household must have the knowledge and the ability to produce or resources to procure the food that it needs on a sustainable basis.

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31.1 Concept framework of the food and nutrition security and nutritional status at the household level [8].

As evident in Figure 31.2, the following four fundamental elements are essential: adequate food availability, adequate access to food, appropriate food utilization and its usage as well as food stability. More recently, the ethical and human rights dimension of food security has also come into focus.

31.2 Conceptual framework of food security [9].

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Public health nutrition in developing countries

Food availability is the amount of food that is physically present in a country or area through all forms of domestic production, stocks, commercial imports and food aid. Availability, in the context of food security, refers to the physical existence of food, be it from own production or the market trade. At the national level, food availability derives from the combination of domestic food stocks, commercial food imports, food aid and domestic food production, as well as the underlying determinants of each of these factors. Food can be accessed through trade, barter, collection of wild foods and community support networks; it can also be received as a gift (or even through theft). Access is ensured when all households and all individuals within those households have sufficient resources to obtain appropriate foods for a nutritious diet. It is dependent on the household’s ability to get food in the marketplace or from the other sources (gift, transfer etc.). Thus food access depends on household resources – labour, knowledge and purchasing power, which vary in relation to market integration, price policies and temporal market conditions. The primary determinants of food security for the majority of poor people are their income levels and the cost of food. Utilization is commonly understood as the way the body makes the most of various nutrients in the food. This food security dimension is determined primarily by people’s health status. Food use and utilization is determined by how much a person eats and how well a person converts food to energy, all of which affects proper biological use of food, nutritional status and growth. Adequate food utilization requires a diet providing sufficient energy along with all essential nutrients and potable water, adequate sanitation and access to health services and proper feeding practices and illness management. Use and utilization thus have a socioeconomic and a biological aspect. If sufficient and nutritious food is both available and accessible, the household has to make decisions about what food is consumed (demanded) and how the food is allocated within the household. In households where distribution is unequal, even if the total quantity and nutritional value of food is sufficient, some individuals may suffer from food deficiency. The same is true if different persons receive different types of food which have greater or lesser nutritional value. The phrase “at all times” mentioned in the definition of food security earlier in this section refers to the stability dimension of food security. It emphasizes the importance of having to reduce the risk of adverse effects on the other three dimensions: food availability, access to food or food utilization. Stability of food supplies refers to those situations in which populations are not vulnerable to losing access to resources and other forms of livelihoods due to extreme weather events, economic or market failure,

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civil conflict or environmental degradation and, increasingly, conflict over natural resources. Food security must be determined and ensured at the macro (national), meso- (district, village etc.) and micro (household, family, individual) level by availability (agricultural, production and marketing), access (own income, transfer income) and use and utilization (nutrition behaviour, caring practices, as well as health status and its determinants) of food. Stability of availability, access and utilization is a further important aspect. It is important to note that there has to be a paradigm shift from emphasis on food security at the macro level to nutrition security at the individual level. The overall outcome for food security is the nutritional status of the population. All three key elements (availability, access and utilization of food discussed above) are important for achieving a good nutritional status as highlighted in the Food Insecurity and Vulnerability Information and Mapping Systems (FIVIMS) framework (Figure 31.3). The framework suggests a hierarchical relationship where food security results from adequate food availability and access, as well as proper food utilization. Further the house-hold food access, care practices, health and sanitation coupled with adequate food consumption and utilization influence the nutritional status. Food use translates food security into nutrition security.

31.3 The Food Security and Vulnerability Information and Mapping System (FIVIMS) framework [5].

Food security therefore depends on adequate and stable food availability, access to adequate and appropriate food, and proper use and good health to ensure that individual consumers enjoy the full nutritional benefits of available and accessible food. Availability is necessary but not enough to

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ensure access, which is necessary but not enough for effective use. But for most of the undernourished, the lack of access to food is a greater problem than food availability. Nobel Laureate Amartya Sen has famously written that “starvation is a matter of some people not having enough food to eat, and not a matter of there being not enough food to eat”.

31.3

Agriculture: central to food and nutrition security

31.3.1 The global perspective The world is generally food secure, producing enough food to meet the dietary needs of today’s global population though future global food security should not be taken for granted because of uncertainties from growing resource scarcity and climate change. Though, the world has more than enough food to feed everyone, yet 850 million are food insecure. Achieving food security requires adequate food availability, access, and use as already highlighted above. Agriculture, therein, plays a key role in (1) food availability globally (and nationally and locally in some agriculture-based countries); (2) income source to purchase food; and (3) foods with high nutritional value status. Agriculture is central to poverty reduction and higher agricultural productivity is critical to the attainment of the MDGs. By increasing food availability, generating income for farmers, and improving the purchasing power and asset level of the poor, agricultural growth can contribute directly to MDG1 of halving hunger and poverty by 2015 and reducing childhood undernutrition [10]. Agriculture can also contribute to maternal and child health, nutrition and survival (MDG4 and MDG5) and to combating HIV/AIDS and other diseases (MDG6) by increasing the diversity of the food supply, increasing the micronutrient density of the staple crops (e.g. through biofortification), improving the overall quality of diets as well as by increasing income and making more resources available to prevent and manage illnesses [11, 12]. The five main pathways by which agriculture affects nutrition can be summarized as follows [13]: ●

●

●

● ●

Increased consumption from increased food production (for own consumption), Increased income from sale of agricultural commodities (production for income), Empowerment for women agriculturalists and related gains in children’s nutrition and welfare, Lower real food prices resulting from increased food production, and Macroeconomic growth arising from agricultural growth.

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However, there is recent evidence that the global food production system is at an unprecedented level of risk from extreme supply deficits, particularly with respect to cereals. This trend could be amplified by climate change, which is expected to have significant impacts on agriculture and food production patterns world over through three major pathways: global warming, change in rainfall patterns and the increase in carbon dioxide concentration in the atmosphere. In a scenario of moderate climate change, it is projected that those most vulnerable to these changes would be the poor and landless in rural areas that are dependent on isolated rain-fed agricultural systems in semi-arid and arid regions. The future of global food supply is highlighted in Box 31.2. Box 31.2 Future of the global food scenario [10] Agriculture has been largely successful in meeting the world’s effective demand for food. Yet more than 800 million people remain food insecure, and agriculture has left a huge environmental footprint. The future is increasingly uncertain. Models predict that food prices in global markets may reverse their long-term downward trend, creating rising uncertainties about global food security. Climate change, environmental degradation, rising competition for land and water, higher energy prices, and doubts about adoption rates in future for new technologies present huge challenges and risks that make predictions difficult. To meet the projected demand, cereal production will need to increase by nearly 50 percent and meat production by 85 percent from 2000 to 2030. Added to this is the burgeoning demand for agricultural feedstocks for biofuels, which have already pushed up world food prices.

31.3.2 The Indian perspective Agriculture in India has contributed substantially to the national level food security through increased productivity and reduced dependence on imports. At the national level, a major achievement on the agricultural front in the post-Independence period has been the expansion of food grain production, enabling the country to acquire a degree of self-sufficiency in cereals production. The production of few important agricultural commodities in India is highlighted in Figure 31.4. International commodity prices are used to calculate the total value of each commodity produced and subsequently used in the ranking of the commodity. This is done to facilitate international comparative analysis of productivity at the national level. Agriculture situation of India [15] is summarised below: ●

With a production reaching ten times in past five years, India is today the second largest wheat producer in the whole world. India has the largest area in the world under wheat. India is also the second largest rice producer in the world. Pulses are sometimes called “poor man’s meat”. India’s export of pulses has increased from Rs. 589.85 crores (USD million 131.46) in 2004–05 to Rs. 770.64 crores (USD Million 170.95) in 2006–07.

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The production in India in (2009)

31.4 The agricultural production in India [14]. ●

● ●

India is the fruit and vegetable basket of the world. India is the second largest producer of vegetables that account about 16 per cent of the world production. India ranks fifth in the world in cropped area under cultivation and production of potatoes. India is second largest onion growing country in the world. India produces 41% of world’s mangoes, 23% bananas, 24% cashew nuts, 36% green peas and 10% onion. India is a world leader in the production of dairy and animal products. India retained its rank as the largest milk producer in the world with a total production of 100 million tonnes.

For operational purpose these statistics can be assumed to indicate that at the national level the aggregate production and supply of food is adequate to meet target consumption levels of our current population groups. However, despite the fact that India has attained near self-sufficiency in food grains, and the region as a whole was surplus in food grains, this food adequacy scenario did not translate into an increase in food grains consumption by the poor and improvement in the nutritional status of undernourished people in India. The limitation is not food supply, but food distribution. A detail review on food insecurity and vulnerability in India follows in Section 31.4.

31.4

Food insecurity and vulnerability

31.4.1 The global perspective About 850 million people in the world are undernourished – a number that has hardly changed since the 1990–92 base period for the World Food

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Summit and Millennium Development Goal commitments on reducing hunger by half by 2015. Of particular concern are hunger hotspots, marked by the widespread persistence and prevalence of food insecurity, especially in protracted crises. As of May 2006, 39 countries in the world were experiencing serious food emergencies and required external assistance for dealing with critical food insecurity: 25 in Africa, 11 in Asia and near East, 2 in Latin America and 1 in Europe [16]. A case study for food security in Cambodia is highlighted in Box 31.3. Box 31.3 Food security in Cambodia – a case study [9] Food security is a cross-cutting issue, and in a country such as Cambodia, rural poverty and food insecurity are strongly interlinked. In Cambodia most people depend, to an important extent, on their own capacity to produce food to meet their needs. They grow crops including their staple food (rice) as well as other annual and perennial crops, raise livestock, and harvest wild foods from fisheries and forests for food and income. Despite Cambodia being self-sufficient in rice at the national level, the country’s rice balance varies significantly from area to area within the country, as well as from year to year. Crop agriculture is largely rice-based, with very limited diversification in many food-insecure areas of the lowland flood plains, while fish production (a main source of protein) is declining and increasingly under threat. Many rural households have insufficient land for crop production. Many rural people also depend on casual low-wage labour or informal-sector enterprises to make income with which to buy at least part of their food needs, and the food security of poor rural people can often depend mainly on income from such activities. Farmers seeking to sell their crops face a poorly developed road and market infrastructure, limited storage capacity, and high transaction costs. Net returns from rice production are very low, and the marketing strategies of households earn little profit. Purchasing power to buy food is generally very limited in rural areas due to the high incidence of poverty. Rice shortages (rice gaps for two months or more) at the household level are frequent and contribute to the indebtedness of rural households, which in turn leads to chronic food insecurity. High health expenditures erode the asset base and purchasing power of food-insecure and vulnerable households. Income and food from common-property resources (forests and fisheries) are particularly important for the poor, but concessions and environmental degradation have restricted their access to these resources. Cambodia has some of the highest malnutrition rates in Asia, with 44% of children under five years of age stunted and 15% wasted. Micronutrient deficiencies such as Iodine Deficiency Disorder (IDD), Vitamin A Deficiency (VAD) and Iron Deficiency Anemia (IDA) are widespread and hamper the full use of human potential for development. There is limited access to safe water and proper sanitation. People’s poor health status (resulting from limited access to quality health services and preventive health) impairs optimal utilisation of food, while poor quality diet and inadequate feeding and caring practices further exacerbate the problem. In recent years, flooding and drought have become more frequent, but emergency response capacities remain insufficient. The current production system is very vulnerable to drought due to the lack of diversification and irrigation. Depletion of productive assets, as a result of indebtedness, leads to chronic food insecurity. The food needs of permanent vulnerable groups (female-headed households with children, elderly, disabled, people living with HIV/AIDS) are not sufficiently addressed as a result of disrupted rural social institutions and lack of

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Public health nutrition in developing countries

social safety nets. While women in Cambodia play a major role in all components of food security, whether in food production, marketing, household income/ budgeting or as care takers, their role is negatively impacted by issues such as high illiteracy rates among women, lack of education and knowledge, and poor health and nutritional status (e.g. very high maternal mortality rates and irondeficiency anemia prevalence of 65% among pregnant women). The elimination of food and nutritional insecurity in Cambodia, and the attainment of Cambodian Millennium Development Goal 1 to eradicate extreme poverty and hunger, demands a specific, comprehensive and integrated approach focusing on all three dimensions of food security: availability, access and use and utilization. Furthermore, food security and vulnerability need to be tackled at the national, household and individual level.

31.4.2 The Indian perspective India is home to the world’s largest food insecure population, with more than 200 million people who are hungry. On the 2008 Global Hunger Index (GHI), India ranks 66 out of 88 countries. Like the GHI, the 2008 India State Hunger Index (ISHI) has been calculated which shows that all Indian states have at least a “serious” level of hunger; there is not a single state with low or even moderate levels. India’s poor performance on the GHI is primarily due to its relatively high levels of child malnutrition and undernourishment resulting from calorie deficient diets [17]. Though India has nearly attained self-sufficiency in food grains, and the region as a whole was surplus in food grains as mentioned earlier, this did not translate into an increase in food grains consumption by the poor. On the contrary, the calorie and protein intake of the poor in the country has declined over the years. Data from the National Sample Surveys [18– 20] show a clear trend of decline in calorie intake. In rural India, the average calorie intake per capita per day fell from 2266 kcal in 1972–73 to 2183 in 1993–94, to 2149 in 1999–2000 and further to 2047 kcal in 2004–05. Between the same period, average per captia calorie intake in urban sector declined from 2089 to 2020 kcal. With reference to the names 2400 kcal for the rural sector and 2100 kcal for urban sector, the calorie deprivation extent increased from 69 to 85 percent in rural India and from 60 to 65 percent in urban India. The data also show a decline in cereal intake, a phenomenon clearly driven by distress rather than choice since it has occurred in a situation of declining overall calorie intake and persistence of high levels of malnutrition. Further, average daily intake of protein by the Indian population has also decreased from 60.2 to 57 grams in the rural area between 1993–94 and 2004–05 and remain stable around 57 grams in the urban area during the same period. However, a significant rise in per capita daily average intake of fat is observed during the decades (1993–94 to 2004–05) in both rural and urban areas. It has increased from 31.4 g to 35.5 g (13.1 percent) in rural areas and from 42 g to 47.5 g (13

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percent) in urban areas. In spite of increasing oil and fat intake, the proportion of dietary energy from fat remains lower than 15 per cent. In addition to energy deficiency, a lack of diversity in the diet is a key issue (e.g. cereals contribute a disturbingly high proportion of calorie intake, more than 80 percent, for the lowest decile, compared to approximately 50 percent for the highest decile). The Food Insecurity Atlas of Rural India, published by the Swaminathan Research Foundation 2001, gives a fairly complete picture of India’s performance. In all the selected states for the study (Table 31.1), the average per capita consumption of cereal exceeds the norm of the Indian Council of Medical Research (ICMR) while that of other foods falls far short. Cereals seem to be the main dietary item and chief source of energy. Table 31.1 Food adequacy in India and in few selected Indian States relative to ICMR norms [21] Food items

Unit consumption (state-wise)* Andhra Pradesh

Madhya Pradesh

Cereal 1.05 1.13 Cereal 0.00 0.01 substitutes Pulses 0.58 0.81 Vegetables 0.53 0.45 Fruit 0.45 0.21 Milk and 0.52 0.55 milk products Oils 0.56 0.45 Meat 0.29 0.08 Fish 0.15 0.08 * ICMR norms equivalent to one unit.

Orissa

West Bengal

India

ICMR norm (grams/person per day

1.26 0.00

1.19 0.00

1.04 0.05

420 75

0.38 0.47 0.27 0.15

0.35 0.51 0.38 0.31

0.58 0.48 0.45 0.97

40 125 50 150

0.27 0.08 0.39

0.52 0.17 0.72

0.52 0.15 0.28

22 25 25

The consumer expenditure survey of the NSSO during the 55th round covering the period from 1999 to 2000 [19] show that out of the total calorie intake of the average Indian, 68% in the rural areas and 55% in urban areas were derived from cereals alone. The contribution of cereals to the average intake of protein in the country was 67% in the rural sector and 57% in the urban sector. In rural areas, oils and fats accounted 7% of total calorie intake, milk and milk products accounted for 6%, pulses, nuts and oilseeds for 5% and sugar and honey for 5%. These contributions were somewhat higher in urban India – oils and fats 11%, milk and milk products 8%, pulses, nuts and oilseeds 7% and sugar and honey 6%. Food security has come to be regarded principally as food grain security, mainly meeting the requirements of energy and proteins. However, for nutrition security, food production should ensure availability of diverse foods, which can ensure both macronutrients as well as micronutrient security. Food grains (cereals and millets) alone cannot meet the requirement of micronutrients like vitamins and minerals, and health

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promoting phyto-chemicals. It is not the case of “either/or” but “all”. Nutrition security is a broader term and implies food grain security as well. In fact, diversification even within food grains to increase the production and availability of millets and legumes should be the demand. Having reviewed the food and nutrition security scenario in India above, it is evident that currently we are in a paradoxical situation where somewhat food surpluses at the aggregate national level coexist with large undernourished and poor population. This scenario is well documented in the case study of food security in Orissa and Himachal Pradesh presented in Box 31.4. It is important to understand that the agriculture productivity and increased production can only ensure food security of the country and not that at individual or more precisely household level, which assumes a complex function of various socio-economic–environment factors as discussed in the next section. Box 31.4 Food security in Orissa – a case study [22] Orissa is among the poorest of India’s poor states. It depends largely on an undiversified agricultural economy. The poverty headcount rate is 47 percent. Poverty is an overwhelmingly rural phenomenon and is clearly linked to low land productivity, limited diversification of the agricultural economy (primarily paddy) and the lowest agricultural wages in the country. While the state, including some of the poorest districts, is virtually self sufficient in food grains, there is a significant portion of chronic food insecurity associated with particular areas and population groups. Inequalities are greater between the relatively better-off coastal areas and the more remote and inaccessible southern region. Regional differences are closely linked to differences among social groups, with poverty among castes and especially indigenous tribal people being strikingly higher than for other groups. The pervasive and chronic food insecurity of poor communities in Orissa is captured by anthropometric measures as over half of the children between 1 and 5 are stunted. Almost half of all adult women and three quarters of all children under three in Orissa are undernourished. The infant mortality rate for Orissa is higher than any other state in India, while child malnutrition in Orissa is significantly higher than the national among the highest in India. The proportion of labouring rural households with an average daily energy intake of less than 1800 kcal (less than 75 percent of the recommended minimum intake) was found to be 43 percent for the Coastal Plains, 57 percent for the Northern Plains and 69 percent for the Eastern Ghats. The vulnerable group category with the greatest prevalence of extreme food insecurity (defined as calorie intake per capita per day below 1800 kcal for people who are 40 percent below a poverty line income) was rural artisan households (73 percent), while more than half of all marginal farming households and labouring rural households (52 to 58 percent) were also considered extremely food insecure. Children of labouring rural households and marginal farming households emerged as the most affected by extreme undernourishment (hunger), particularly in the districts of Gajapati and Nuapada where between 56 and 80 percent were found to be consuming less than 1800 kcal per day. Findings contributing the poor scenario of Orissa include (a) Human capital – Alarmingly poor education levels and awareness of basic health and sanitation issues among poor communities. (b) Social capital – Traditional extended family and community and civil society support systems have been significantly undermined as a result of entrenched poverty and shocks such as natural disasters. (c) Natural capital – Unsustainable farming practices and declining soil fertility are key factors

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causing slow growth in the agricultural sector and worsening rural livelihood conditions. (d) Physical capital – Poor rural connectivity is a major factor underlying limited market development. In addition, the low capital value of the dwellings of vulnerable households has negative implications for access to formal credit services. (e) Financial capital – More than 75 percent of all poor rural households are found to be indebted (mostly through informal and often exploitative arrangements). The majority of loans are taken to meet basic consumption requirements. In most households more than 50 percent of income is regularly used for repayments. The central challenge facing policy makers in Orissa involves managing a transition away from an underdeveloped agricultural economy, while ensuring basic levels of human welfare and equitable access to resources. Central to this achievement is an increase of labour productivity within agriculture and, simultaneously, expansion of non-agricultural employment opportunities in both rural and urban areas. Eleven specific priority areas of intervention for reduced vulnerability and enhanced food security following a twin-track approach addressing both rural/agricultural development while addressing also immediate food needs of the most vulnerable in Orissa have been suggested:

●

TRACK 1 Rural development greater investment in dryland/ agricultural technology adaptive agricultural research

●

watershed development

●

irrigation and water management

●

pro-poor land policy reform

●

●

● ●

● ●

●

TRACK 2 Addressing immediate food needs ● strengthening of disaster management capacities ● strengthening anti-poverty programmes for enhanced social protection ●

food storage

joint forest management and Non Timber Forest Products (NTFP) promotion developing financial services diversification e.g. through horticulture, animal husbandry and fish production improved agro-processing promotion of small scale industries and micro-enterprises developing tourism and mining sectors

Food security in Himachal Pradesh: a case study [5, 22] Whilst Himachal Pradesh is comparably less food insecure, the state does face a range of challenges related to undernourishment and malnutrition. Anthropometric measures show that close to every second child under five in HP are underweight and 41 percent of adult women are anaemic, only slightly lower than the national figure. The main causes of food insecurity and vulnerability include increased fragmentation of land, limited or no access to welfare provisions and public services related to migration, weak infrastructure and lack of accessible credit institutions. Key interventions to address the causes of food insecurity and vulnerability in Himachal Pradesh have been identified. These include increased investment in irrigation; improved extension services; ensuring social service provision and basic human welfare; and continued assurance of high levels of investment in constructing and maintaining rural infrastructure as a prerequisite for sustainable and broad-based economic growth.

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!.5

Factors underlying the current state of food and nutrition security

As will be discussed in this section, many factors have contributed to the current food insecurity situation prevailing worldwide, though it is difficult to quantify their contributions. Among the most important factors it is possible to list environmental factors such as climatic changes, stock levels, increasing food prices, biofuel and agricultural commodities, food supply etc. A briefly review of these factors follows.

31.5.1 Global perspective (i) Food pricing and food security Agricultural commodity prices rose sharply in 2006 and 2007 and continued to rise even more sharply in the first three months of 2008. The continuing surge in prices is led by vegetable oils, which on an average increased by more than 97 percent during the same period, followed by grains with 87 percent, dairy products with 58 percent and rice with 46 percent. This is a very large increase for poor people who depend on a single staple food (particularly cereals) for the bulk of their caloric intake, and typically spend 20–40 percent of their income on this one commodity alone. A critical trigger for the price hikes has been the decline in the production of cereals in major exporting countries, which beginning in 2005 and continuing in 2006, declined annually by 4 and 7 percent, respectively. The gradual reduction in the level of stocks, mainly of cereals, since the mid-1990s, is another supply side factor that has had a significant impact on markets recently. However, in spite of the soaring prices in global commodity markets, in particular of tradable cereals such as wheat, rice and maize, the most recent data on the food use of these key cereals have not shown much of a decline on a per capita basis. These trends however, must be interpreted cautiously. Even if cereal consumption of the poor does not change, this does not imply that there are no important welfare effects. The poor may defend their intake of cereals, but only at the expense of reduced consumption of more nutritious foods such as meat and dairy products, and reduced expenditures on education and health. As one example, Block et al (2004) [23] found that when rice prices increased in Indonesia in the late 1990s, purchases of more nutritious foods were reduced in order to afford the more expensive rice. This led to a measurable decline in blood haemoglobin levels in young children (and in their mothers), increasing the probability of developmental damage. A negative correlation between rice prices and nutritional status has also been observed in Bangladesh [24]. Reductions in expenditures on education and health care can also

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obviously have adverse long-term consequences on their efforts to escape poverty. Households under distress may liquidate assets (distress sales) and deplete savings with uncertain prospects for re-building them. (ii) Climate, agriculture and food security Climate change is expected to have significant impacts on agriculture and food production patterns through three major pathways: global warming, change in rainfall patterns and the increase in carbon dioxide concentration in the atmosphere [25]. The present crisis of food insecurity world over is a combination of rising demand for agricultural products, due to population growth and economic development in emerging countries; the rapid expansion of biofuels; insufficient supply as production is negatively affected by climate change, in particular drought and floods, and water availability. Developing countries are particularly vulnerable because their economies are closely linked to agriculture, and a large proportion of their populations depend directly on agriculture and natural ecosystems for their livelihoods. The Asian countries most vulnerable to climate change are Afghanistan, Bangladesh, Cambodia, India, Lao PDR, Myanmar and Nepal. Afghanistan, Bangladesh, India and Nepal are particularly vulnerable to declining crop yields due to glacial melting, floods, droughts, and erratic rainfall, among other factors. Several studies have looked at the sensitivity of specific crops to projected changes in the climate, to assess vulnerability of systems based on these crops. These are highlighted in Box 31.5. Box 31.5 Assessing and mapping vulnerability [26] Wheat in the Indo-Gangetic Plains. Wheat is a crop of temperate climate, and rising temperatures may make many currently important wheat areas too hot for the crop. A study from the International Maize and Wheat Improvement Center (CIMMYT) details possible climate shifts in the Indo-Gangetic Plains of South Asia, a region of 13 million hectares that extends from Pakistan across northern India, Nepal and Bangladesh, and which grows 15% of the world’s wheat. According to the study, by 2050 more than half of its area may become heatstressed for wheat, with a significantly shorter season for the crop. Rice in the mega-deltas of Asia. The Mekong and Red River Deltas in Vietnam, the Irrawaddy Delta in Myanmar and the Ganges–Brahmaputra Delta in Bangladesh and India are vital for world rice production. But the impacts of climate change – increased flooding and salinity – pose a major threat. Maize in sub-Saharan Africa and Latin America. Scientists at the International Center for Tropical Agriculture (CIAT) and the International Livestock Research Institute (ILRI) have taken outputs from climate simulation models and data from various sources to simulate the growth, development and yield of maize crops over sub-Saharan Africa and Central and South America. The results showed an aggregate yield decline by 2055 for smallholder rain-fed maize production of 10%, representing an annual economic loss of the order of US$2 billion.

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It is important to understand that climate change has the potential to act as a ‘risk multiplier’ in some of the poorest parts of the world, where agricultural and other natural resource-based systems are already failing to keep pace with the demands on them. Some of the anticipated costs of climate change are highlighted in Box 31.6. Box 31.6 The costs of climate change [26] A recent study by the International Food Policy Research Institute (IFPRI), highlights some of the anticipated costs of climate change, which include: ●

●

●

●

25 million more children will be malnourished in 2050 due to climate change without serious mitigation efforts or adaptation expenditures Irrigated wheat yields in 2050 will be reduced by around 30% and irrigated rice yields by 15% in developing countries Climate change will increase prices in 2050 by 90% for wheat, 12% for rice and 35% for maize, on top of already higher prices. At least US$7 billion a year are necessary to improve agricultural productivity to prevent adverse effects on children.

It is estimated (Figure 31.5) that, twenty five million more children will be malnourished in 2050 due to effects of climate change (Figure 31.5). Further, with climate change, average calorie availability in Asia in 2050 is expected to be about 15 percent lower and cereal consumption is projected to decline by as much as 24 percent compared to a no climate change scenario. To counteract the effects of climate change on nutrition, additional annual investments of 7 billion USD per year is estimated (Figure 31.5).

31.5 Number of malnourished children in 2050 with and without climate change [27].

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(iii) Biofuels and agricultural commodities There is a growing international consensus that the rapid increase in demand for biofuel feedstocks has contributed significantly to the current rise in food prices. The emerging biofuels market is a new and significant source of demand for some agricultural commodities such as sugar, maize, cassava, oilseeds and palm oil. The increase in demand for these commodities has been one of the leading factors behind the increase in their prices in world markets which, in turn, has led to higher food prices. The most important biofuels today are ethanol and biodiesel. Ethanol is produced predominantly from sugar cane and maize and, to a far lesser degree, from wheat, sugar beet and cassava. Biodiesel mostly uses rapeseed but also palm oil, soybean oil and jatropha. Sugar from Brazil and maize from the United States of America (USA) dominate global ethanol production. Together they comprise around 80 percent of global production. China, the European Union (EU) and India are other significant ethanol producers. In 2007, approximately 23 percent of USA coarse grain production was used to produce ethanol, as was about 54 percent of Brazil’s sugar-cane crop. In the EU, about 47 percent of vegetable oil production was used in the production of biodiesel causing higher imports of vegetable oil to meet domestic consumption needs. These commodities, which have predominantly been used as food and/ or feed, are now being grown as raw material (feedstock) for producing biofuels. Significant increases in the price of crude oil allow them to become viable substitutes in certain important countries that have the capacity to use them. Availability of food can be threatened to the extent that land, water and other productive resources are diverted from food production to biofuel production. This competition for natural resources occurs whether edible or non-edible crops are cultivated for bioenergy purposes. The degree of competition among food, feed and fuel uses of biomass hinges on a variety of factors, including crop selection, farming practices, agricultural yields and the pace at which next-generation biofuel technologies develop. Utilization of food, as discussed earlier refers to peoples’ ability to utilize, i.e. absorb, nutrients. This is closely linked to health and nutrition factors, such as access to clean water, sanitation and medical services. When biofuel feedstock production competes for water supply, it could make water less readily available for household use, threatening the health status and, thus, the food security status of affected individuals. Further growth in biofuels could exert additional pressure on the stability of food supplies. The use of food crops (or crops which compete with them for land resources) for biofuels may establish an effective floor price for these commodities, and price volatility from the petroleum

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sector will be more strongly transmitted to the agricultural sector, increasing the risk of food insecurity. This impact will be enhanced as import dependence is expected to grow for most low income food deficit developing countries, and as price transmission increases between global and national markets with greater market liberalization and the forces of globalization.

31.5.2 Indian perspective (i) Impact of Green Revolution on food security As a result of the Green Revolution (1) , India’s total food grain production increased from 50 million tons in 1950–51 to over 200 million tons in the year 2000–01 – a four-fold increase. The population during the same period increased from 300 millions to 1000 millions (1 billion) [28]. Thus, the increase in food grain production surpassed population growth and India turned from a ‘nation’ with a ‘begging bowl’, to a country with food grain reserves to provide some degree of national food security. This impressive achievement, however, has some worrisome aspects. ●

●

The Green Revolution concentrated primarily on cereals like rice and wheat, which responded to innovations in agriculture technologies leading to development of high yielding varieties. However, these crops are water guzzling – particularly paddy and have had adverse environmental impact. Production of millets (referred as coarse cereal), legumes/pulses and oil seeds, which are less water demanding and nutritionally better endowed, has remained almost static. Apart from scientific and technological reasons, the pricing policy of the government in terms of minimum support price and procurement price as well as PDS has favoured production of rice and wheat, leading to the neglect of millets and legumes.

Higher support price for fine cereals is responsible for the accumulation of cereal stocks, which reached 60 million tons in mid 2002; but has come down since. Farmers, who traditionally raised millets, have shifted to growing and eating fine cereals with adverse impact on nutrition, environment, and threat to biodiversity with regard to some of the local minor millets. (1)

A significant increase in agricultural productivity resulting from the introduction of high-yield varieties of grains, the use of pesticides, and improved management techniques.

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Box 31.7 Green Revolution in India The term “Green Revolution” is a general one that is applied to successful agricultural experiments in many Third World countries. It is not specific to India. But it was most successful in India. The world’s worst recorded food disaster happened in 1943 in British-ruled India known as the, Bengal Famine, an estimated four million people died of hunger that year alone in eastern India that included today’s Bangladesh. The initial theory put forward to ‘explain’ that catastrophe was that there was an acute shortfall in food production in the area. While food shortage was a contributor to the problem, a more potent factor was the result of hysteria related to World War II which made food supplies a low priority for the British rulers. The hysteria was further exploited by Indian traders who hoarded food in order to sell at higher prices. Nevertheless, when the British left India in 1947, food security was a paramount item on free India’s agenda. This awareness led to the Green Revolution in India and also framing legislative measures to ensure that businessmen would never again be able to hoard food for reasons of profit. The term “Green Revolution” in India is specifically applied to the period from 1967 to 1978. The Green Revolution changed India from a starving nation to one of the world’s leading agricultural nation. There were three basic elements in the method of the Green Revolution in India: (1) Continued expansion of farming areas; (2) Double-cropping existing farmland; (3) Using seeds with improved genetics. The most noteworthy high-yield value (HYV) seed was the K68 variety for wheat. The Green Revolution resulted in a record grain output of 131 million tons in 1978–79. This established India as one of the world’s biggest agricultural producers. No other country in the world which attempted the Green Revolution recorded such level of success. India also became an exporter of food grains around that time. Yield per unit of farmland improved by more than 30 per cent between 1947 (when India gained political independence) and 1979 when the Green Revolution was considered to have delivered its goods. The crop area under HYV varieties grew from 7 per cent to 22 per cent of the total cultivated area during the 10 years of the Green Revolution. More than 70 per cent of the wheat crop area, 35 per cent of the rice crop area and 20 per cent of the millet and corn crop area, used the HYV seeds.

(ii) Food supply – situation in India The decline in per capita net availability of cereals and pulses over the last 15 years (from 510 g per capita a day in 1991 to 463 g in 2004) in India has been unprecedented. While a few years ago, it appeared that there was no threat to self-sufficiency in food grain production, the situation is of concern. The estimates for the requirement of cereals in 2020 range from 224 to 296 million tonnes. The High Level Committee on Long Term Grain policy (Abhijit Sen Committee) arrived at an intermediate projection of 260 million tonnes. To achieve this, starting from the production level of 191 million tonnes of cereals in 2004–05, in the next 15 years, production will

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have to increase by 69 million tonnes to meet the demand of 2020. In the last 15 years, cereal production increased by only about 29 million tonnes. In the next 15 years, the achievement needs to be doubled to meet the projected requirement. The present rate of growth of cereal and food grain production will not be adequate to meet these demands. Major changes are needed in terms of agricultural strategy, as spelt out in the Reports of the National Commission on Farmers [29]. (iii) Land fragmentation One clear cause of food insecurity and vulnerability in some parts of the Indian region is the increased fragmentation of land. The fragmentation has made farming households more vulnerable to weather-induced or market-based shocks and many farming households have difficulty maintaining sufficient food production with only a marginal piece of land. However, households with access to proper irrigation seem to be better off in terms of coping with marginal land areas. The fragmentation has also led to an increase in both agricultural and non-farm labourers putting a downward pressure on wages and thereby increasing the vulnerability of these livelihoods. (iv) Poverty, purchasing power and food security In India, availability of foodgrains is not the real problem since the country has achieved self-sufficiency in the matter of foodgrains. This implies that there is no longer a requirement to import foodgrains. In fact, the country is in a position to export same food items. However, the problem of suppressed demand, due to poverty, is of concern since the prevailing poverty amongst a large number of household essentially those living below poverty line (BPL) is the major constraint for achieving household’s food security. In 2004–2005, the Planning Commission based on National Sample Survey (NSS) estimated that 27.5% of the population was living below the poverty [30]. The criterion used by 61st round of the National Sample Survey (NSS) was monthly per capita consumption expenditure below Rs. 356.35 for rural areas and Rs. 538.60 for urban areas. It is estimated that 75% of the poor are in rural areas, most of them are daily wagers, self-employed householders and landless labourers. More recently, an expert group constituted by the Planning Commission, Government of India, to review the methodology for estimation of poverty line recommended that actual private expenditure per capita on food, education and health consistent with optimal nutrition, educational and health outcomes should be used to define poverty line. It has been estimated that if these revised criteria are

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applied, poverty at all India level in 1993-94 was 51% in rural areas, 31.8 in urban areas and 45.3% in the country as a whole compared to the 199394 official estimation of 37.2% rural, 32.6% urban and 36% combined. A 2007 report by the state-run National Commission for Enterprises in the Unorganised Sector (NCEUS) reported that 25% of Indians, or 236 million people, lived on less than 20 rupees per day with most working in “informal labour sector with no job or social security, living in abject poverty”. In India, large scale unemployment is a great aggravating factor and in conjunction with rapidly growing population, severely impairs the purchasing power of a large number of households or forces the families to acquire purchasing power at a certain social cost like child labour. To ensure food security, we have to ensure adequate supply (also called availability) as well as intake. Intake by individuals depends on many factors, most importantly on purchasing power and availability of food of appropriate quantity and quality at affordable prices. The contributions that agriculture makes to food security need to be complemented by medium-term programs to raise incomes of the poor, as well as insurance and safety nets, including food aid, to protect the chronic and transitory poor. The Government of India (GoI) has, since independence, implemented multiple initiatives – policies, programmes. In the next section we focus on such initiatives and strategies.

31.6

Policies and programmes for reducing food insecurity and vulnerability in the Indian context

To address widespread poverty, food insecurity and vulnerability, the Government of India (GoI) has, since independence, implemented multiple initiatives such as the Integrated Child Development Services (ICDS) Programme, the Mid Day Meal (MDM) Programme, the Mahatma Gandhi National Rural Employment Guarantee Act (MGNREGA), social protection initiatives (Anti-poverty programmes, Public Distribution System or PDS), community-based food and nutrition programmes, and, in recent years, the National Plan of Action on Nutrition and the National Rural Health Mission. Though macro-level food self-sufficiency has been achieved, partly through the establishment of national systems for public grain procurement and distribution, this has proved insufficient to ensure micro-level food security for the poor. A brief description of the programmes and initiatives taken by the government to address the food insecurity and vulnerability issue are highlighted herewith.

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31.6.1 Social protection initiatives It is now well recognized that the availability of food grains is not a sufficient condition to ensure food security to the poor. It is also necessary that the poor have sufficient means to purchase food. The capacity of the poor to obtain food can be ensured in two ways – by raising the incomes or supplying food grains at subsidized prices. While employment generation programmes attempt the first solution, the Public Distribution System (PDS) is the mechanism for the second option. Our government has made consistent efforts to improve availability of food for the poor. Besides the PDS, other programmes such as, the Antyodaya Anna Yojana (AAY), the Annapurna Scheme, National Food for Work Programme (NFFW) have also been launched. Few of these central government sponsored social protection initiatives are presented below: (i) The Public Distribution System (PDS) and the Targeted Public Distribution System (TPDS) PDS continues to be a major instrument of Government’s economic policy for ensuring food security to the poor. ‘Rationing’, as it was originally called, has a long history in India, dating from the Second World War. Introduced by the British government, the PDS was retained after independence as a deliberate social policy. Over time, the PDS, evolved into a national social safety system. In 1984, Government of India created the Ministry of Food and Supplies with the Department of Civil Supplies in charge of the PDS. With a network of more than 4.62 lakh Fair Price Shops (FPS) distributing commodities worth more than Rs 30,000 crores annually to about 160 million families, the PDS in India is perhaps the largest distribution network of its kind in the world. The Central government, through Food Corporation of India (FCI), has assumed the responsibility for procurement, storage, transportation and bulk allocation of food grains to the State Governments. The operational responsibility, including identification of families below the poverty line, issue of Ration Cards and supervision of the functioning of Fair Price Shops (FPS), rest with the State Governments. Under the PDS, presently the commodities, namely wheat, rice, sugar and kerosene, are being allocated to the States/UTs for distribution. Some States/UTs also distribute additional items of mass consumption through the PDS outlets such as cloth, exercise books, pulses, iodized salt and tea, etc. The PDS gave way to the Revamped PDS (RPDS) in 1992 with focus on disadvantageous area. The PDS as it was being implemented, was widely criticized for its failure to serve the population Below the Poverty Line (BPL), its urban bias, limited coverage in the States with high concentration of the rural poor and lack of transparent and accountable

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arrangements for delivery. Therefore, in June 1997, the Government of India modified the PDS into a two-tiered structure known as The Targeted Public Distribution System (TPDS) with focus on the poor. This was the new beginning of targeting the PDS. TDPS beneficiaries The beneficiaries of the TPDS were identified on the basis of a specific poverty line: (i) (ii)

Households existing below the poverty line (BPL households), whose entitlements were subsidized, and Above-the-poverty-line households (APL) who were allocated food grain at cost price.

The BPL households were determined on the basis of population projections of the Registrar General of India for 1995 and the state-wise poverty estimates of the Planning commission for 1993–94.

At present the Government provides 35 kg of food grains, including wheat and rice to 65.2 million families classified as living below the poverty line (BPL). These subsidized rations are made available at a price of Rs. 4.15 per kg for wheat and Rs. 6.65 per kg for rice. To focus the TPDS further, Antyodaya Anna Yojana (AAY) was launched. The TPDS is often considered a key initiative in promoting food security. However, a number of implementation challenges are evident such as non-availability of rationed foodstuffs, problems faced by the poor in accessing BPL entitlement cards, corruption etc. Critics of India’s long standing grain procurement and distribution systems have also raised concerns regarding poor cost efficiency and long-term market distortion resulting from such a system. (ii) Antyodaya Anna Yojana (AAY) Antyodaya means “uplift of the last”. The Antyodaya Anna Yojana scheme, launched in 2000, is to provide special food-based assistance to destitute households. The scheme reflects the commitment of the Government to ensure food security for all and improve the PDS so as to serve the poorest in the rural and urban areas. It is estimated that 5% of the population are unable to get two square meals a day on a sustained basis through out the year. Their purchasing power is so low that they are not in a position to buy food grains round the year even at BPL rates. It is this 5% of the population (ten million of the poorest BPL families) which constitutes the target group of AAY. The scheme provides food grains at the rate of 35 kg per family per month. The food grains are issued by the Government of India @ Rs.2/- (US cents 4.25) per kg for wheat and Rs. 3/- (US cents 6.5) per kg for rice. After the identification of Antyodaya families, distinctive ration cards known as ‘Antyodaya Ration Cards’ are issued to the families based on which the ration is provided.

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(iii) Sampoorna Gramin Rozgar Yojana (SGRY) The Prime Minister in his Independence Day speech in 2001 announced the introduction of a Food for Work Programme to be called “Sampoorna Gramin Rozgar Yojana” (meaning Complete Rural Village Scheme) in all the States/UTs for organizing various employment generation programmes. The main objective of the scheme is to give security to the rural poor. Generation of supplementary employment for the unemployed poor in the rural area is the focus of the scheme. Under the Scheme, food grains are given as part of wages to the rural poor at the rate of 5 kg per man-day. Fifty lakh tonnes of foodgrains are distributed to the labourers as a part of wages at the BPL rate under this programme. Special component of Sampoorna Gramin Rozgar Yojana is also initiated with a view to extending support to the people affected by natural calamities in States/UTs. (iv) National Food for Work Programme (NFFWP) The National Food for Work Programme has been conceived with the objective to provide additional resources apart from the resources available under the Sampoorna Grameen Rozgar Yojana (SGRY) to 150 most backward districts of the country so that generation of supplementary wage employment and providing of food-security through creation of need based economic, social and community assets in these districts is further intensified. Distribution of foodgrains as part of wages under the NFFWP is the focus of the programme and based on the principle of protecting the real wages of the workers besides improving the nutritional standards of the families of the rural poor. Under the scheme, foodgrains are given as part of wages to the rural poor at the rate of 5 kg per man-day. More than 5 kg foodgrains can be given to the labourers under this programme in exceptional cases subject to a minimum of 25% of wages to be paid in cash. The State Governments also takes into account the cost of foodgrains paid as part of wages, at a uniform BPL rate. The workers are paid the balance of wages in cash, such that they are assured of the notified minimum wages. (v) Mahatma Gandhi National Rural Employment Guarantee Act (NREGA) The scheme known as the National Rural Employment Guarantee Act (NREGA) was launched in February 2006 in 200 districts, and was expanded to cover additional 130 districts in 2007–08 and eventually covered all the 593 districts in India by 2008. On October 2, 2009, the scheme has been renamed as Mahatma Gandhi National Rural Employment Guarantee Act or NREGA. The scheme is a landmark in the history of

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social security legislation in India and promises to be a major tool in the struggle to secure the right to food. The scheme provides for the enhancement of the livelihood security of the households in rural areas of the country by providing at least one hundred days of guaranteed wage employment in every financial year to every household whose adult members volunteer to do unskilled manual work at the statutory minimum wage of Rs. 100/day. The scheme has been introduced with the aim of improving the purchasing power of the rural people, primarily semi or un-skilled work to people living in the rural India, whether or not they are below the poverty line. About one-third of the stipulated work force is women. The Central Government outlay for the scheme is Rs. 39,100 crores (US$ 50 m) in the financial year 2009–10. (vi) The Right to Food Act The President of India in August 2009 announced that India would soon pass a Food Security Act which will ensure at least 25 kg of grain (wheat/ rice) at Rs. 3/kg to every household below the poverty line. Aside from an overarching obligation to protect everyone from hunger, as well as to promote sustainable and equitable food production, essential provisions of the proposed Right to Food Act include: ●

●

●

●

a universal Public Distribution System (providing at least 35 kgs of grain per family); special food entitlements for destitute households (including an expanded Antyodaya programme); consolidation of all entitlements created by recent Supreme Court orders (e.g. cooked mid-day meals in primary schools and universalization of ICDS); support for effective breastfeeding (including maternity entitlements and crèches); safeguards against the invasion of corporate interests in food policy; and elimination of all social discrimination in food–related matters.

31.6.2 Programmes/assistance targeted toward specific needy sections of the population In addition, following programmes targeting specific sections of the society, often at individual level to address intra-household inequities or to address the issue of meeting the gap in nutritional requirements and other social needs have been launched. (i) National Social Assistance Programme (NSAP) The National Social Assistance Programme (NSAP) came into effect from

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15th August, 1995. It introduces a National Policy for Social Assistance benefit to poor households in the case of old age, National old Age Pension Scheme (NAOPS), death of primary bread-winner National Family Benefit Scheme (NFBS) and maternity National Maternity Benefit Scheme (NMBS). Under the maternity scheme, benefit is provided in the form of a lump sum cash assistance (Rs. 500) to pregnant women of households below the poverty line. The benefit is restricted to pregnant women for upto the first two live births provided they are of 19 years of age and above. The Schemes under NSAP are implemented through the State/UT Governments with assistance from the Panchayat and Municipal functionaries. (ii) Annapurna Scheme Annapurna is yet another scheme started in 2000, addressing the food security of senior citizens, who though eligible have remained uncovered under the National Old Pension Scheme. Under the Annapurna Scheme, 10 kg of food grains per month are to be provided ‘free of cost’ to the beneficiary. The gram panchayat is required to identify, prepare and display list of persons eligible to receive benefits under the Annapurna Scheme. The Department of Public Distribution, Ministry of Consumer Affairs and Public Distribution ensure the supply of the required food grains. (iii) Village Grain Bank Scheme Village or Community Grain Bank Scheme was launched during 1996–97 by the Ministry of Tribal Affairs with a focus on remote tribal-dominated areas for the prevention of starvation deaths. A revised Village Grain Bank Scheme for establishment of Grain Banks in chronically food scarce areas was approved by Ministry of Finance in February 2006 for the period 2005– 07 subject to its evaluation in the 11th Five Year Plan. The main objective of the scheme is to provide safeguard against starvation during the period of natural calamity or during lean seasons. The grain banks are set up in food scarce area like the drought prone areas, the hot and cold desert areas, tribal areas and the inaccessible hilly areas. An evaluation of the Grain Bank Scheme implemented in Andhra Pradesh is presented in Box 31.8. (iv) Nutritional Programme for Adolescent Girls (NPAG) A Pilot Project – “Nutritional Programme for Adolescent Girls”(NPAG) – was launched by the Planning Commission initially for a period of two years (2002–04) in 51 identified districts on a pilot project basis to provide free food grains to undernourished (weight < 35 kg.)

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Box 31.8 Evaluation of Grain Bank Scheme in tribal areas of Andhra Pradesh [31] The community managed grain banks have been established in the tribal areas of Andhra Pradesh during 1990s under externally aided Andhra Pradesh Tribal Development Project (APTDP) and Andhra Pradesh Participatory Tribal Development Project (APPTDP), funded by IFAD, Rome. Besides, Government of India have also formulated the scheme of grain bank in the year 1996–97 to arrest the starvation deaths in the vulnerable areas of 12 States identified by the Central Planning Committee which included the Chenchu areas of Andhra Pradesh. The main objectives in establishing the grain bank are ●

to combat the problem of food grains scarcity during the lean season.

●

to avoid or reduce dependency on local money lenders or traders for borrowing grains during the lean season at exorbitant rates of interest. to promote the habit of self-help among the tribals.

●

The Tribal Cultural Research and Training Institute (TCR & TI) has conducted Evaluation of Grain Banks in the year 2001 established under APTDP in Tribal Sub Plan areas of East Godavari District and also in Sundipenta ITDA area where the Government of India Scheme of Grain Banks has been under implementation. The specific objectives underlying the study were as follows: ●

Community mobilization strategies adopted in the formation of grain banks.

●

Modus operandi of grain banks.

●

Physical and financial targets and achievements under different schemes.

●

●

Impact on already existing local lending system operated by money lenders and traders. Identifying the factors contributing to the success/failure of grain banks.

●

Lacunae in the implementation of the scheme.

●

Perceptions of the beneficiaries and functionaries for effective functioning of the scheme.

Observations and recommendations ●

●

●

●

●

There was no follow-up after establishing grain banks which led to closure of most of the grain banks. Hence, it was suggested to ensure sustainability of all grain banks by way of motivation, training of beneficiaries and regular monitoring. Constitution of mandal-level community mobilization committees by involving local functionaries to ensure timely motivation especially during harvesting season and also prompt recoveries. There are no permanent storage structures in most of the areas and the collected grain are stored in private houses which are not in good condition. It is essential to ensure construction of storage structures with a part of beneficiary contribution and the beneficiaries should be trained in safe storage methods. Under Government of India scheme, rice was distributed at the rate of 1 quintal per family without educating the beneficiaries regarding the modalities of the scheme and repayment procedures. Hence they are under the impression that it was a free supply of rice and need not be paid back. It is required to educate all the beneficiaries regarding the modalities of the scheme before distributing rice for the sustainability of the scheme. The functionaries of grain banks should be imparted proper training for ensuring transparency in recording the details of loan transactions. If necessary, one of the educated local functionaries should be attached to them for maintenance of the accounts.

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adolescent girls (11–19 years) and expectant and nursing mothers. This scheme was restarted in 2005–06, with the coverage confined to only adolescent girls. As per the revised guidelines of the programme, undernourished adolescent girls as identified by weight would be beneficiaries under the programme, irrespective of financial status of the family which they belong. Free foodgrains, 6 kg per beneficiary per month, is provided to the adolescent girls initially for a period of three months. Those beneficiaries, who cross the cut off point for weight, are discontinued from the programme. Those who in spite of receiving food grains for three consequent months do not show improvement in nutritional status, are investigated by ICDS workers and, if necessary referred to doctor for investigation and treatment, but continue to receive free foodgrains for the next three months. Besides the free food grains, beneficiaries are given regular health check ups and referral services and are imparted appropriate nutrition education. (v) National Programme of Nutritional Support to Primary education (MidDay Meal Programme) The National Programme for Nutritional Support to Primary Education, (popularly known as the MDM) was launched as a centrally sponsored scheme on 15th August 1995. Its objective was to boost “universalization of primary education, by increasing enrolment, retention and attendance and simultaneously impact on nutrition of the students in primary classes”. It was implemented in 2408 blocks in the first year, and covered the whole country in a phased manner in the year 1997–98. The programme originally covered the children of primary stages (classes I to V) in Government, localbody and Govt.-aided schools and was extended in October 2002 to cover children studying in Education Guarantee Scheme (EGC) and Alternative and Innovative Education Centres. The revised MDM scheme is entitled “National Programme of Nutritional Support to Primary Education (NP– NSPE), 2004 and covers over 100 million school children. The central Government provides the following assistance to the States under the MDM programme (a) Free supply of food grains through Food Corporation of India (FCI) @ 100 g of wheat/rice per student per day, and (b) Subsidy for the transport of the food grain from the nearest FCI depot to the primary school – subject to a maximum of Rs. 50 per quintal. MDM provides either cooked lunches or foodgrains to assure food security without caste or gender bias. Its goal is to eliminate classroom hunger and promote balanced socialization along with free and compulsory education to all children. As per provision mentioned in the programme, the meal is to be provided for 200 working days in a year and the rate of mid day meal is Rs. 2 (US 4 cents) per child per day. The meal/food supplement distributed as part of the programme provides roughly 350–450 kcal and 20–30 g protein

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per child per day, which is expected to meet one-third of the energy and half of the protein Recommended Dietary Intakes of the children. The MDM has been successful in significantly increasing school enrolment, improving attendance and keeping students in school. It has been especially beneficial to girls who were earlier discriminated into leaving school prematurely. Conjunctively, the choice of cooks (preferably women) from the lower caste (Dalit) and the construction of cooking sheds have helped to further increase employment and income among the specially targeted socially weaker castes and gender. (vi) Integrated Child Development Services (ICDS) Scheme Started in 1975, the Integrated Child Development Services Programme (ICDS) is one of the most unique, community-based outreach programmes in the world. ICDS is the only major national programme that addresses the health and nutrition needs of children under the age of six. It seeks to provide young children with an integrated package of services, including supplementary nutrition, health care and pre-school education. Since the needs of a young child cannot be addressed in isolation from those of his or her mother, the programme also extends to adolescent girls, pregnant women and nursing mothers. ICDS provides a package of services that consists of supplementary nutrition, immunization, health check-up, referral services, non-formal preschool education, and nutrition and health education. The nutrition norms for the programme are highlighted in Table 31.2. The programme provides an integrated approach for delivering basic services through communitybased Anganwadi workers and helpers, supportive community structures and women groups through the ICDS centres, better known as “Anganwadis”. Besides this, the ICDS Centre is a meeting place where women and mothers’ groups can come together to promote awareness and joint action for child development and women empowerment. The programme is estimated to cover over 4.8 million expectant and nursing mothers and over 23 million children under the age of six. Of these children, more than half participate in early learning activities. Table 31.2 Nutritional norms S. no.

1. 2. 3.

Category

Children (6–72 months) Severely malnourished children (6–72 months) Pregnant women and nursing mothers

Revised (per beneficiary per day) Calories (kcal)

Protein (g)

500 800

12–15 20–25

600

18–20

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31.6.3 Poverty programs and the evolution of public works The ‘Rural Works Programme’, first initiated in 1970/1, was later redesignated as the ‘Drought Prone Areas Programme’ (DPAP). The ‘FoodFor-Work Programme’ was started in 1977 with the aim of utilizing the surplus food stocks of the times. The ‘National Rural Employment Programme’ (NREP) evolved in 1980. The ‘Rural Landless Employment Guarantee Programme’ (RLEGP) was instituted in 1983 to address the plight of the core rural poor. In 1989 NREP and RLEGP were merged to form the Jawahar Rozgar Yojana (JRY) programme that prioritized backward, schedule caste and schedule tribe classes (SC/ST), women and bonded labour. Central and state governments shared the expenses, and wages were paid partly in cash and partly in food. Labour-intensive projects were preferred and operationalized by stipulating a desired wage-tomaterial cost ratio. In 1993 the JRY was again modified, and two of the programme components were dropped and made as independent programmes i.e. – the ‘million wells’ and Indira Awaas Yojana for rural housing – JRY programme, redesigned again in 2001, and renamed as Jawahar Gram Samridhi Yojana. In November 2004 the ‘Food-For-Work’ (FFW) was launched which is planned to be managed with NREGA.

31.6.4 Agriculture initiatives to improve food security Many new initiatives have been undertaken by the governments world over to ensure that the synergies between agriculture and nutrition are successfully exploited and lead to food security and better overall development outcomes. Programmes such as the National Food Security Mission, the Horticulture Mission, the Rashtriya Krishi Vikas Yojana in India and the Conditional Cash Transfer Programmes developed in Mexico in late nineties are reviewed in this section. The National Food Security Mission (NFSM) The objective of the National Food Security Mission is to increase production and productivity of wheat, rice and pulses on a sustainable basis so as to ensure food security of the country. The approach is to bridge the yield gap in respect of these crops through dissemination of improved technologies and farm management practices. The programme has three missions – one each for rice, wheat and pulse. The implementation of the NFSM is expected to result in increasing the production of rice by 10 million tones, wheat by 8 million tones and pulses by 2 million tones by 2011–12.

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National Horticulture Mission National Horticulture Mission was launched by the Government of India during the year 2005–06 (Tenth Five Year Plan) with the objective to promote holistic growth of the horticulture sector in India and to enhance horticulture production. To achieve the above objectives, the mission has adopted the following strategies: 1. Ensure an end-to-end holistic approach covering production, post harvest management, processing and marketing to assure appropriate returns to growers/producers. 2. Promote R&D technologies for production, post-harvest management and processing. 3. Enhance acreage, coverage, and productivity through. ● Diversification from traditional crops to plantations, orchards, vineyards, flower and vegetable gardens. ● Extension of appropriate technology to the farmers for high-tech horticulture cultivation and precision farming. 4. Assist setting up post harvest facilities such as pack house, ripening chamber, cold storages, Controlled Atmosphere (CA) storages etc, processing units for value addition and marketing infrastructure. 5. Adopt a coordinated approach and promotion of partnership, convergence and synergy among R&D, processing and marketing agencies in public as well as private sectors, at the national, regional, state and sub-state levels. 6. Promote National Dairy Development Board (NDDB) model of cooperatives which are appropriate and feasible to ensure support and adequate returns to farmers. 7. Promote capacity-building and human resource development at all levels. Rashtriya Krishi Vikas Yojana The Rashtriya Krishi Vikas Yojana was launched as a central and state sponsored scheme by Government of India in August 2007 with the aim of achieving 4% annual growth in the agricultural sector during the XI Five Year Plan period by ensuring a holistic development of agriculture and allied sectors. The beneficiaries to the programme include individual, families, communities, women and children. The objectives of the scheme, in general, are (i) to provide incentives to the State for increasing public investment in agriculture and allied sectors, and in particular, to ensure that agriculture for the State and districts are prepared based on agroclimatic conditions, availability of technology and natural resources; (ii) local needs/crops/priorities are better reflected in the agricultural plan

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of the State; (iii) reduce yield gaps in important crops through focused interventions; (iv) maximum returns is obtained by farmers in agriculture and allied sectors; (v) increase in production and productivity of various components of agriculture and allied sectors by addressing them in a holistic manner. Conditional Cash Transfer Programme (CCT) Conditional Cash Transfer Programme is a novel approach to social safety net developed in Mexico in the late nineties. CCT programme involves the direct transfer of cash to poor households, with the condition that the household undertake specific actions such as enrolling and maintaining their children in schools, and complying with a schedule of health visits for mothers, young children and other household members. CCT programmes are usually targeted to the poor households or other vulnerable population groups, and benefits are often specifically targeted to the women in the household [32]. The overarching goal of CCTs is to reduce poverty and food insecurity in the short term while providing an incentive for poor families to invest in their children and hence alleviate poverty in the long term. The CCT programme is expected to influence nutrition through a combination of several pathways; one potential pathway is through increasing income and access to food, thereby increasing household food consumption, another pathway may be through improved water and sanitation and/or greater use of health services and the resulting prevention and better control of infectious diseases. The CCT programme of Mexico is being critically reviewed for adoption in India policy. Global and the Indian perspective of food and nutrition security, presented in the chapter, highlights the fact that access to food and good nutrition is largely governed by socio-economic, environmental factors. An integrated approach to address poverty, unemployment, targeting alternate and sustainable livelihood and economic empowerment is essential. Social protection initiatives, rural development schemes and policies, micro-enterprises, employment generation schemes etc., are all vital links to ensure food security at household level, particularly in rural areas. An integrated approach together with economical agricultural productivity is critical to mitigate food security challenges, to a great extent, in developing countries.

References 1. SWAMINATHAN MS, Oct 2, 2008, Hindu. 2. India at a Glance. http://devdata.worldbank.org/AAG/ind_aag.pdf. Accessed on 11/7/08.

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3. FAO Statistical Year Book. www.fao.org/statistics/yearbook/vol_1_2/pdf/ India.pdf. Accessed on 11/7/08. 4. Agriculture for Development, World Development Report, 2008. The World Bank, Washington DC. Accessed on 14 December 2009. 5. Understanding the Dynamics of Food Insecurity and Vulnerability in Himachal Pradesh, India. ESA Working Paper No 07-22. FAO, May 2007. 6. FOSTER P. (1992). The world food problem: Tackling the causes of undernutrition in the Third World. Boulder. 7. QUISUMBING AR et al. (1995). Women: The key to food security. IFPRI Food Policy Report. Washington. 8. GROSS , R . et al. (1998). Community nutrition: definition and approaches. Encyclopedia of Human Nutrition. M. Sadler, S. Strain and B. Caballero (eds). 9. Food Security and Nutrition. Cambodian Food Security and Nutrition website. http://www.foodsecurity.gov.kh/CamSituation.aspx 10. ROSEGRANT MW, MSANGI S, SULSER T and RINGLER C (2007). “Future Scenarios for Agriculture: Plausible Futures to 2030 and Key Trends in Agricultural Growth.” Background paper prepared for the World Development Report 2008. 11. BOUIS H (2002). Plant breeding: A new tool for fighting micronutrient malnutrition. Journal of Nutrition. 132(3):491S. 12. VON BRAUN J, SWAMINATHAN MS, ROSEGRANT MW (2004). Agriculture, Food Security, Nutrition and the Millennium Development Goals. 2003–2004. Annual Report Essay. IFPRI: Washington DC. 13. World Bank and International Food Policy Research Institute (2007). From agriculture to nutrition, Pathways, Synergies and Outcomes. Report No. 40196GLW. Washington DC. 14. The Agricultural Production in India. http://faostat.fao.org, Accessed 15 December 2009. 15. Agricultural and Processed Food Products Export Development Authority. http:/ /www.apeda.com/apedawebsite/six_head_product/FFV.htm. (Accessed on 27/ 8/08). 16. Food Security, Policy Brief. Issue 2, FAO, June 2006. 17. 2008 India State Hunger index: Key Findings and Facts. http://www.ifpri.org/ publication/2008-india-state-hunger-index-key-findings-facts. Accessed 30th January 2010. 18. Nutritional Intake in India, 2004-2005, NSS 61st Round. July 2004 – June 2005. National Sample Survey Organisation. Report No. 513 61/1.0/6). Ministry of Statistics & Programme Implementation. Government of India, May 2007. 19. Nutritional Intake in India 1999-2000. NSS 55th Round. July 1999 to June 2000. Report No. 471(55/1.0/9). National Sample Survey Organisation. Ministry of Statistics & Programme Implementation. Government of India. August 2001. 20. Reported Adequacy of Food Intake In India: 1993–94, Fifth Quinquennial Survey of Consumer Expenditure, Nss 50th Round July 1993 – June 1994, Report No.415; National Sample Survey Organisation, Department of Statistics, Government of India. http://mospi.nic.in/rept%20_%20pubn ftest.asp?rept_id=415&type=NSSO. Accessed on 11/7/08. 21. The Food Insecurity Atlas of Rural India, Swaminathan Research Foundation (2001). 22. Understanding the Dynamics of Food Insecurity and Vulnerability in Orissa, India. ESA Working Paper No 07-28. FAO, October 2007 (22).

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23.

BLOCK S , KIESS L , WEBB P, KOSEN S, MOENCH - PFANNER R, BLOEM MW

24.

25.

26. 27.

28. 29. 30.

31. 32.

and TIMMER CP (2004). Macro shocks and micro outcomes: child nutrition during Indonesia’s Crisis. Economics and Human Biology, 2(1): 21–44. TORLESSE H , KIESS L and BLOEM MW (2003). Association of household rice expenditure with child nutritional status indicates a role for macroeconomic food policy in combating malnutrition. J Nutr, 133(5): 1320–1325. Climate Change, Water and Food Security. Technical Background Document From the Expert Consultation Held on 26 to 28 February 2008, FAO, Rome. ftp://ftp.fao.org/docrep/fao/meeting/013/ai783e.pdf. Accessed on 24-7-08. Climate Change: Impact on Agriculture and Costs of Adaptation, International Food Policy Research Institute (IFPRI), 2009 (26). Projections by the International Food Policy Research Institute. http:// www.ifpri.org/pressroom/briefing/impact-climate-change-agriculture. Accessed 15th January 2010. Government of India. Planning Commission, Report of the Steering Committee on Nutrition for the Tenth Plan (2002–2007), September 2002. National Commission on Farmers. http://kisanayog.gov.in/. Accessed on 28-8-08. Poverty Estimates for 2004–05, Planning Commission, Government of India, March 2007, http://www.planningcommission.gov.in/news/prmar07.pdf. Accessed 21 July 2008. Evaluation of the Grain Bank Scheme in Andhra Pradesh. Tribal Cultural Research and Training Institute. www.aptribes.gov.in. Accessed 15-12-09 (31) ADATO AND HODDINOTT (2007). Conditional Cash Transfer programme. A magic bullet for reducing poverty? 2020 Focus Brief on Worlds poor and hungry people IFPRI : Washington DC.

32 Food and nutrition situation in India K. Vijayaraghavan

K. Vijayaraghavan, formerly Head of Department of the Division of Community Studies at the National Institute of Nutrition, India, is a medical graduate with Masters in Community Health and Nutrition from the University of London. During his forty years of research experience, Dr. Vijayaraghavan was involved with the National Nutrition Monitoring Bureau (NNMB) and is recognized for his research contributions in the areas of prevention of vitamin A deficiency, household food security studies, micronutrients deficiencies of iron and iodine, and development and implementation of behavioural change communication.

32.1

Introduction

India, though has made substantial progress in improving life expectancy at birth and reducing infant and maternal mortality since independence, still it shelters a large proportion of population suffering from ill-health and preventable undernutrition. Undernutrition contributes to 35% of all deaths due to all major causes like diarrhea, pneumonia, malaria, measles etc [1]. Despite an unequivocal commitment in the Constitution of India that “State shall regard the raising of the level of the nutrition and the standard of living of its people and the improvement of public health among its primary duties”, malnutrition continues to be an important public health problem in India even after about 60 years of independence, with a major share of undernourished people in the world. The UN General Assembly, in the year 2000, adopted the Millennium Development Declaration [2] with nutrition related goals: to halve the proportion of the world’s people who suffer from hunger by the year 2015; to reduce maternal mortality by three quarters; and under five year child mortality by two thirds, of their current rates. India is signatory to the Millennium Development Goals. Adequate food and good nutrition being the basic human need, is recognized in the Millennium Development Goals (MDGs), which emphasize eradication of extreme poverty and hunger and

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promote the empowerment of women as effective ways to combat poverty, hunger and disease and to stimulate sustainable development.

32.1.1 Hunger in India The International Food Policy Research Institute (IFPRI) developed the Global Hunger Index (GHI) [3] as an approach to measuring and tracking progress on hunger, and seeking solutions to preventing hunger and improving nutrition (See Box 32.1). Box 32.1 Global Hunger Index (GHI) ●

●

●

●

●

The GHI has been developed by the International Food Policy Research Institute (IFPRI) as a tool for calculating hunger and malnutrition. It supports the measurement of progress of the global fight against hunger and thus helps in monitoring of the UN Millennium Development Goals. The GHI was established in 2008 for 120 developing countries and newly industrialized countries. It combines three equally weighted indicators: (a) the percentage of the population undernourished (reflecting the share of the population with insufficient dietary intake); (b) the prevalence of underweight children among under-fives (indicating the proportion of children suffering from weight loss and/or reduced growth); and (c) the mortality rate of children under the age of five (partially reflecting the mortality as a result of synergy between dietary intake and unhealthy environments). The GHI contributes to a comprehensive understanding of hunger; provides for a quick overview; makes visible factors characterizing the specific food security situation in a country and facilitates making apparent the progress and failures in the fight against poverty and hunger. The GHI is, of course, limited by the collection of accurate data by various governments and international agencies.

India’s GHI score is 23.7, which ranks it 66th out of 88 countries. The GHI of some of the developing and third world countries for the year 1990 and 2008 is presented in Table 32.1 which shows that as compared to the year 1990, there is an improvement in the over all situation of global hunger in 2008. The GHI of India is worse than all its neighbouring countries, except Bangladesh. Table 32.1 Global Hunger Index of some developing countries 2008 Country Mauritius Malaysia China Thailand Sri Lanka Nepal Pakistan India Bangladesh

GHI 5.0 6.5 7.1 9.9 15.0 20.6 21.7 23.7 25.2

1990 Rank 1 10 15 23 39 57 61 66 70

GHI 6.1 9.5 11.6 18.4 19.1 27.6 25.3 32.5 32.3

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32.1.2 Indian State Hunger Index (ISHI) It was calculated on the same lines as Global Huger Index for 17 states in 2008 (See Box 32.2). Box 32.2 India State Hunger Index (ISHI)

●

The ISHI is a tool to calculate hunger and malnutrition at the regional level in India. It is constructed in the same fashion as the Global Hunger Index (GHI) 2008 for 17 states in India, covering more than 95 percent of the population. The India State Hunger Index (ISHI) represents the index calculated using a calorie undernourishment cut-off of 1,632 kcal per person per day to allow for comparison of the India State Hunger Index with the Global Hunger Index 2008. The ISHI score for India using this cut-off is 23.3 and corresponds more closely with the GHI 2008 score for India of 23.7 than any other calorie cutoff. The ISHI ranges between 13.6 in Punjab and 30.9 in Madhya Pradesh.

●

Punjab is ranked 34 in the 2008 country rankings while MP is ranked 82.

●

Twelve of the 17 states fall into the “alarming” category, and Madhya Pradesh into the “extremely alarming” category. ISHI scores though are closely aligned with poverty, there is little association with state level economic growth. High levels of hunger are seen even in states that are performing well from an economic perspective. Inclusive economic growth and targeted strategies to ensure food sufficiency, reduce child mortality and improve child nutrition are urgent priorities for all states in India.

●

●

●

●

●

●

All the 17 states had Inter State Hunger Index (ISHI) scores well above the “low” and “moderate” hunger categories and 12 states fall into the “alarming” category, with Madhya Pradesh in the “extremely alarming” category (Figure 32.1). While the ISHI scores are closely aligned with poverty, there is little association with economic growth at the state level. Therefore, high levels of hunger are seen even in states that are performing economically well. Inclusive economic growth and targeted strategies to ensure food sufficiency, reduction in child mortality and improvement in child nutrition are urgent priorities for all the states in India. It is particularly essential to improve the food security among the socio-economically vulnerable sections of the society through out all the seasons but especially during the times of stress and disasters such as drought.

32.2

Food security

The FAO (1992) [4] reported that at least one fifth of the world’s population – about 800 million people of the developing countries – suffer from chronic

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32.1 Interstate Hunger Index – India (IFPRI, 2009).

undernutrition. These undernourished millions are trapped in a vicious cycle of not getting adequate food regularly, unable to lead a healthy and active life and inability to either produce or procure required food. In India, the results of the National Sample Survey Organization (NSSO) indicate that self-reported hunger at the national level is about 2%; in the rural areas it is 2.4% while in the urban areas it is only 0.5% (5). In other words, the household food security, in the opinion of the community, is satisfactory. Access to adequate food, which is one of the fore-most basic needs of life, is the fundamental right of every single human being on this earth. There can be food security in the population only when every one at all the times has both physical and economic access to sufficient food to meet their dietary needs for a productive and healthy life (USAID, 1992) [6]. The FAO Committee on World Food Security (1983) [7] incorporated the following specific goals for food security (i) ensuring adequacy of food supplies and (ii) maximizing stability, emphasizing thus that availability, access, affordability and adequacy are essential for food security. Food security, thus, should include physical, economic and social access to a balanced diet, safe drinking water, environmental hygiene and primary health care. This requires concurrent attention to the availability of food, the ability to buy needed food and the capability to absorb and utilise the food in the body. Thus, food as well as non-food factors, such as drinking water, environmental hygiene and primary health care are involved in food security.

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32.2.1 Production and availability of foods in India The food security in India, at the national level, is reportedly improving with the estimated overall production of food grains at 217.3 MT in 2006– 07 as compared to about 108 MT in 1970–71. In India, though apparently food security at the national level may have been achieved, household and/or individual food security continues to be an important problem particularly among the low socioeconomic groups of population. The productions of food grains, between 1950–51 and 2006–07, increased at an average annual rate of 2.5 per cent, marginally higher than the average annual population growth rate of 2.1% during the corresponding period. As a result, India almost became self-sufficient in food grains with hardly any imports during 1976–77 to 2005–06. However, the production of pulses shows no increase in the fifteen years in the period 1990–2005 (Figure 32.2). Consequently, the consumption of pulses has declined from 42 g per capita per day (72 g in 1956–57) to 33 g per capita per day during the same period. Table 32.2 Production of food grains – time trends [8] Year Crop

2003–04

Rice Wheat Coarse cereals Pulses Total foodgrains

88.5 72.2 37.6 14.9 213.2

2004–05 83.1 68.6 33.5 13.1 198.4

2005–06

2006–07

91.8 69.4 34.1 13.4 208.6

93.4 75.8 33.9 14.2 217.3

2007–08* 94.1 74.8 36.1 14.3 219.3

*Estimates

32.2 Total production of food grains in India by year.

India ranks first in the world with respect to milk production, which increased from 17 MT in 1950–51 to about 102 MT by 2007–08. The per

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Public health nutrition in developing countries

capita availability of milk has also increased from 112 g in 1968–69 to 246 g per day during 2006–07. Though it is still low compared to the world average of 265 g per day, it is more than the recommended intakes per consumption unit (sedentary adult male) (Figure 32.3) [9]. The efforts of the governments in the dairy sector are currently concentrated on the promotion of dairy activities in non-Operation Flood area with emphasis on building up cooperative infrastructure, revitalization of sick dairy cooperatives and federations and creation of infrastructure at state level for production of quality milk and milk products.

32.3 Production and availability (per capita) of milk in India – Time Trends.

While there are debates and concerns about food security, it is important to recognize that we are yet to achieve nutrition security, meaning that the diets do not yet provide all the nutrients in proper amounts. Though the production of cereals appears adequate, the per capita availability of pulses, the only rich source of protein for the poor, actually shows a decline as compared to that in 1960–61. Unfortunately, the food insecurity is observed all round the year for protective foods like pulses, milk and milk products, making it difficult for the individuals to meet their nutrient requirements.

32.2.2 National Food Security Mission The Government of India has launched a National Food Security Mission (NFSM) to increase the production of rice, wheat and pulses. The Mission aims at increasing food grains production of the above crops through expansion in the area and enhancement in productivity; restoring soil

Food and nutrition situation in India

885

fertility and its productivity; creating employment opportunities; and enhancing farm level economy to restore confidence of farmers of 305 targeted districts. The districts are selected in different states with emphasis on specific food crops and are referred as (1) Rice districts, (2) Wheat districts, and (3) Pulse districts [10]. Besides the NFSM, the government launched the National Horticulture Mission (NHM), which was initiated during 2005–06 for holistic development of the sector with the objectives to enhance horticulture production through area-based regionally differentiated strategies; improve nutritional security and income support to farm households; establish convergence and synergy among ongoing programmes for horticulture development; and, promote, develop and disseminate technologies. The area and production of horticultural crops is presented in Table 32.3. Following the launch of the NHM, an increase in area and production is evident. In 2006–2007, of the total horticulture production, vegetables contributed to 59.8% and fruits to 30.9%. Table 32.3 Area production of vegetables, roots and tubers and fruits [9] 2004–05

2005–06

2006–07

Area (‘000 ha)

Production (‘tonnes)

Area

Production

Area

Production

6744

101246

7131

110106

7211

111770

32.3

Dietary consumption pattern in India

Indian population, by and large, depends, on foods of plant origin with cereals – rice and wheat – forming the bulk of the dietaries. NNMB surveys [11, 12] reveal that the consumption of protective foods like pulses, vegetables, milk and milk products is woefully inadequate and much below the ICMR recommended dietary allowances (Table 32.4). Table 32.4 Consumption of foods (g/day) among rural communities – NNMB Food

Cereals

Millets

Pulses

GLV

Other vegetables

Roots and Milk tubers

Oils

Consumption unit*

344

52

28

16

49

60

82

14

14

460

40

40

60

50

150

20

300

RDI (ICMR)

Sugar and jaggery

* For consumption unit, see Box 32.3.

Over the years, the practice of consumption of qualitatively superior diet consisting of mixed cereals, containing particularly coarse grains

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Public health nutrition in developing countries

Box 32.3 Consumption unit Diet surveys involve assessment of diet and nutrient intakes of different individuals belonging to different ages and physiological groups. In such cases, the usual practice is to assess the requirements of different groups in terms of those of the average man by applying calorie coefficients, which are referred to as consumption units. The energy consumption of an average male doing sedentary work is taken as one consumption unit, which corresponds to energy requirements of 2400 kcal/day. The other coefficients are worked on the basis of their calorie requirements as a proportion of the above. For more information on the consumption units for different age and physiological groups details are available in a document on nutritive value of foods [13].

like millets, is showing a significant decline. The surveys conducted by the NNMB [11] indicate that the intake of coarse grains like millets is confined mostly to the States of Gujarat (maize, bajra), Maharashtra (Jowar), Karnataka (ragi) and Madhya Pradesh. Even the NSSO surveys indicate that there has been a significant decline in the consumption of coarse cereals like millets during 1972–73 and 1999–2000 (Table 32.5). Table 32.5 Time trends in consumption of coarse cereals in India [14] Group

Rice and Wheat (kg/month) 1972–73 1999–2000

Lowest income Pooled

3.4 10.5

8.3 11.3

Coarse cereals (kg/month) 1972–73 1999–2000 2.4 4.8

1.4 1.4

Though a large majority of the population is non-vegetarian, the contribution of animal foods is very small and infrequent, mainly due to economic reasons. The diets, thus, are poor in micronutrients. High levels of poly-phenols and phytates in the Indian diets further interfere with the absorption of nutrients leading to inadequacy of micronutrients. The National Nutrition Monitoring Bureau (NNMB) under the auspices of the Indian Council of Medical Research (Box 32.4) has been presenting annual data on diet and nutritional status for the past 40 years.

32.4

Trends in nutrient intake

The nutrients intakes for the age group 1–3 years and 4–6 years against the RDA are presented in Tables 32.6 and 32.7, respectively. The data is based on the 2002 and 2006 NNMB report for the rural region in 9 states (Andhra Pradesh, Gujarat, Karnataka, Kerala, Madhya Pradesh, Maharashtra, Orissa, Tamil Nadu and West Bengal) of the country [11, 12].

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Box 32.4 National Nutrition Monitoring Bureau (www.nnmbindia.org) ●

●

●

●

●

●

●

●

The Indian Council of Medical Research (ICMR) established the National Nutrition Monitoring Bureau (NNMB) in 1972 – with Head quarters in National Institute of Nutrition, Hyderabad – in the States of Kerala, Tamil Nadu, Karnataka, Andhra Pradesh, Maharashtra, Gujarat, Madhya Pradesh, Orissa, West Bengal and Uttar Pradesh. The main objectives of the NNMB are to collect data on a continuous basis on dietary and nutritional status of the population in each of the States, and to evaluate the on-going National Nutrition Programmes, identify their strengths and weaknesses and recommend mid-course corrections to improve their effectiveness. Initially, the Bureau carried out annual surveys in four randomly selected districts from four strata formed on the basis of certain developmental criteria at the district level, from each State. From the year 1982, the NMMB has been adopting the sample frame of National Sample Survey Organization (NSSO) developed for its Consumer Expenditure Surveys covering a subsample of villages, which enabled sufficient spatial representation of the sample. The NSSO adopts a two stage stratified random sampling method in which the villages formed the first stage units (FSU), while the households (HHs) formed the second stage units (SSU). For the purpose, each State is divided into different agro-economic regions. Each region within a State consists of groups of contiguous districts having similar cropping pattern and population density. A district or part of the district with rural population of less than 1.8 millions forms one stratum. Districts with rural population of more than 1.8 million are divided into two or more strata by grouping contiguous talukas/tehsils having similar cropping pattern and population density. Such an approach helped in calculating, in future, unbiased estimates of the diet and nutrition situation of the community by applying design-based multipliers obtained from the NSSO. The unique feature of NNMB is conducting two repeat surveys in rural areas in the same villages which were surveyed in the years 1975–79. The results of the repeat surveys helped in assessing the changes in diet and nutritional status of rural communities. The results of all the annual surveys are published in the form of technical reports – to date 25 technical reports have been published. The results of the surveys carried out till the year 1995 were compiled as a publication entitled “25 years of National Nutrition Monitoring Bureau” (1997). The National Nutrition Monitoring Bureau (NNMB) also carried out special studies on micronutrient deficiency (MND) survey in 10 states including biochemical estimations of serum vitamin A, hemoglobin and urinary iodine. The bureau also conducted a cross-sectional survey of assessment of hypertension and diabetes mellitus in the rural areas.

Source: www.nnmbindia.org

About 70% of the children in the age group of 1–3 years and 4–6 years consume inadequate amounts of energy (Tables 32.6 and 32.7). The protein intake is inadequate (<70 percent RDA) in 40 percent of 1–3 year old children, while less than 10 percent of the 4–6 year old children consume inadequate protein daily. Thus, it is clear that the primary limiting factor in the Indian dietaries, among the poorest segments of rural India, is ‘food

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Public health nutrition in developing countries

Table 32.6 Trends in intakes of nutrients for preschool children (1–3years) [11, 12] Nutrient

RDA

2002 Intake % RDA %consuming % RDA > 70

Energy (kcal) Protein (g) Fat (g) Calcium (mg) Iron (mg) Vitamin A (µg) Thiamin (mg) Riboflavin (mg) Niacin (mg) Vitamin C (mg) Free Folic

719 729 22 19.5 – 12.1 400 221 12 5.3 400 106 0.6 0.4 0.7 0.3 8 5.1 30 17 30 20.4

101.3 88.6 – 55.2 44.1 26.5 66.6 42.8 63.7 56.6 68.0

29.5 62.3 22.7 18.5 15.1 8.0 39.1 18.7 36.2 23.0 40.0

Intake

2006 %RDA %consuming %RDA

< 50 38.0 17.4 63.1 69.7 72.1 87.5 43.7 69.8 41.8 66.1 37.5

719 20.2 10.7 245 5.7 129 0.5 0.3 5.2 17 20.3

100.0 91.8 – 61.2 47.5 32.2 83.3 42.8 65.0 56.6 67.6

> 70

< 50

28.9 63.3 – 29.6 19 9.4 42.5 21.6 38.7 14.8 38.8

41.7 18.9 – 58.3 66.8 85.8 42.9 66.4 40.7 76.5 41.1

Acid (µg)

Table 32.7 Trends in mean dietary intakes of nutrients for preschool children (4–6 years) [11, 12] Free Folic Nutrient

RDA

2002

2006

Intake % RDA % consuming %RDA % consuming %RDA %RDA >70% <50% Intake >70% 50% Energy (kcal) Protein (g) Fat (g) Calcium (mg) Iron (mg) Vitamin A (µg) Thiamin (mg) Riboflavin (mg) Niacin (mg) Vitamin C (mg)

1690 30 – 400 18 400 0.9 1 11 40

Free Folic Acid (µg) 40

1066 63.0 28.2 94.0 15 – 239 59.7 8.1 45.0 127 31.7 0.7 77.7 0.4 40.0 8.1 73.6 24 60.0

30.6 73.4 29.7 28.1 15.3 9.6 44.6 5.6 49.1 25.3

24.1 6.5 51.2 55.3 70.7 87.3 26.3 83.0 23.4 60.7

1020 28.7 12.7 272 8.6 166 0.7 0.4 7.9 25

60.3 95.6 – 68.0 47.7 41.5 77.7 40.0 71.8 62.5

25.9 72.9 – 34.0 18.3 10.9 45.0 6.4 45.8 25.8

31.3 8.6 – 49.5 66.4 84.0 28.6 82.5 27.9 63.1

30.2

49.0

24.9

28.8

72.0

44.7

31.7

75.5

gap’ and not protein deficiency as was, hitherto, believed. However, decreasing trend in consumption of pulse is of concern since it would adversely influence the quantity and quality of protein. More than twothirds of the households and individuals consume less than 70% of RDA of other vital nutrients like vitamin A, iron and vitamins B-complex. In the case of younger children in the age group of 1–3 years, over 80 percent children consume less than 70 percent RDA of vitamin A, while almost 70 percent consume less than 50% RDA of iron. The nutrient intakes of adolescent girls in the age group of 10–12 years are presented in Table 32.8. The proportion of the adolescent girls consuming less than 50 percent RDA of energy seems to increase between the years 2002 to 2006. The intake of iron, calcium and vitamin A is rather low.

Food and nutrition situation in India

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Table 32.8 Trends in mean dietary intakes of nutrients for adolescent girls (10–12 years) [11, 12]

Nutrient

RDA

Intake

Energy (kcal) 1970 1500 Protein (g) 22 39.4 Fat (g) 57 18.9 Calcium (mg) 600 304 Iron (mg) 19 12.1 Vitamin A (µg) 600 174 Thiamin (mg) 1.0 1.0 Riboflavin (mg) 1.2 0.5 Niacin (mg) 13 11.7 Vitamin C (mg) 40 32 Free Folic Acid (µg) 70 42.4

2002

2006

% consuming Intake (% RDA) >70 % < 50 %

%consuming (% RDA)

56.6 41.1 51.3 22/0 11.2 9.2 65.6 10.5 70.4 35.0 29.0

8.5 23.8 30.5 63.2 77.5 87.8 19.0 74.0 8.5 51.9 42.0

1389 37.8 14.8 307 11.5 205 0.9 0.5 11.1 33 39.3

>70 %

<50%

46.7 35.5 – 21.8 27.5 9.2 59.7 8.2 63.0 36.8 25.4

16.6 27.5 – 65.2 51.9 87.4 21.7 78.7 16.2 50.5 46.9

The average energy nutrient intake among adult women seems to decrease in all these groups of adult women such as non-pregnant-nonlactating as well as pregnant and lactating women (Tables 32.9, 32.10 and 32.11). In the case of pregnant women, almost a third have energy intake of less than 70 percent RDA. In the case of micronutrients, a very high percentage of women consume less than 50 percent of RDA. Table 32.9 Trends in mean dietary intakes of nutrients for adult women [11, 12] 2002 Nutrient

2006

RDA

Intake

% consuming (% RDA) >70% <50%

Intake

% consuming (% RDA) >70%

<50%

Energy (kcal) 1875 Protein (g) 50 Fat (g) – Calcium (mg) 400 Iron (mg) 30 Vitamin A (µg) 600 Thiamin (mg) 0.9 Riboflavin (mg) 1.1 Niacin (mg) 12 Vitamin C (mg) 40 Free Folic Acid (µg) 100

1878 48.2 27.6 445 14.1 219.8 1.2 0.6 14.9 44.7 51.6

89.1 78.3 77.0 60.9 14.7 11.2 86.1 26.7 91.1 51.4 17.0

1738 46.5 21.8 443 13.8 254 1.1 0.6 14.2 47 50.6

81.0 76.3 – 60.5 15.3 11.8 83.2 24.4 86.6 51.2 16.1

4.2 5.9 – 23.2 68.6 84.3 5.6 50.8 4.3 33.3 55.9

1.4 4.7 10.9 24.5 67.9 85.7 4.5 47.9 1.9 14.4 55.3

32.4.1 Intrafamily distribution of nutrients An analysis of intra-family distribution of dietary energy in the households was carried out by comparing the adequacy of energy intakes, as per the RDI, of those of preschool children in each household with those of their parents and other elders. The intra-family distribution of dietary energy was assessed from 24-hour dietary recall data collected by the NNMB in seven states in India during 1996–97. The energy consumption, expressed

890

Public health nutrition in developing countries

Table 32.10 Trends in mean dietary intakes of nutrients for pregnant women [11, 12] 2002

Nutrient

RDA

Intake

Energy (kcal) 2175 1933 Protein (g) 65 49.7 Fat (g) – 25.9 Calcium (mg) 1000 463 Iron (mg) 38 14.0 Vitamin A (µg) 600 227 Thiamin (mg) 1.1 1.2 Riboflavin (mg) 1.3 0.7 Niacin (mg) 14 15.1 Vitamin C (mg) 40 45 Free Folic Acid (µg) 400 53.1

2006

%consuming (% RDA) < 50 > 70

Intake

%consuming (% RDA) < 50 > 70

1.6 15.4 12.8 24.5 68.1 82.4 8.5 54.8 3.2 36.2 55.3

1726 46.8 22.5 456 14.0 261 1.1 0.6 13.7 42 50.3

7.5 18.2 – 67.4 80.2 83.4 15.0 62.6 8.6 36.9 100.0

75.5 48.4 75.0 61.2 15.4 13.3 82.4 16.0 87.8 50.5 21.8

63.6 46.5 – 17.1 5.3 12.3 73.8 15.5 73.8 45.5 0.0

Table 32.11 Trends in mean dietary intakes of nutrients for lactating women [11, 12] Nutrient

RDA

2002 Intake

Energy (kcal) 2425 Protein (g) 75 Fat (g) – Calcium (mg) 1000 Iron (mg) 30 Vitamin A (µg) 950 Thiamin (mg) 1.2 Riboflavin (mg) 1.4 Niacin (mg) 16 Vitamin C (mg) 80 Free Folic Acid (µg) 150

2028 50.3 25.9 408 14.6 212 1.3 0.6 16.3 48 57.6

2006

% consuming (% RDA) > 70 < 50 82.3 46.9 74.9 54.9 15.3 9.3 83.8 15.1 83.8 53.9 23.4

1.3 13.9 13.2 27.4 71.1 86.7 7.8 64.1 3.0 32.3 45.4

Intake

1878 49.6 22.1 447 14.7 249 1.2 0.6 15.5 46 55.2

% consuming (% RDA) > 70 < 50 71.6 47.1 – 17.6 17.6 7.9 84.4 15.2 81.9 24.2 3.5

3.7 13.4 – 72.0 66.5 89.9 6.6 63.7 4.2 64.3 83.5

as percentage of recommended dietary intake (%RDI) for preschool children, schoolchildren, and adolescents was compared with that of adult men and women in the same households. The data on energy consumption of adult males and females and children from +1 to +4 years is presented in Table 32.12, which presents the comparison of the percentage of preschool children consuming adequate energy according to different ages with that of adults when their diets were either adequate or inadequate. The results revealed that about one third of the preschool children had inadequate intakes of energy even when their adult counterparts had an adequate intake [15]. There were no difference between sexes in any of the age groups, with respect to intra-family food distribution. The time trends in the intra-family distribution of dietary energy were assessed by comparing the data with those collected in 1975–80 using the

Food and nutrition situation in India

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Table 32.12 Adequacy (%) of energy consumption by age – preschool children and adults Energy consumption category

% of children age-wise (years) in specific energy consumption category

Adult male (M) and female (F)

Child

1+

2+

3+

4+

Both M and F adequate Both M and F adequate Either M or F inadequate Either M or F inadequate Both M and F inadequate Both M and F inadequate

Adequate Inadequate Adequate Inadequate Adequate Inadequate

13.0 57.7 1.8 17.6 1.0 8.9

33.9 41.1 4.6 12.9 1.2 6.3

42.5 33.1 6.6 10.2 1.3 6.3

32.0 42.1 4.0 14.0 0.5 7.4

same procedures in the same villages. The analysis revealed a significant increase in the proportion of preschool children consuming inadequate energy, although both adult men and women were consuming energyadequate diets during 1996–97 as compared to those surveyed in 1975– 80. These results reflect the inappropriate child feeding and caring practices prevailing in the community, perhaps, due to mothers’ ignorance about the child’s energy requirements indicating the need for effective nutrition education for parents regarding appropriate feeding of their children for meeting the nutritional needs.

32.4.2 Socioeconomic status and diet The socioeconomic status of the households plays an important role in the dietary pattern of the families. The dietary consumption among the landless agriculture labor and the socially backward scheduled castes and scheduled tribes, particularly, is not satisfactory. Poverty and ignorance are the major determinants of dietary consumption in these households. Even if all their income is spent on food, the poor families will not be able to meet the nutrient requirements. The average per capita consumption expenditure for rural and urban population as per 61st Round of NSSO (2004–05) is Rs. 558.78 and Rs. 1,052.36, respectively. In the rural households, on an average the consumption expenditure on food is about 55 per cent and remaining 45 per cent on non-food items. Rural population divided on the basis of their monthly per capita expenditures (MPCEs) exhibit consumption patterns as presented in Table 32.12. Rural poor (below poverty line/BPL) are spending about 31–35 per cent of their total consumption expenditure on non-food items and remaining on food items (Table 32.13). NSSO consumption expenditure surveys indicate that expenditure on food has declined without any apparent increase in the cereal consumption, except in the lowest income group. It might be because cereal requirements, perhaps considered to be important by the community, are being met.

892

Public health nutrition in developing countries Table 32.13 Expenditure on food and nonfood items according to MPCE** MPCE Classes of Rural Population (Rs) 0–235 235–270 270–320 320–365 365–410 410–455 455–510 510–580 580–690 690–890 890–1155

Expenditure % Food Non-food 68.45 67.16 66.35 64.78 63.99 62.93 61.61 60.11 58.02 53.92 49.80

31.55 32.84 33.65 35.22 36.01 37.06 38.39 39.88 41.98 46.08 50.20

*BPL – Below Poverty Line **MPCE – Monthly Per Capita Expenditure of BPL is Rs. 356.30 (Source: NSSO, 2004–05)

Unfortunately, the pulse consumption among all the segments showed a decline due to the continuous escalation of prices. Consequently dietary diversification is observed mainly in middle and high-income groups in urban and rural areas. There has been only a small increase in energy consumption among the poor despite widespread distribution of subsidized foods through Public Distribution System (PDS) to the BPL families. On the other hand, the energy consumption of the urban high-income group is achieved through increased quantities of sugar, oil, milk and milk products and lowering quantities of cereals. Such changes in the energy density of the diet and sedentary lifestyles are likely to lead to steep increase in over weight and obesity among this group.

32.5

Nutritional status – trends in children and adults

NNMB surveys indicate that Indians of lower socio-economic group, in general, are shorter and lighter as compared to the international standards. In fact, the median heights and weights of Indian preschool children of rural areas are comparable to the 5th percentile of the international standards. In other words, only the upper 5% of Indians have measurements comparable to an average well fed normal child. Until recently, for comparison purposes and to assess the extent of undernutrition, the heights and weights of National Centre for Health Statistics (NCHS) of USA were being used as international standards. The earlier NNMB data was based on the NCHS standards. The analysis of data by the NNMB using the NCHS standards and the recently developed WHO Multicentre Growth Reference Study (MGRS) revealed that the overall prevalence of underweight and stunting is less when the MGRS standards are used on

Food and nutrition situation in India

893

the same children, as compared to the figures arrived by using NCHS reference standards, while the prevalence of wasting is higher [12]. The data for the national survey, National Family and Health Survey, 2006, are calculated on the basis of the WHO–MGRS Standards [17]. Trends in the nutritional status of children 1–5 years are presented in Figs. 32.4, 32.5 and 32.6. This is based on the surveys conducted by the NNMB [16] at different points of time for the 10 states covered by the NNMB between 1975 and 2006. It should be recognized that while in the repeat surveys, the same villages were surveyed in 1975–79 and 1996–97, the sample covered in the routine annual surveys during the years 2002 and 2006 is an independent sample selected using NSSO sample frame [11, 12]. They are presented based on Mean-2SD classification using NCHS standards for reference. The anthropometric values below Mean-3SD represent severe underweight, stunting or wasting. It should be noted that Mean-2SD values in the Figs. 32.4, 32.5 and 32.6 also include Mean3SD. The values between <Mean-2SD and Mean-3SD represent moderate undernutrition. The data reveals that there has been a gradual reduction in the prevalence of underweight and stunting among the Indian preschool children during the last 3 decades. However, with respect to wasting in preschool children during the same period, the prevalence of wasting did not show any appreciable change, except for a small increase in 2002. This is not surprising since there have been changes in both height and weight. The samples in 2002 and 2006, as already indicated are independent samples based on NSSO sample frame.

32.4 Trends in underweight (weight for age) for preschool (1-5 years) children.

32.5 Trends in stunting (height for age) for preschool (1-5 years) children.

894

Public health nutrition in developing countries

32.6 Trends in wasting (weight for height) for preschool (1–5 years) children.

A comparison data on underweight, stunting and wasting in under 5 years children between NNMB-2006 and NFHS-3 using WHO-MGRS standards are presented in Fig. 32.7.

32.7 Nutritional status of under five year children - NNMB - 2006 and NFHS - 3.

In the case of adults, nutritional status is assessed by body mass index or BMI (weight in kg divided by height in m2). The classification of James et al [18] using BMI index is presented in Table 32.14. The adults with BMI less than 18.5 in general are considered as chronic energy deficient, while those with values between 20 and 25 are treated as normal. The values 25+ and <30 indicate overweight (pre-obese), while >30 is considered to indicate obesity. Based on the BMI, overweight and obesity have been classified into various categories of I, II and III as

Food and nutrition situation in India

895

Table 32.14 Classification of nutritional status by BMI Classification Underweight Normal range Pre-obese (Overweight) Obese class I Obese class II Obese class III

BMI (kg/m 2 ) <18.5 18.5–24.9 25.0–29.9 30.0–34.9 35.0–39.9 > 40.0

shown in Table 32.14. The BMI provides a reliable estimate of body fat in a great majority of individuals and has been recommended by the WHO. In view of the relative ease and accuracy of the basic measurements required for assessment, the BMI is widely used as an indicator of the risk of underweight as well as for classification of overweight. The major limitations of BMI are that it does not distinguish between weight associated with either muscle or fat. Heavily muscled athletes will have a higher BMI but a relatively low fat content and conversely with increasing age, the lean tissue of the body decreases, so elderly subjects may have a normal BMI but excessive amount of fat. Also, BMI does not assess the fat distribution in the body. NNMB surveys [12] indicate that about 37% of the males and 39% of the females have chronic energy deficiency (CED: <18.5), while 57% of the males and 52 % of females have normal BMI. The prevalence of central obesity was about 33% in men (Waist–Hip Ratio >0.95) and 77% in women (Waist–Hip Ratio >0.80). Figures 32.8 and 32.9 present the national data on nutritional status of adult men and women.

32.8 Nutritional status (BMI) of adult men and women [17].

The classification of BMI in children and adolescent is complex as they are still growing and their stature and body composition is changing at different rates and times in different populations. The International Obesity Task Force (IOTF) based on the data obtained of BMI of more than 10,000 children in the age group of 6–18 years from each of the six countries –

Public health nutrition in developing countries

896

32.9 Trends in nutritional status (MBI) of adult men and women.

Hong Kong, the Netherlands, Singapore, Brazil, Great Britain and the United States suggested the IOTF classification. According to this classification, children with BMI value between 85th and 95th percentile are considered as overweight and those with BMI value above 95th percentile for specific age and sex as obese [19].

32.6

Conclusion

Despite large investments by the governments, the extent of undernutrition remains high mainly due to unsatisfactory implementation of the programmes. This is evident from the reports that only a third of the eligible persons are reported to be using any services under the Integrated Child Development Services (ICDS) while only a quarter are availing supplementary feeding [17]. Inappropriate child feeding practices, poor food availability in the family, unsafe drinking water and lack of sanitation lead to high child undernutrition and mortality. With the threat of double burden of undernutrition and diet related non-communicable diseases glaring at the country, it is critical to ensure that there is intensive effort to reduce undernutrition through proper implementation of the existing programmes and working with the community to address the problem of child feeding, maternal care, large family size, poverty and ignorance.

References 1.

JONES G , STEKETEE RW , BLACK RE , BHUTTA ZA , MORRIS SS

and the Bellagio Child Survival Study Group (2003). How many child deaths can we prevent this year? Lancet, 362, pp. 65–71. 2. United Nations (2001). General Assembly, 56th session. Road map towards the implementation of the United Nations Millennium Declaration: report of the Secretary-General. New York: United Nations. 3. MENON P , DEOLALIKAR A and BHASKAR A (2009). Inter State Hunger IndexComparisons of Hunger Across States, Washington, DC: IFPRI.

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4. Food and Agriculture Organization (1992). Malnutrition in the World. Nutrition the Global Challenge. International Conferences on Nutrition, p. 3. Rome: FAO. 5. SAXENA NC (2008). Hunger, Under-nutrition and Food Security in India, UNDP workshop, Delhi, December. 6. USAID (1992). Policy Determination PD-19, Definition of Food Security, USAID, New York 7. FAO (1983). World Food Security: A Reappraisal of the concepts and approaches, Rome: FAO. 8. Ministry of Agriculture (2009). Agriculture statistics at a glance, Department of Agriculture and cooperation, Government of India. 9. Ministry of Finance, Govt. of India, Economic Survey 2007–08, (http:// indiabudget.nic.in/ub2007-08/ubmain.htm 10. Ministry of Agriculture (2007). National Food Security Mission-Operational Guidelines, New Delhi: Department of Agriculture and Cooperation, Government of India. 11. National Nutrition Monitoring Bureau (2001). Diet and Nutritional Status of Rural Population, NNMB Technical Report No. 21, NNMB, NIN, Hyderabad. 12. National Nutrition Monitoring Bureau (2006). Diet and Nutritional Status of Rural Population and Prevalence of Hypertension among adults in Rural Areas, NNMB Technical Report No. 24, NNMB, NIN, Hyderabad. 13. GOPALAN , C et al. (1995). Nutritive Value of Indian Foods, Hyderabad: National Institute of Nutrition. 14. National Sample Survey Organization (2001). Department of Statistics, Government of India. 15. VIJAYARAGHAVAN K, SURYA PRAKASAM B and LAXMAIAH A (2002). Time Trends in the intrafamily distribution of dietary energy in rural India, Food & Nutrition Bulletin, 23, pp. 390–394. 16. National Nutrition Monitoring Bureau, Report of Second Repeat Surveys 1996– 97– Rural (1999), Technical Report No.18, National Nutrition Monitoring Bureau, National Institute of Nutrition, Hyderabad. 17. International Institute for Population Sciences (IIPS) and ORC Macro, 2007. National Family Health Survey (NFHS) III, 2005-06, India, Mumbai: IIPS. 18. JAMES WPT , FERRO- LUZZI A and WATERLOW JC (1988). Definition of chronic energy deficiency in adults. Report of Working Party of IDECG. Eur J. Clin. Nutr 42, pp. 969–981. 19. COLE JC, MARY CB, KATHERINE MF, WILLIAM HD (2000). Establishing a standard definition for child overweight and obesity worldwide: international survey. Br Med Journal, 320, pp. 1240–1243.

33 Food and nutrition in natural and manmade disasters Deepti Gulati

Deepti Gulati, MSc (Food and Nutrition), is currently a Senior Programme Associate with Global Alliance for Improved Nutrition (GAIN). Prior to GAIN, she was a Senior Nutritionist with UN World Food programme. She has extensive experience of working with the government as Deputy Director, National Institute of Public Cooperation and Child Development, Government of India. Deepti is Masters in Foods and Nutrition from MS University, Baroda, India. The author has received fellowships from the International Agriculture Centre, Netherlands and from the United Nations University in ‘Management of Community Nutrition Programmes’.

33.1

Natural and manmade disasters

There are various definitions of disaster. WHO defines disaster as “an occurrence disrupting the normal conditions of existence and causing a level of suffering that exceeds the capacity of adjustment of the affected community” [1]. The definition by UN/ISDR is “a serious disruption of the functioning of a community or a society causing widespread human, material, economic, or environmental losses which exceed the ability of the affected community or society to cope using its own resources” [2]. Disasters whether natural or man-made, cause immense stress and instability. High profile disasters, like earthquakes, cyclones, floods, tsunamis, landslides, avalanches, conflicts etc., take heavy toll of life, while silent disasters like drought, starvation, epidemics, chronic malnutrition etc., take an even heavier toll of life. The disasters may be brief or protracted. All disasters – silent or otherwise – result in emergencies. In the unstable aftermath of disasters, there are periods in which conditions become more or less acute, and the sequence and duration of these periods are unpredictable. The acuity of conditions may build to a peak (as in a drought or floods) or start at a pinnacle and then taper down

898

Food and nutrition in natural and manmade

899

and start mending (as in an earthquake). Transition from disasters to normality takes time and people affected by disasters usually need external support to cope and to return to normalcy. Disasters can be categorized broadly into three categories: ●

● ●

Sudden disasters – natural disasters, which affect food access and / or cause population displacements (floods, cyclones, earthquakes etc.). Slow-onset disasters – these are usually droughts and crop failures. Complex emergencies – these can involve conflict, widespread social and economic disruption and large population displacements, within the country or outside.

Whatever be the type of disaster, availability of food and its access to people affected by disaster, always gets highly compromised. The nature of food and nutrition problems depends on the type of disaster, its duration and size of the area affected, and the nutritional status of population prior to disaster. Disasters demonstrate their serious adverse impact on the nutritional status. Both protein energy malnutrition (PEM) and micronutrient malnutrition can occur. Malnutrition contributes to mortality amongst those affected by the disasters. Such mortality is often more pronounced in disasters such as internal political conflicts and wars, which result in large scale displacements of population groups within and outside the country, forcing people to stay in the refugee camps. In such situations, water and sanitation facilities are poor or non-existent and people’s access to food is minimal. This results in high levels of malnutrition. Ethiopia, Somalia and Sudan have been affected by war/conflict over a very long period. In the worst phase of conflict in these countries, malnutrition incidence was reported to be as high as 80% in Somalia in 1992 and Southern Sudan in 1993. Micronutrient deficiencies – vitamin A, vitamin C, iron deficiency anemia and niacin are also commonly observed in refugee camps [3]. Thus, human nutrition is nowhere more critically grave than in the situations where the normal channels of food access have been disrupted or cut off because of natural or man-made disasters. Nothing is more important than providing food when people find themselves suddenly, and often critically, in need, following a storm, earthquake, flood or other disaster emergency. Besides just the food and nutrition scenario, the environment itself gets greatly affected and contributes to the multiplier effect of the disaster. In fact, disasters trigger on a cycle of malnutrition, infection and ill health: disease burden increases and the malnourished individuals are many times more likely to succumb to infectious diseases resulting from environmental degradation perpetuated by the disaster. Hunger, poor performance of health and social service systems, low immunization coverage, and poor

900

Public health nutrition in developing countries

provision of primary care, render people more susceptible to disease and death.

33.1.1 Nutritional emergencies in natural or manmade disasters Emergencies resulting from natural or man-made disasters are characterized by abnormal conditions of stress and instability (Box 33.1 and 33.2). Even though every emergency is unique and challenging, certain departures from normal, characterize nutritional emergencies. These include: ●

●

●

●

●

Changes in livelihood strategies. Normal strategies for earning income and obtaining essential goods and services are interrupted or become less efficient. Less desirable (begging/selling off jewellery or household goods) and less-efficient strategies (eating lesser amounts of food or working on compromised wages) are referred to as coping strategies and these are adopted or expanded (Box 33.3). Expansion of poverty, both in prevalence and intensity. Incomes drop and possessions, necessary to households’ short- or long-term viability, are lost. Reduced availability of and/or access to staple foods. Food and productive resources are destroyed, production fails, trade is interrupted and/or access to markets is blocked. Changes in household and community structures and functions. Death, disability, migration or conscription to armed forces removes people from households and communities. Those who remain must compensate, assuming new roles. Political rifts, armed conflict or competition for diminishing resources increases intra- and intercommunity tensions, disrupting normal operations. Increased susceptibility to death and disability. Several new threats, such as malnutrition, increased disease transmission, interruption of or blocked access to health services, inadequate water and sanitation and loss of protective infrastructure, goods and services, increase the susceptibility to death and disability (Box 33.2).

Disasters are major challenges to nutrition, health and food security. People in the areas with recurrent disasters face the problem of “transitory food insecurity” due to displacement or damage to household stocks. Inadequacy and uncertainty of food supply makes them food insecure and undernourished. Populations that are chronically undernourished are less likely to survive these crises. Disasters reduce a community’s ability to effectively mobilize resources for the crisis management, making it difficult for people to cope up with the situation.

Food and nutrition in natural and manmade

901

Box 33.1 India's vulnerability to natural disasters India has been traditionally vulnerable to natural disasters on account of its unique geo-climatic conditions. Floods, droughts, cyclones, earthquakes and landslides have been a recurrent phenomena. About 60% of the landmass is prone to earthquakes of various intensities; over 40 million hectares is prone to floods; about 8% of the total area is prone to cyclones and 68% of the area is susceptible to drought. In the decade 1990–2000, an average of about 4344 people lost their lives and about 30 million people were affected by disasters every year. The loss in terms of private, community and public assets has been astronomical. [4]

People are thus caught in a hunger trap. Within these population groups, women and children are the worst affected. Familiar images of mothers with their children, standing amidst the wreckage of floods, cyclones, earthquakes, and other major disasters, reinforce the correct scenario that women and children are the first and foremost victims; they are vulnerable, poor, marginalized, and lack socio-political influence. Worldwide, women and children are 14 times more likely to die in a disaster than men are. [6] In the critical situations arising from disasters, the humanitarian aid agencies step in to provide various types of assistance. Food assistance is of paramount importance as without enough food, any other humanitarian assistance intervention is likely to be less effective. Health interventions alone will not be enough to prevent illnesses that are compounded by lack of adequate nutritional intake, and even if there are adequate hygiene facilities, people will continue to be susceptible to risk of disease because of weakened immune systems and diminished bodily reserves. Box 33.2 Global scenario Earthquakes, floods, drought, and other natural hazards continue to cause tens of thousands of deaths, hundreds of thousands of injuries, and billions of dollars in economic losses each year around the world. According to the EM-DAT global disaster database maintained by the Centre for Research on the Epidemiology of Disasters (CRED) in Brussels, 354 natural disasters were recorded in 2008. Asia remained the most affected continent. Nine of the top 10 countries with the highest number of disaster-related deaths were in Asia. The human and economic losses caused by natural disasters in 2008 were devastating. More than 235,000 people were killed, 214 million people were affected and economic costs were over 190 billion US$ [5]. Disasters represent a major source of risk for the poor and wipe out development gains and accumulated wealth in developing countries.

Purpose of food aid Very often during the disasters like floods/cyclones/earthquakes, there is widespread destruction, resulting in reduced access to food due to diminished household food stocks, crop destruction, easy access to markets etc. In such situations, food aid may perhaps be the only way of restoring people’s access to food.

Public health nutrition in developing countries

902

Box 33.3 How people respond in disasters? Recurrent natural disasters undermine people's livelihoods, force poor households to resort to unsustainable practices in order to meet basic food needs: ● ● ● ● ●

Reduce food – fewer meals – low cost food Work as labour/service-job Seasonally migrate for employment Sell animals – jewellery, land, self Permanent out-migration

When people are unable to gain access to enough food, they are more likely to engage in short-term survival strategies like excessive disposal of household assets, leading to destitution, ill health and other long-term negative consequences. Food aid can thus act as one of the most crucial interventions and an important mechanism to sustain life, protect or restore people’s self-reliance, reduce the need for them to adopt potentially damaging coping strategies and help to re-establish their capacity to respond to future shocks. The purpose of food aid is to: (a) Sustain life by ensuring adequate availability and access to food by people affected by disaster. (b) Provide sufficient food resources to eliminate the need for survival strategies, which may result in long-term negative consequences to human dignity, household viability, livelihood security and the environment. (c) Provide a short-term income transfer or substitution to people to allow household resources to be invested for recovery. Hence whenever situational analysis demands that food aid is an appropriate response, it should be undertaken in a manner that not only meets short-term needs but also, as far as possible, contributes to restoring long-term food security.

33.1.2 Planning for an effective food aid Measures to prevent malnutrition following a disaster include assuring that food supplies are nutritionally complete, that food is distributed equitably among affected population, safe drinking water is available and there is adequate sanitation. In the absence of both, adequate nutrition and proper sanitation, it is difficult to prevent the onset of malnutrition. Following steps are to be followed in order to ensure effective food aid programme: ● ●

Estimate the quantity of food available. Calculate the dietary needs of the affected population.

Food and nutrition in natural and manmade ●

903

Determine the food rations in accordance with the characteristics of the population and estimated duration of the effects of disaster.

Food aid and feeding interventions have demonstrated that these play a vital role in disaster management and have made a difference. However, these need to be coupled with a development approach. The transition from receiving relief aid to community development can be difficult. Agencies may withdraw their personnel and resources, leaving the community with some of the immediate needs met but little reserves to cope long term. On the other hand, the community may become overdependent on outside help if the agencies remain for too long. Neither approach enables the underlying vulnerability to be addressed, nor capacity and preparedness to develop. Local data highlighting rising rates of malnutrition (refer to section 33.5 for details) can lead to increased efforts directed at prevention or if necessary, application for food intervention. Building capacity of vulnerable community should be the focus with emphasis on multidisciplinary involvement for addressing nutrition concerns during disasters.

33.2

Understanding concepts of vulnerability, disaster-preparedness and building capacities

During the last 30 years, there has been a manifold increase in the number of disasters and complex humanitarian emergencies and food insecurity of the community has been the core issue. Individuals, communities, and countries face various challenges in different ways; some seem well able to cope with adverse situations and overcome them, and others are completely overwhelmed. Box 33.4 Disaster and malnutrition Malnutrition is commonly associated with food insecurity and poverty. In most developing countries, the malnutrition is high amongst all population groups and amongst these, women and children have much higher levels of malnutrition. Disasters perpetuate environment degradation. So in any disaster situation, when the access and availability to adequate food and safe water is highly compromised, reduced food intake and lack of varied diet during a disaster predisposes people to protein-energy malnutrition and micronutrient deficiencies. Malnutrition, lack of safe water supply and any sanitation services, displacement due to loss of property, etc. make people highly vulnerable and they have an increased risk of infectious diseases such as cholera, typhoid fever, diarrhea, acute respiratory infections and measles. Malnourished individuals are many times more likely to succumb to infectious diseases that result from environmental degradation perpetuated by the disasters.

It is important to prepare the communities to deal with the disasters and build their coping capacity so that their vulnerability is reduced (Box 33.4).

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Hence it is essential to understand the concepts of vulnerability, disaster preparedness and capacity building. It is also essential to understand the importance of the interaction between vulnerability, and disasterpreparedness as these are inextricably linked. Therefore, the agencies providing aid to the disaster-affected populations also need to direct their efforts at enabling populations to build their own capacity and decrease their vulnerability – communities need to be enabled to mobilize as much of their own strengths as possible, so that their preparedness for any future disaster is enhanced. Vulnerability In the disaster reduction context, vulnerability has been defined as “the conditions determined by physical, social, economic, and environmental factors or processes, which increase the susceptibility of a community to the impact of hazards” [1]. WHO defines vulnerability as “the predisposition to suffer damage due to external events” [2]. For example, those people living near the coastal areas are vulnerable to cyclones and tsunamis; those near the rivers are vulnerable to annual floods; those people who are living in the arid zones, are highly vulnerable to hunger as these areas are drought-prone, and those living in the seismic zones are vulnerable to earthquakes. These people suffer colossal damages whenever there are external events like droughts/cyclones/floods/ earthquakes, etc. Unless the capacity of these people is built and they are supported to cope with these hazards, they would always be at the receiving end of the calamity or such external events. In a disaster, vulnerability of communities will be influenced not only by the nature, extent, and time-scale of the disaster but also by community’s capacity to cope with it, which means “the ability of the community to use available resources and abilities to face adverse consequences”. This capacity to cope is influenced by factors such as prior experience, access to information, and cultural norms. In fact, the following formula has been proposed which indicates the relationship of vulnerability, hazards and coping capacity: V = H – C, where V is vulnerability, H is hazards/disasters and C is the coping capacity. Addressing vulnerability and capacity to cope aims to increase disaster preparedness i.e. the measures taken in advance to help ensure effective response to the impact of hazards [2]. To illustrate this, let us take an example of Orissa. Orissa has a very big coastline (over 430 km) and is visited by cyclones almost annually, making the people in the coastal areas very vulnerable to the cyclone fury. In October 1999 when the super cyclone hit Orissa, there were only 23 cyclone shelters of the Red Cross operating under the Orissa Disaster Mitigation Programme (ODMP) where people could seek rescue. About 2,000 persons

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occupied each shelter, which was designed only for about 1,500 people. Nevertheless, according to the Orissa Government’s Relief Commissioner, these Red Cross shelters saved around 40,000 lives. Equipment of the shelters such as megaphones, generators, first aid kits, water containers etc. ensured that at least no one staying in these shelters died. In this case, the vulnerability is the exposure of people to recurrent cyclones (which is the hazard) and the coping capacity is the availability of shelters. Hence, if the coping capacity to meet with the hazards/disasters is enhanced, the vulnerability due to hazards/disasters is reduced. Since the super cyclone, Government of Orissa has constructed many such cyclone shelters across the cyclone-prone areas so that the vulnerability of the people to hazards of cyclones is greatly reduced. Recognizing and understanding vulnerability in the context of disaster preparedness is fundamental in designing programmes for appropriate capacity building of the community and aiding in their quick recovery from the aftermath of the disasters. However, in order to help the communities to build their coping capacity for facing the challenges of disasters, it is critical to interact with and listen to the local community. This will help to understand what factors onset the disasters and make these communities vulnerable. For example, activities like indiscriminate digging of deep bore-wells for water without any mechanism of water harvesting/re-charging, depletes water table leading to severe water crises, and arbitrary tree-felling leads to low rain falls. Many similar activities exploit and degrade the environment, which results in making the area become arid and drought prone. Displacement, loss of buying power and erosion of coping and caring capacities, limit people’s access to health services and often contribute to an overall increase in morbidity and mortality. Discussions with community members help in identifying key issues that explain why a community is not able to cope with the disasters. Once the dynamics of vulnerability and inability of community to cope is understood, it becomes easier to partner with the community to develop mechanisms for reducing their vulnerability. Disaster preparedness Disaster preparedness refers to “activities and measures taken in advance to ensure effective response to the impact of hazards” [2]. This includes the use of early warnings and measures to evacuate people from areas that might be affected. The WHO definition of preparedness is “the measures that ensure the organized mobilization of personnel, funds, equipment and supplies within a safe environment for effective relief ” [1].

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However, the extent to which vulnerability is addressed by building a community’s capacity is a key factor in determining its disaster preparedness (Box 33.5). When preparedness is directed towards the threat of a specific phenomenon like an earthquake, flood, or famine, knowledge gained from experience of comparable situations should be of value. A key issue in nutrition and disaster preparedness is that development of capacity in vulnerable populations and disaster management must go hand in hand. Food aid and feeding interventions from outside have been vital in disaster management and have made a difference, but these need to be coupled with a development approach. Box 33.5 ASHRAYA project Due to the Super Cyclone, around 800,000 homes were demolished and 1.9 million badly damaged. CARE initiated ASHRAYA project to build better, stronger homes that could withstand future punishing storms, in the worst affected villages of Astarang, Balikuda, Mahakalpara and Rajnagar. The project was undertaken in partnership with local people. Rather than adopt a small number of villages, CARE spread the intervention over a larger area by building only 10 to 15 'core houses' in each village usually having a population of about 100 people and handed it over to the community for use during emergencies. The core house is designed to withstand cyclones, has a flat roof so that people can shelter from floods, and is not vulnerable to fire and can therefore also act as a safe storage place for grain. In addition, local people were encouraged to build their own core houses – and to learn new building methods as a result.

Capacity building According to UN/ISDR, capacity to address disaster is “a combination of all the strengths and resources available within a community, society or organization that can reduce the level of risk, or the effects of a disaster” [2]. This includes physical and human resources as well as leadership and management. Box 33.6 The National Disaster Management Authority, India The National Disaster Management Authority (NDMA) with Prime Minister of India as its chairperson is the lead agency in India, which is authorized to deal with all types of natural and man-made disasters. It deals with prevention, mitigation and preparedness in pre-disaster phase, and response, rehabilitation and reconstruction in post-disaster phase. NDMA has a "National Disaster Management Operations Centre" with the state-of-the-art multi-faceted communication systems, to carry out the tasks of capacity development, training and knowledge management.

WHO indicates that capacity for emergency management consists of timely sharing of all the relevant information with people in authority and with the community so that the resources and procedures can be activated

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instantly to minimize the impact of disasters [1]. This can happen only if there is a systematic approach and well-laid out advance plans, which people in authority have been trained to understand and execute efficiently and effectively; and there is a receptive and responsive community that has been readied before hand to meet with such exigencies. Hence, a country’s ability to deal and manage a disaster in an urgent, organized and effective manner depends upon its advanced planning and effective systems that have been put in place, which can be activated as and when the need arises. Capacity building for disaster prevention and mitigation also implies that there is a clear line of command authorizing the trained personnel at different levels to take quick decisions and implement the set of actions without the tardy processes of sanctions and approvals. Therefore, for the areas prone to disaster, we must develop an early warning system, which provides accurate “information” about the impending disaster. Then, there must be specifically designated people/ officers who receive this information, interpret it and are authorized to initiate action without delay. Each country must have its own specified agency/department/partner institution(s) that have the responsibility to put into action the mechanism to deal with any kind of disaster or any eventuality that may take place. Enabling communities for disaster preparedness and building their capacity to cope with the disasters and enhancing the ability for disaster management at the country/state/district level must be addressed together if we wish to reduce the vulnerability from future eventualities. Unless the underlying vulnerability and its relation to disaster preparedness are addressed, the damage from the disasters cannot be minimized.

33.2.1 Role of humanitarian aid organization In the immediate response to disaster, the affected community uses its own knowledge about local needs and capabilities and this helps in the speedy recovery and development processes. The role of humanitarian aid organisations is not to take over the affected communities unnecessarily, but to enable these communities to take control over the decisions. The humanitarian aid organisations must take account of potential expertise and contribution from within the affected populations and offer help and support that is culturally appropriate and acceptable. Otherwise their support / programmes may be limited in time and effectiveness.

33.2.2 Early warning systems (EWSs) Early warning is “provision of timely and effective information, through identified institutions, that allows individuals exposed to a hazard

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(impending risk/danger) to take action to avoid or reduce their risk and prepare for effective response” [1]. Effective EWSs can predict a specific sequence of events that may result in disasters. This EWS helps in the identification and understanding of the hazard, the related impending risk and the extent of damage that can result. Hence, by using an EWS, the impending events are forecast and monitored, and understandable warnings disseminated to the population and those in authority, leading to an appropriate and timely action in response. This can thus minimize the havoc and reduce the loss of life, property and livestock. Using preliminary indicators of natural disasters, EWSs can predict most of the disasters. However, EWSs have been mostly used in the area of drought prediction, possibly due to its slower onset and the large numbers of people potentially affected. Also, EWSs related to ‘food security’ use indicators like information on rainfall, state of crops, market prices, migration of workers, population movement, changes in nutritional status, and mortality rates, etc., which are easier to predict [7]. Based on the EWSs, impending crisis can be assessed and its management is planned accordingly. EWSs can be a very useful tool in helping the humanitarian aid organisations to estimate the seriousness of the impending disaster and help the organisations to decide when best to intervene for maximum effectiveness and prepare plans. These plans should be used as intervention strategies ready for immediate implementation if required. It is advisable that planned interventions, based on the EWSs are implemented before any population displacement begins. The commencement of migration often reflects that the situation is already serious.

33.3

Food insecurity and malnutrition – identification and measurement

Nutrition and health are inextricably linked and the factors that influence nutrition, ultimately affect health. Dietary inadequacies are a major contributing factors resulting in malnutrition, which influences and compromises resistance to diseases. It is well understood that poor nutritional status leads to lowered immunity and thus to increased morbidity from infectious diseases such as measles, malaria, or tuberculosis. The disease/nutrition cycle affects infants and young children in particular. The nutritional status in children under 5 years responds rapidly to acute food shortages and high levels of malnutrition in this age group are used as proxy indicator of acute malnutrition in the overall population. Hence, in populations affected by disasters and complex emergencies, ascertaining the level of malnutrition should be given priority.

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Marasmus (severe wasting), kwashiorkor (where oedema is a key feature), or a combination (marasmic kwashiorkor) are often present in children affected by disasters. Besides “protein energy malnutrition” (PEM), there may be micronutrient deficiencies in the population. The body also requires adequate stores of micronutrients to prevent deficiency in times of crises such as food shortages or trauma as these are associated with increased morbidity and mortality. Guidelines for the identification and management of malnutrition have been published by various international and non-governmental organizations. These include Medicines Sans Frontiers’ [8], the World Health Organization [9, 10], and UNHCR/UNICEF/WFP/WHO [11]. In addition, food security, nutrition, and food aid are included in the minimum standards set by “The Sphere Project [12]” (Box 33.7).

Box 33.7 The Sphere Project The Sphere Project (the name conveys the sense of universality of this initiative), launched in 1997 by the Red Cross and Red Crescent movement and several non-government organizations (NGOs), aims to improve the effectiveness and accountability of humanitarian assistance. Their Humanitarian Charter and Minimum Standards in Disaster Response set standards in several areas including provision of shelter, safe water and sanitation and food security (2004)

33.3.1 Food insecurity and malnutrition Identification of food insecurity and malnutrition normally commences with a rapid assessment of the general situation. When people are not able to access adequate food to assuage hunger and to meet their physiological needs, they are termed as food insecure. Such food insecurity could be transit or chronic in nature. Transitory food insecurity results from temporary disruption of access to food due to disasters or any other compelling circumstances while chronic food insecurity results from unavailability of adequate food over a long period (Box 33.8). Box 33.8 Concepts of Food Security Chronic Food Insecurity is the result of a consistently inadequate diet due to problems of food availability, food access and/or food utilization. More than 200 million Indians are undernourished; and chronically food insecure.

Transitory Food,

Insecurity in food among households who normally can meet their minimum dietary need but are not able to cope with natural disasters. About 35 million Indians are affected by recurrent disasters every year; they are victims of transitory food insecurity.

Interviews and focus group discussions are carried out with members of the general population, as well as community leaders to get information

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on food availability and access, food beliefs, estimated population size, possible increases in illness and death, and information about water, sanitation, and food crops. This information is most essential in planning an effective food support programme as the cause of poor access to food can be identified and addressed; and sustainable systems can be initiated that would streamline the access of the affected population to adequate food. Measuring malnutrition The most widely accepted practice is to assess malnutrition levels in children aged 6–59 months as a proxy for the population as a whole. It is usually the young children between 6 and 59 months who are measured in nutrition surveys, because these young children are the first to show the signs of malnutrition in times of food shortages and they are the most severely affected. In cases where the ages of children are not known or cannot be assessed easily, children measuring between the length/ height of 65 cm and 110 cm are used to represent the children in the agegroup of 6–59 months. However, other groups may be affected to a greater extent or face greater nutritional risk. When this is the case, the situation of these groups should be assessed, although measurement can be problematic. Malnutrition can be assessed by clinical signs and by anthropometry. Anthropometric measurements such as weight-for-height are used as an objective assessment of nutritional status, which quantifies the nutritional situation at one point of time and allows comparisons over time. Information on child mortality and child morbidity assists in understanding the underlying causes of malnutrition and the relationship characterised between malnutrition and mortality to determine the focus on specific interventions. Child mortality rates are particularly important. International guidelines stipulate that a representative sample should be used for surveys; adherence to national guidelines can promote coordination and comparability of reporting. Where representative data are available on trends in nutritional status, these are preferable to a single prevalence figure. Weight-for-height in children The “weight for height” (WFH) index is most commonly used to detect acute malnutrition (wasting) in surveys. WFH in children is the best indicator to assess and monitor nutritional status of populations and is normally estimated by surveying children aged 6 to 59 months, using cluster sampling. It compares weight with the median weight of a sample of children of the same height.

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The actual weight of a child is calculated as a percentage of the standard weight for a normal child of that height, or as a Z-score. Z-scores are the standards and a preferred mode of presenting anthropometric indicators in nutrition surveys (Table 33.1). Thus a Z score of < –3 and/or oedema indicates severe acute malnutrition [13]. Moderate acute malnutrition is indicated if the WFH is between 70% and 80% of the median, or between –3 and –2 Z scores. The term “global acute malnutrition” (GAM) refers to the total number of children with severe acute malnutrition plus those with moderate acute malnutrition, that is all those with WFH < 80% of median, or < –2 Z scores. In selective feeding programmes percentage of median can be presented in addition to Z-scores in survey reports if there is a specific need, e.g., if it is required as a programmatic tool in selective feeding programmes. Until recently, United States National Centre for Health Statistics/ Centers for Disease Control (NCHS/CDC) and Prevention reference tables adopted by the World Health Organization [14] were in use, but now the recently launched WHO Child Growth Standards provide a new international standard [15]. When anthropometric measurements are used in conjunction with clinical observations, these together provide a very clear picture of malnutrition, including micronutrient malnutrition. WFH less than 70% of the median and/or oedema indicates severe acute malnutrition while pallor indicates anemia, and signs of night blindness or bitot’s spot indicate vitamin A deficiency. Table 33.1 Classification of acute malnutrition in children [12]

Children 6.0-up to months * **

Total malnutrition*

Moderate malnutrition

Severe malnutrition

<–2 Z scores WFH** or 80% median and/or nutritional oedema

–3 to <–2 Z scores or 70%–80% median WFH

<–3 Z score WFH or < 70% median WFH and / or nutritional oedema

This is also called global acute malnutrition. Weight for height.

WHO has set emergency thresholds, above which nutritional intervention is indicated for the population. A critical situation is reached when over 15% of the children surveyed have global acute malnutrition. There are no agreed anthropometric cut-offs for acute malnutrition in infants below six months, apart from the presence of nutritional oedema. The NCHS/CDC growth references are of limited use since they are drawn from a population of babies fed artificially, whereas breastfed babies grow at a different rate. This means that malnutrition will tend to be overestimated in this age group (WHO). It is therefore important to assess

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infant feeding practices, particularly access to breast milk, and any medical conditions in order to determine whether malnutrition in this age group may be a problem. Delayed growth in height for age, i.e. “stunting”, can be found in situations of chronic malnutrition. In this case, weight for age (WFA) may be a preferred indicator as this indicator captures recent undernutrition, which often results in disasters when there is poor access to adequate food due to the disruption in normal food supply chain. Body mass index Body mass index (BMI) is measured as weight in kg/height in m2 and is used for assessing the nutritional status of adults by assessing the degree of thinness. A ratio of ≥16–18 indicates moderate malnutrition and <16 severe malnutrition (Table 33.2). Mid-upper arm circumference Where large numbers of children have to be screened, mid-upper arm circumference (MUAC) can be used to identify wasting. MUAC is a simple and practical tool which can be used by minimally trained workers for detecting the severely malnourished in the community and for achieving high programme coverage. MUAC measurements <115 mm in children of <5 years are indicative of severe acute malnutrition and are of value in predicting mortality. MUAC has also been used to identify malnourished adolescents, and adults including pregnant women, in need of admission to feeding programmes. A MUAC of <20.7 cm indicates severe risk [12]. Nutritional survey reports should always describe the probable causes of malnutrition. Explanation on probable causes of malnutrition helps to effectively address the root-cause and provide some tangible solutions to reduce the magnitude of malnutrition. Also, nutritional oedema should be reported separately. Presence of nutritional oedema is an indicator of protein deficiency and thus needs special attention and care. Also, while assessing the nutritional status using weight for age, children having nutritional oedema are excluded as the presence of oedema may show higher weight of the child due to the fluid accumulation and retention, thus interfering with correct assessment of malnutrition. Trends in mortality are important in the interpretation of nutrition data. Crude mortality rate (CMR) is the number of deaths in the population, for example per 1,000 per month, or per 10,000 per day. A doubling of CMR above the baseline indicates a public health emergency [12].

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Table 33.2 Summary of key malnutrition indicators [10] Malnutrition Children <5 years old

Adults

WFH (W/H)%of WFH (W/H) in Z scores or median NCHS/WHO SD’s of the median reference values NCHS/WHO reference values

MUAC

BMI

Moderate

70–79%

–3 to 2 Z scores

115 mm to 16 to <17 <125 mm

Severe

—

< 3 Z scores or oedema

<115 mm

Less than 16

On-going nutrition surveillance should be a standard practice in every country so that a deteriorating situation can be identified early. This requires developing the expertise of fieldworkers to carry out data collection, and strengthening the ability of the programme managers to seek access to logistical, statistical, and nutritional expertise to analyse and interpret finding.

33.4

Nutritional interventions

In any emergency or disaster, the first and foremost need is assuaging (assessing) hunger. Providing food and other nutritional interventions to the disaster affected persons is one of the most important activities of the collective response of the humanitarian aid agencies. For planning nutrition intervention, it is important to undertake the initial assessment and analysis of the emergency situation and focus on people’s own food and income sources, and assess the quantity and type of food assistance required to maintain adequate nutritional status for the general population, as well as of the vulnerable groups (Box 33.9). Moreover, it is important to understand the underlying causes of malnutrition and analyse information provided through the anthropometric surveys. Information on the causes of malnutrition can be gathered from primary or secondary sources, including existing health and nutrition profiles, research reports, early warning information, health centre records, food security reports and community welfare groups, and can comprise both quantitative and qualitative information. An early assessment of nutritional status of the disaster-affected population helps to plan emergency response, the components of rations and the requirement for any additional selective feeding programme. Decision-making should rely on an understanding of all the possible underlying causes of malnutrition as well as results from anthropometric surveys. In an acute crisis, however, decisions to implement general food distribution need not await the results of anthropometric surveys, as these

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can take up to three weeks. It should, however, be possible to use anthropometric survey findings to inform decisions on responses aimed at correcting malnutrition. Box 33.9 Essentials of planning It is important to consider factors, such as cultural acceptability of the food ration and the choice of suitable foods. Providing a diverse diet, with culturally appropriate foods that are rich in micronutrients, is a major food aid challenge. The participation of disaster-affected people in decision-making, programme design and implementation, helps to ensure that programmes are equitable and effective. Special effort should be made to ensure the participation of women and a balanced male and female representation within the assistance programme. Participation in the food aid / support programme may also serve to reinforce people's sense of dignity and worth in times of crisis. It generates a sense of community ownership, which can help ensure the safety and security of those who are receiving assistance, as well as those who are responsible for its implementation.

The standard for food aid requirements is based on WHO’s planning estimate for a typical population. Nutritional interventions, primarily consisting of feeding, fall into two main categories: (i) General feeding programmes and (ii) Selective feeding programmes The objectives of the feeding programme should be realistic and should be achieved within a period determined in advance. Figure 33.1, based on the Nutrition Guidelines; MSF, 1995 [8] helps to understand the seriousness of the situation and decide on the type of nutrition programme that should be started. Supplementary feeding programmes provide nutritious food in addition to the general ration. They aim to rehabilitate malnourished persons or to prevent a deterioration of nutritional status of those most at-risk by meeting their additional needs, focusing particularly on young children, pregnant women and nursing mothers. General feeding programs These are designed to meet the needs of the overall population, and should adhere to the minimum standards set by The Sphere Project (2004). In situations where the ration provided by the aid agency is the sole food source, ration size is planned in such a way that it meets an average daily energy requirement of 2100 kcal per person (adult). This ration size is designed to address hunger and prevent further deterioration of the nutritional status. Calorie requirements of ration per person are increased

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in conditions where malnutrition is present, heavy physical work is being carried out, or population is living at low atmospheric temperatures.

33.1 Nutrition interventions and selective feeding programs.

The initial planning estimates of WHO for nutritional requirements for the general feeding programme and supplementary feeding programme are based on the following: These feeding programmes are designed as a “safety net” to prevent further deterioration of nutritional status and reduce mortality. While for supplementary feeding programme, the nutritional requirement and the ration size would depend upon the nutrition gap between what is required vis-à-vis what the people are getting; for general feeding programme, the nutritional requirements of the daily ration include the following: ●

● ●

2,100 kcal per person per day. (This is the basis used for population, irrespective of age group – Table 33.3.) 10–12% of total energy is provided by protein. 17% of total energy is provided from fat.

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Adequate micronutrient intake through fresh or fortified foods (refer Table 33.4).

In general rations, supplies are provided preferably as dry food rations, the basic commodities being cereals, pulses, and vegetable oil, to be prepared at home. As a short-term measure, rations may be provided as cooked meals. In most emergency situations like the earthquakes, floods etc., the people get displaced and/or their house are damaged or destroyed. In the first few days following such disasters, on-spot cooking of food is nearly impossible, hence rations may be provided as cooked meals. As a short-term measure, the most appropriate foods are the ‘High-energy biscuits’ or similar ‘Readyto-eat’ (RTE) foods, as these can be mobilized quickly and are logistically easy to distribute. Reported difficulties with emergency food aid fall roughly into the following three categories: 1. The quantity of rations provided; 2. The quality of rations, particularly their micronutrient content and the appropriateness of foods in the ration; and 3. The coordination of food aid programming with the health and personal care components required for protecting the nutrition of people affected by emergencies. However, biscuits and RTE need to be replaced by foods that would not only pacify hunger but would also be nutritionally appropriate. These can be replaced by a steady supply of a complete basket of food commodities in quantities sufficient to meet requirements. Thus, the dry food rations would include basic commodities such as cereals, pulses, and vegetable oil, which can be prepared at home. But, the unprocessed grains, though easy to procure, are not the ideal food choice in emergency situations because they need milling and cannot be consumed otherwise. Hence, foods like wheat flour/corn flour or the wheat–soya / corn–soya blends should be considered as an important part of the food basket as these can be cooked with minimal fuel and fuss. Another advantage of these floors/blends is the ease with which these can be fortified with micronutrients, which are critical for meeting the micronutrient needs of the population groups. When foodstuffs like fruits and vegetables that provide naturally occurring essential vitamins and minerals to population groups are not available, the use of food fortified with micronutrients; following the principles outlined in Codex Alimentarius, should be the most appropriate alternative. At a minimum, the micronutrient fortification for all the processed grains can be undertaken with elemental iron and B vitamins, plus vitamin A.

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Factors, such as cultural acceptability of the food ration and the choice of suitable foods, must be considered. There are many challenges in ensuring fair distribution of food aid. Food aid targeting should help identify the most vulnerable areas and households. This requires the use of various indicators, such as health status and food security, in addition to nutritional status. In brief, commodity selection should consider the following: ● ● ● ●

Local availability and market impact. Local acceptability and preparation. Fitness and nutritional composition. Fuel requirements for cooking.

Selective feeding programmes (SFP) These aim to ensure that individuals in specific vulnerable groups receive adequate nourishment. Typically, such groups would include malnourished infants and young children and/or pregnant or nursing mothers. In SFP, the food rations either provide one or two food commodities to complement existing foods available and accessible to the affected population (for example, pulses and oil might be provided to complement locally accessible cereals), or provide specific foods as a supplement to the general ration, in order to cover the needs of particular groups. In SFP, the selection of food items to be included in the food basket is based on people’s food and income sources and the availability and access to food. Estimates of people's food and income sources include consideration of: ● ● ● ●

Market and income opportunities. Foraging and wild food potential. Agricultural seasons and access to productive assets Sources of income and coping strategies

There are two types of selective feeding programmes: ● ●

Supplementary feeding programmes (SFP) and Therapeutic feeding programmes (TFP).

The Supplementary feeding programmes aim to provide extra food to the groups at risk in addition to the general ration. The ration provided could be as a dry, take-home ration or a wet, on-the-spot feeding. These are of two types: Blanket SFP and Targeted SFP. The blanket SFP provides a food and/or micronutrient(s) supplement to

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all members of a certain vulnerable group, regardless of their individual nutritional status in order to prevent a further deterioration in the nutritional status of those groups most at risk (usually children <5 years of age, pregnant women and nursing mothers). The targeted SFP aims to rehabilitate those who are moderately malnourished. These could be infants, children, adults or older people and/or individuals selected on medical or social grounds, e.g. pregnant and nursing mothers and the sick. This is the most common type of SFP. As far as infants are concerned, breastfeeding, if possible, should always be encouraged. For older children and adults, in addition to the general food ration, the SFP should supply an extra 1000–1200 kcal/person/day (dry rations), or 500–700 kcal/person/day (cooked meal), as the need may be. Therapeutic feeding programmes (TFP) generally target the severely malnourished, particularly infants and young children who are severely malnourished and critically ill with high rates of mortality. The TFP can either be implemented in special feeding centres or in a hospital or clinic or at the community level. TFP involves intensive medical and nutritional treatment. The management of severe malnutrition in children can take place through facility-based management and community-based therapeutic care. Facility-based management refers to treatment in a hospital or a centre that provides skilled medical and nursing care where the affected infants and young children are treated under medical supervision. The priority in the first 1–2 days in such cases includes treating dehydration, infections, hypoglycaemia, fluid and electrolyte imbalance, and hypothermia. If the infant is being breastfed, this is encouraged to be continued. Once the child’s appetite has returned (usually after 2–7 days), several weeks of rehabilitation follow and micronutrient supplements especially vitamin A (dosage specific for the age) is given. The children are then discharged to the care of their own families with weekly monitoring at the feeding centre [10]. Community-based therapeutic care (CTC) refers to diagnosing the condition, instituting treatment and monitoring the condition of child at home with some external input, such as the presence of a health worker/ trained community-based programme worker. Community-based therapeutic care includes treatment of severely malnourished child with vitamin/mineral supplements and/or Ready-to-Use Therapeutic Foods (RUTF). RUTFs are available as energy-dense pastes or biscuits, which are resistant to bacterial growth, unlike milk-based liquid products and are useful for treating severe malnutrition in children who have limited access to local family diets for nutritional rehabilitation. When RUTF is given to children with severe malnutrition, 150–220 kcal/kg/day should

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Box 33.10 Facility-based management Severely malnourished children in institutional setting are given F-75, a "starter formula", which is administered frequently - every 2-3 hours and in small amounts. Naso-gastric tube feeding may be required in this stage. Additionally, micronutrient supplements are given. Usually, the child's appetite returns to normal after 2-7 days. F-75 is gradually replaced with another formula F-100 or the "catch-up" formula. Both F-75 and F-100 are therapeutic milk products designed to treat severe malnutrition. F-75 contains 75 kcal of energy and 0.9 g protein per 100 ml, and F-100 contains 100 kcal of energy and 2.9 g proteins per 100 ml. Both are very high in energy, fat, and protein, and provide a large amount of nutrients. These are now used by all major humanitarian aid organizations to treat acute malnutrition. Ingredients include concentrated milk powder, food oil, and dextrin vitamin complexes. The formulas may be prepared by mixing with the local water supply. Sometimes 'Plump nut/peanut butter' is substituted for F-100. F-75 may be constituted using a cereal base in place of milk. However, it is important that child feeding should be accompanied with other components of child care such as social contact, simulation, play etc. Rehabilitation at institutional level should be followed by family level care and weekly monitoring at the institutional level.

be provided. This energy-dense fortified therapeutic food may be given in two-three doses depending upon the age, and severity of malnutrition. In case of moderate to severely malnourished children, anorexia may be a problem and hence the portion size of food has to be small. Box 33.11 Read-to-Use Therapeutic Foods (RUTF) RUTF have a similar nutrient composition to F100, which is the therapeutic diet used in hospital settings. But unlike F100, RUTF are not water-based, meaning that bacteria cannot grow in them. Therefore these foods can be used safely at home without refrigeration and even in areas where hygiene conditions are not optimal. When there are no medical complications, a malnourished child with appetite, if aged six months or more, can be given a standard dose of RUTF adjusted to their weight. Guided by appetite, children may consume the food at home, with minimal supervision, directly from a container, at any time of the day or night. Because RUTF do not contain water, children should also be offered safe drinking water to drink at will. The technology to produce RUTF is simple and can be transferred to any country with minimal industrial infrastructure. RUTF cost about US$3 per kilogram when locally produced. A child being treated for severe acute malnutrition will need 10–15 kg of RUTF, given over a period of six to eight weeks.

Ready-to-use therapeutic foods Ready-to-use therapeutic foods (RUTF) are high energy, fortified, readyto-eat foods suitable for the treatment of children with severe acute malnutrition. These foods should be soft or crushable and should be easy for young children to eat without any preparation. At least half of the proteins contained in the foods should come from milk products. RUTF contains iron and F-100 does not contain this micronutrient.

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Public health nutrition in developing countries

Nutritional composition of RUTF [9, 16] Moisture content Energy Proteins Lipids Sodium Potassium Calcium Phosphorus (excluding phytate) Magnesium Iron Zinc Copper Selenium Iodine Vitamin A Vitamin D Vitamin E Vitamin K Vitamin B1 Vitamin B2 Vitamin C Vitamin B6 Vitamin B12 Folic acid Niacin Pantothenic acid Biotin n-6 fatty acids n-3 fatty acids

– – – – – – – – – – – – – – – – – – – – – – – – – – – – –

2.5% maximum 520–550 Kcal/100 g 10–12% total energy 45–60% total energy 290 mg/100 g maximum 1,110–1,400 mg/100 g 300–600 mg/100 g 300–600 mg/100 g 80–140 mg/100 g 10–14 mg/100 g 11–14 mg/100 g 1.4–1.8 mg/100 g 20–40 μg 70–140 μg/100 g 0.8–1.1 mg/100 g 15–20 μg/100 g 20 mg/100 g minimum 15–30 μg/100 g 0.5 mg/100 g minimum 1.6 mg/100 g minimum 50 mg/100 g minimum 0.6 mg/100 g minimum 1.6 μg/100 g minimum 200 μg/100 g minimum 5 mg/100 g minimum 3 mg/100 g minimum 60 μg/100 g minimum 3%–10% of total energy 0.3%–2.5% of total energy

Children below 6 months should neither receive RUTF nor solid family foods. These very young infants need milk-based diets and their mothers to re-establish breastfeeding. These new methods of therapeutic feeding make it easier to care for moderately severely malnourished children at home, who have no medical complications, are alert and have reasonable circumstances at home for rehabilitation. Children, who develop medical complications, become anorexic and develop pedal oedema, should be referred to an inpatient facility based management where trained staff can provide all the required medical and nutritional care.

Food and nutrition in natural and manmade

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When families have access to nutrient-dense foods, severe malnutrition without medical complications can be managed in the community without RUTF, by means of carefully designed diets using low-cost family foods that are preferably prepared using fortified flour blends of cereals and lentils, and enriched with oil/butter/ghee. In addition, these children should be provided, appropriate mineral and vitamins as supplements.

33.5

Nutritional requirements

33.5.1 Energy requirements The need for food assistance in the disasters / emergency situations has been discussed in details in the preceding sections. Table 33.3 presents the energy requirements for the different sections of population and has been adapted from “The Management of Nutrition in Major Emergencies, WHO, 2000” and these recommendations form the basis for deciding the food commodities to be given and the ration size. Table 33.3 Energy requirements for emergency-affected populations, developing country profile (demography and anthropometry) in kilocalories per day [10] Age/sex Male(a) Female(a) Male and female(a) group (years) % of total Energy % of total Energy % of total Energy population requirement population requirement population requirement per caput per caput per caput 0 1(b) 2(b) 3(b) 4(b) 0–4 5–9 10–14 15–19 20–59(c) +60(c) Pregnant Lactating Whole population (a) (b)

(c)

1.31 1.26 1.25 1.25 1.24 6.32 6.00 5.39 4.89 24.80 3.42

850 1250 1430 1560 1690 1320 1980 2370 2700 2460 2010

50.84

2250

1.27 1.20 1.20 1.19 1.18 6.05 5.69 5.13 4.64 23.82 3.82 2.4 2.6 49.16

780 2.59 1190 2.46 1330 2.45 1440 2.44 1540 2.43 1250 12.37 1730 11.69 2040 10.53 2120 9.54 1990 48.63 1780) 7.24 285 (extra 2.4 500 (extra) 2.6 2010 2080

820 1220 1380 1500 1620 1290 1860 2210 2420 2230 1890 285 (extra) 500 (extra)

adult weight: males: 60kg, female: 52 kg. population estimates for years 1, 2, 3 and 4 were not available from the United Nations so estimates were made by the interpolation of UN data for 0–5 years. Figures in the Table are for the energy requirements of light activity levels (1.55 × BMR for males and 1.56 × BMR for females).

For moderate and heavy activity levels, the energy requirements would need a revision and should be calculated as:

(d)

(c)

(b)

10.0 10.0 10.0 10.0 10.0 10.0 2.5 2.5 2.5 2.5 2.5 2.5 2.5 2.5 2.5 2.5 +7.5 +7.5 3.2 3.2 3.2 3.2–3.8(d)

Vitamin D (µg calciferol) 0.3 0.5 0.55 0.60 0.65 0.5 0.75 0.95 0.8 0.9 1.1 0.9 1.0 1.0 0.8 0.9 +0.1 +0.2 0.9 0.75 0.8 0.9

Thiamine (mg)(c)

0.5 0.8 0.9 1.0 1.1 0.8 1.2 1.6 1.35 1.5 1.8 1.4 1.6 1.7 1.4 1.55 +0.1 +0.3 1.4 1.2 1.3 1.4

Riboflavin (mg)(c)

4.2 6.4 7.5 8.2 8.9 7.1 10.3 13.1 11.3 12.2 15.3 11.9 13.6 14.5 11.5 12.9 +1.1 +2.7 11.9 10.3 10.9 12.0

24 50 50 50 50 45 80 150 130 140 200 170 185 200 170 185 +250 +100 200 170 185 160

Niacin Folic acid equivalents (µg) (mg)(c) 0.1 0.45 0.53 0.61 0.69 0.50 0.82 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0 +0.4 +0.3 1.0 1.0 1.0 0.9

Vitamin B12 (µg) 20 20 20 20 20 20 20 25 25 25 30 30 30 30 30 30 +20 +20 30 30 30 28

VitaminC (mg)

13 8 8 9 9 9 16 24 27 26 15 32 24 15 32 23 120 17 15 15 15 22

Iron (mg)(d) Low (5– 9%) 50–90(d) 90 90 90 90 90 110 140 140 140 150 150 150 150 150 150 +50 +50 150 150 150 150

Iodine (µg)

Vitamin A requirements may be met by absorption of vitamin A itself (retinol) or provitamin A carotenoids, which have varying equivalence in terms of vitamin A activity. The requirement is expressed in terms of the retinol equivalent (RE) which is defined by the following relationships: 1ug retinol = 1.0mg RE; 1mg beta-carotene = 0.167 g RE; 1ug other provitamin A carotenoids = 0.084 mg RE. B-vitamin requirements are proportional to energy intake and are calculated: Thiamine: 0.4 mg per 1000 kilocalories ingested; Riboflavin: 0.6 mg per 1000 kilocalories ingested; Niacin equivalents: 6.6 mg per 1000 kilocalories. Iron requirements are based on the premise that in the developing countries, bioavailability of iron from the dietary sources is only 5–9%. The higher figure is used for developing countries because of the larger proportion of children under 5 years whose requirement is greater.

350 400 400 400 400 390 400 550 550 550 600 500 550 600 500 570 +100 +350 600 500 540 500

0 1 2 3 4 0–4 5–9 10–14 M 10–14 F 10–14 M/F 15–19 M 15–19 F 15–19 MF 20–59 M 20–59 F 20–59 M/F Pregnant Lactating 60+ M 60+ F 60+ M/F Whole population

(a)

Vitamin A (μg retinol equivalent RE(b))

Age/sex group (years)

Table 33.4 Vitamin and mineral requirements – safe levels of intake (summary)(a) [10]

922 Public health nutrition in developing countries

Food and nutrition in natural and manmade

923

Moderate activity levels for males: 1.78 × BMR and for females 1.64 × BMR; Heavy activity levels for males: 2.10 × BMR and for females; 1.82 × BMR.

33.5.2 Micronutrient requirements Since the emergency programmes aim to cover the complete nutritional requirements of the target population, food fortification should be given active consideration. Food rations must be designed to meet these needs and to prevent micronutrient deficiency diseases. Table 33.4 gives the requirements of various micronutrients for different population groups. Levels of fortification, however, should be evaluated and adjusted according to bioavailability of the nutrient(s) in the diets of target populations. Most countries in need of food aid do not have the capability to implement adequate food control procedures locally. Thus based on a realistic estimate of food intake, adequate levels of micronutrients at the point of consumption should be ensured, either through fortification or through supplementation. All required nutritional information must be provided through appropriate labeling. Also, it is important to monitor the levels of micronutrient, bioavailability, stability and shelf-life of fortified food used. However, foods fortified with micronutrients may not meet fully the needs of certain nutritionally vulnerable subgroups such as pregnant and lactating women, or young children. For this reason UNICEF and the WHO have developed the daily multiple micronutrient formula shown in Table 33.5 to meet the daily recommended nutrient intake (RNI) of these vulnerable groups during emergencies [17, 18, 19]. Table 33.5 The composition of multiple micronutrient supplements for pregnant women, lactating women, and children from 6 to 59 months of age [18–22] Micronutrients

Pregnant women

Children (6–59 months)

Vitamin A (µg) Vitamin D (µg) Vitamin E (mg) Vitamin C (mg) Thiamine (vitamin B 1) (mg) Riboflavin (vitamin B2) (mg) Niacin (vitamin B3) (mg) Vitamin B6 (mg) Vitamin B12 (µg) Folic acid (µg) Iron (mg) Zinc (mg) Copper (mg) Selenium (µg) Iodine (µg)

800.0 5.0 15.0 55.0 1.4 1.4 18.0 1.9 2.6 600.0 27.0 10.0 1.15 30.0 250.0

400.0 5.0 5.0 30.0 0.5 0.5 6.0 0.5 0.9 150.0 10.0 4.1 0.56 17.0 90.0

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Based on the detailed requirement for energy and micronutrients stated in Tables 33.3 and 33.5, the following figures for macro and micronutrients can be used for planning purposes in the initial stage of a disaster [10]. Table 33.6 Recommended nutritional composition of a general food ration for the disaster affected population [10] S. No. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Nutrient

Mean population requirement

Energy Protein Fat Vitamin A B1 B2 Folic acid B3 B12 Vitamin C Vitamin D Iron Iodine Magnesium* Zinc* Selenium* Vitamin E* Vitamin K* Biotine* Pantothenic acid*

2100 kcal 10–12% of total energy (52–63 g) but <15% 17% of total energy (40g) 1660 IU (or 0.5 mg retinol equivalent) 0.9 mg (or 0.4 mg per 1000 kcal) 1.4 mg (or 0.6 mg per 1000 kcal) 160 mcg 12.0 mg (or 6.6 mg per 1000 kcal) 0.9 mcg 28.0 mg 3.2–3.8 mcg calciferol 22 mg (low-bioavailability, i.e. 5–9%) 150 mcg 201 mg 12.3 mg 27.6 mcg 8.0 mg alpha – TE 48.2 mcg 25.3 mcg 4.6 mcg

* provisional requirements

It may however be noted that the above mentioned requirements of various nutrients are based on a reference population as given in the following table: Table 33.7 Reference population [12] S. No.

Group

% of population

1. 2. 3. 4. 5. 6. 7. 8. 9.

0–4 years 5–9 years 10–14 years 15–19 years 20–59 years 60+ years Pregnant Breastfeeding Male/Female

12 12 11 10 49 7 2.5 2.5 51/49

As the demographic structure of different populations varies, this will affect the nutritional requirements of the population concerned. For example, if 26% of the affected population is aged under five, and the

Food and nutrition in natural and manmade

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population consists of 50% males and 50% females, the energy requirement is reduced to 1,940 kcal. Energy and protein requirements should be adjusted for the following factors [12]: 1. The demographic structure of the population, in particular the percentage of those under five years of age and the percentage of females (this may change in populations affected by HIV/AIDS); 2. Mean adult weights and actual, usual or desirable body weights – Requirements will increase if the mean body weight for adult males exceeds 60kg and the mean body weight for adult females exceeds 52 kg; 3. Activity levels to maintain productive life – Requirements will increase if activity levels exceed light (i.e. 1.55 × Basal Metabolic Rate for men and 1.56 × Basal Metabolic Rate for women); 4. Average ambient temperature and shelter and clothing capacities. Requirements will increase if the mean ambient temperature is less than 20°C; 5. The nutritional and health status of the population – Requirements will increase if the population is malnourished and has extra requirements for catch-up growth. HIV/AIDS prevalence may affect average population requirements. Whether general rations should be adjusted to meet these needs will depend on current international recommendations. If it is not possible to incorporate this kind of information into the initial assessment, the figures in the table above may be used as a minimum in the first instance.

33.6

Addressing food security

Normal food production and consumption must resume as early as possible and effort should be made that nutrition intervention with community becoming dependent on outside help indefinitely, is discontinued as much as possible. Addressing food security is therefore crucial. Food security depends principally on three variables: availability of food, access to food and a nutritious diet, and proper use of food to ensure maximum nutrition and hygiene. The humanitarian aid agencies along with NGOs, work towards food security through the capacity building initiatives, which provide cash for work or cash as well as food for work. These projects enable communities to build up their assets by working on specific projects. Projects involving cash or food in exchange for work help the communities, not only

Public health nutrition in developing countries

926

financially and nutritionally, but also increase their self-reliance. These projects can lead to infrastructure improvements, such as the rebuilding of roads and bridges, improvements in irrigation and drainage, tree planting, and building health posts and schools. Disadvantages may include a possible negative impact on the health of children whose mothers are enrolled in food for work schemes. While these may increase the level of preparedness of the community for future food shortages, they need to be appropriate for the local agricultural environment and culture. Box 33.12 presents details of food security measures taken in Gujarat. Box 33.12 Addressing food security: WFP experience in Gujarat The District of Kachchh, in the western most part of the State of Gujarat, suffered a continuing drought for the last two years. On the 26 January 2001, a severe earthquake hit the district causing widespread devastation. These factors caused a high degree of food insecurity in the district. Immediately after the earthquake, International Federation of Red Cross and Red Crescent Societies, the World Food Programme, Save the Children and Oxfam conducted a survey to determine the prevalence of acute malnutrition in the District of Kachchh. Its focus was to use the anthropometric measurements of weight and height as the prime determinants of the level of acute malnutrition in the district and to establish baseline nutritional data, which could be used to determine the impact of the earthquake and to target and plan assistance. This survey collected quantitative information on the prevalence of diarrhea and respiratory infections, breastfeeding and the effect of the earthquake on food intake; to support the anthropometric data, through a questionnaire. The survey targeted children aged between 6 and 59 months as a proxy for the rest of the population. Anthropometric measurements were taken from a total of 798 children randomly sampled throughout the District of Kachchh. A caretaker of each child was also interviewed to obtain basic information on the prevalence of diarrhea and respiratory infections, food intake since the earthquake, level of breastfeeding and registration at Anganwadi Centres (child development centre at village level). The nutritional index of weight for height, the statistical description of Z-scores and international reference values (NCHS) were used to interpret the anthropometric data collected by this survey. Based on the survey report, food assistance in the form of India-mix (fortified blended food containing wheat, fullfat soya, sugar and 11 critical micronutrients) was provided to all the ICDS beneficiaries through the Anganwadi workers. ICDS system was useful in identifying and establishing contact with the beneficiaries. After over 8 months of intervention, a repeat survey was undertaken to see if there was any impact of the food-assistance. The results were very encouraging as it helped to not only stall deterioration of nutritional status but in fact helped to improve when compared to the baseline indicators as assessed immediately after the earthquake. The post-phase survey, following 8 months of intervention, presented the following status: Overall malnutrition (weight for age) among children 6–59 months decreased by 9.9% ●

●

percent reduction higher in girls (14.1%) compared to boys (6.3%) in both age groups percent reduction higher in older children (36–59 months).

Food and nutrition in natural and manmade

927

Moderate malnutrition ● ● ●

Percent reduction in moderate malnutrition was 11.3% in the total sample reduction higher amongst younger children 6–35 months reduction was higher in girls than in boys in both age groups

Rural-urban differences in malnutrition ●

●

overall malnutrition was higher in rural areas compared to urban areas (baseline versus post-phase survey) reversal of trends observed in the rural and urban areas in the post-phase.

An improvement over baseline seen in the rural areas was attributed to the concerted efforts in rural areas.

33.7

Types of disasters and disaster management in India

(a) India: a country prone to natural calamities The Asia-Pacific region experiences nearly 60 per cent of the world’s natural disasters. India, on account of its geographical position, climate and geological setting, is the worst-affected theatre of disaster in the South Asian region. India is adversely affected by drought and floods, earthquakes and cyclones year after year. (b) The cost and consequences of disasters The cost of natural disasters in India, in terms of human life, loss of property and assets and loss of shelter and livelihoods, is immense. Between 1980 and 1999 the total number of people killed in disasters was 110,131. Between 1988 and 1997, disasters affected 24.79 million every year in India. In 1998, 9,846 people died and 34.11 million people were affected by disasters. Between 1985 and 1995, disasters caused an annual economic loss of around US$ 1,883.93 million. The economic loss from January 2001 earthquake alone was huge, the official estimate putting the number of human lives lost at 30,000 and the economic loss at US$ 10 billion [23]. According to estimates of the industry and business bodies, Confederation of Indian Industries (CII) and Federation of Indian Chambers of Commerce and Industry (FICCI), the damage to buildings and construction and related cost was Rs 120,000 to 150,000 million. The loss of infrastructure amounted to Rs 30,000 million. The damage to big factories was valued at Rs 15,000 million [24]. (c) Disaster management in India Approach to disaster management in India has been primarily reactive and relief centric. Now, there is a paradigm shift to move from providing

928

Public health nutrition in developing countries

assistance to adopting a holistic and integrated approach with emphasis on prevention, mitigation and preparedness. These efforts are aimed to conserve developmental gains and also minimize losses to lives, livelihood and property. In India the focus of ‘Disaster Management’ is shifting and the present approach comprises: prevention, mitigation and preparedness in predisaster phase, and response, rehabilitation and reconstruction in postdisaster phase. The National Disaster Management Authority (NDMA), headed by the Prime Minister of India, is the apex body for disaster management in India. The setting up of the NDMA and the creation of an enabling environment for institutional mechanisms at the State and District levels is mandated by the Disaster Management Act, 2005. NDMA as the apex body is mandated to lay down the policies, plans and guidelines for Disaster Management to ensure timely and effective response to disasters. Thus, various ministries at the central government level have been specifically identified and entrusted with the task of managing different types of disasters. The responsibility to cope with natural disasters is essentially that of the State Government. The role of the Central Government is supportive in terms of supplementation of physical and financial resources. The Chief Secretary of the State heads a state level committee which is in overall charge of the relief operations in the State and the Relief Commissioners who are in charge of the relief and rehabilitation measures in the wake of natural disasters in their States, function under the overall direction and control of the state level committee. In many states, Secretary, Department of Revenue, is also in-charge of relief. State Governments usually have relief manuals and the districts have their contingency plan that is updated from time to time. The Government of India is a member of various international organisations in the field of disaster response and relief. While, as a policy, no requests for assistance or appeals are made to the international community in the event of a disaster, assistance offered suo moto is accepted. Linkages exist with the following UN organisations: (a) UN Office for Coordination of Humanitarian Affairs (UN OCHA), which is responsible by UN General Assembly mandate for all international disaster response. (b) United Nations Development Programme (UNDP), responsible for mitigation and prevention aspects of disaster management. (c) UN Disaster Assessment and Coordination (UNDAC) System. In most disaster and complex emergency situations that require international humanitarian assistance, the UN Resident Coordinator

Food and nutrition in natural and manmade

929

represents the Office for the Co-ordination of Humanitarian Affairs (OCHA), and its primary function is to facilitate and ensure the quick, effective, and well-coordinated provision of humanitarian assistance to those seriously affected by the complex emergency in question. This assistance includes: assessing and addressing humanitarian needs, humanitarian advocacy, and information dissemination. It also aims at strengthening national and regional disaster response capacity in disaster prone countries. Government of India however, as a policy does not take food aid for managing the disasters as it considers itself capable of mobilizing resources and providing the necessary food aid to the populations affected by any disaster. Way forward Nutritional status of individuals determines the ability to cope with the effect of natural disasters. Women and children are more prone to nutritional deficiencies because of their unique nutritional needs. Women are especially vulnerable when they are pregnant or breastfeeding, and some cultures, have household food hierarchies. This physical and biological difference heightens their vulnerability and their initial response to natural hazards [25]. Social norms and given roles (related to the expected behaviour of women) compounded by inequitable distribution of aid and resources caused by social hierarchies, leads to higher morbidity and mortality amongst women and children during disasters. Hence for effective and preventive management of disasters, it is important for aid-agencies to be sensitive and focus on timely and adequate food aid for these vulnerable groups. However, though women are disproportionately impacted by disasters and swift environmental changes, they also have contributed to curbing the impacts of disasters [26]. Women’s knowledge and responsibilities related to natural resource management have proven to be critical to community survival and hence efforts must be made towards actively building the capacity of women and adolescent girls in planning for preparedness for disaster management. They would be the right resources to identify those in need of food aid within their communities and become powerful allies to reduce the impact of disasters on health, nutrition and survival of the communities.

References 1.

World Health Organization (2002). Disasters and emergencies. Definitions Training Package. WHO/EHA PanAfrican Emergency Training Centre, Addis Ababa. Retrieved August 10, 2006, from www.who.int/disasters/repo/ 7656.pdf

930 2.

3. 4. 5.

6. 7.

8. 9. 10. 11. 12. 13. 14.

15. 16. 17.

18. 19.

20. 21. 22.

23.

Public health nutrition in developing countries United Nations International Strategy for Disaster Reduction (UN/ISDR) (2004). Terminology: Basic terms of disaster risk reduction. Retrieved June 4, 2006, from www.unisdr.org/eng/library/lib-terminology-eng-p.htm NOJI E (1997). Public Health Consequences of Disasters, New York, Oxford University Press. Disaster Management in India – A Status Report, Ministry of Home Affairs, National Disaster Management Division, August 2004 p. 3. JOSE RODRIGUEZ LL , VOS F, BELOW R, SAPIR DG (2009). Annual Disaster Statistical Review: Numbers and Trends 2008, Centre for Research on the Epidemiology of Disasters (CRED), Brussels. Natural Hazards Observer 21(5) May, 1997. Displacement, loss of buying power and erosion of coping and caring capacities, limit people’s access to health services and often contribute to an overall increase in morbidity and mortality. MÉDICINS SANS FRONTIÈRES (1995). MSF Nutrition Guidelines. World Health Organization (1999). Management of severe malnutrition: A manual for physicians and other senior health workers. World Health Organization (2000). The management of nutrition in major emergencies. Geneva: WHO. UNHCR/UNICEF/WFP/WHO (2003). Food and nutrition needs in emergencies. The Sphere Project. (2004). Humanitarian charter and minimum standards in disaster response. YOUNG H , BORREL A , HOLLAND D , and SALAMA P (2004). Public nutrition in complex emergencies. Lancet, 365, pp. 1899–1909. World Health Organization (1987). Global nutritional status, anthropometric indicators. Geneva, Switzerland: WHO Nutrition Unit, Division of Family Health. World Health Organization (2006). The WHO Child Growth Standards. http://www.who.int/child-adolescent-health/New_Publications/NUTRITION/ CBSM/ tbp_4.pdf UNICEF/UNU/WHO (1999). Composition of a multi-Micronutrient supplement to be used in pilot programmes among pregnant women in developing countries. Report of a Workshop. New York, UNICEF. FAO/WHO (2005). Vitamin and mineral requirements in human nutrition, 2nd ed. Geneva, World Health Organization. Institute of Medicine (2001). Food and Nutrition Board Dietary reference intakes. Application in dietary assessment. A report of the Subcommittee on Interpretation and uses of dietary reference intakes and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. National Academic Press, Washington D.C. w w w. s e a r o . w h o . i n t / . . . Nutrition_for_Health_and_Development_ WHO_UNICEF_statement_emergency.pdf FAO/IAEA/WHO (1996). Trace elements in human nutrition and health. WHO. Geneva. WHO. Prevention and control of iodine deficiency in pregnant and lactating women, and in children less than two years old. Report of a consultation. Geneva. GUPTA HK , RAO PN , RASTOGI BK and SARKAR D (2001). Science, 291, pp. 2101– 2102.

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24. Disasters: Background & Perspective by Vinod C Menon and Shirish Kavad – published in www.infochangeindia.org/200310045981/Disasters/Backgrounder/ Disasters-Background-Perspective. 25. CANNON T (2002). Gender and climate hazards in Bangladesh. Gender and Development, 10(2), pp. 45–50. 26. AGUILAR L (2004). Climate change and disaster mitigation: Gender makes the difference: IUCN. Switzerland.

34 Nutrition for the aged Kumud Khanna and Seema Puri

Kumud Khanna is the Director of Institute of Home Economics and the Head of Department of Home Science, University of Delhi. Dr. Khanna is PhD in Community Nutrition from Harvard University, Washington, USA. She has over thirty five years of teaching and research experience. Her research interests include geriatric nutrition, clinical nutrition and public health nutrition. Seema Puri is an Associate Professor at Institute of Home Economics, Delhi University. She is PhD in Nutrition from Delhi University and has undergone specialized training in Social Gerontology. She has over twenty five years of teaching and research experience. Her research interests include geriatric nutrition, bone health, nutrition and HIV/AIDS.

!".1

Introduction

Population ageing is having profound effects on society. It is the most significant result of the process known as demographic transition. Reduction in fertility results in a decline in the proportion of young in the population. Reduction in mortality means a longer life span for individuals. Population ageing involves a shift from high mortality / high fertility to low mortality / low fertility and consequently an increased number of old people in the population. India is undergoing such a demographic transition. Its influence is being felt at every level, from family life and living arrangements, employment, the provision of health services and pension systems, to the state of economy. Ageing will need to occupy the increasing attention of policymakers in the twenty first century.

!".2

Definition of old age

It is difficult to precisely define ageing. Ageing is an inevitable, irreversible and progressive phenomenon and is the last phase of human life cycle. Ageing has also been defined as a progressive loss of adaptability with the passage of time so that the individual is less able to

932

Nutrition for the aged

933

react adaptively to challenges from the external or internal environment. Bagchi [1] has stated that ageing implies predictable, progressive, universal deterioration in various physiological systems - mental and physical, behavioural and biomedical. At the same time, ageing can also involve psychological growth in capacities for creativity, prudence, wisdom and experience. The age at which one's productive contribution declines and one tends to be economically dependent can probably be treated as the onset of the aged state of life. It is usually regarded as synonymous with pensionable age or age at retirement. In India, retirement from active life is equated with old age. In modern India, retirement age is fixed at 60 years in most Government jobs. In academic research too, retirement age is often taken as an index of aged status. For all practical purposes people above 60 years are considered to be "senior citizens". A three-fold classification given by William and Anderson [2] is generally used to distinguish the older adult population: (a) 'Young-Old' is the age group between 60 and 74 years, living in relatively healthy and vigorous state and are retired but remain productive to the extent that they can support themselves without being too heavy a burden on their families and the State. (b) 'Old-Old' comprises the aged between 75 and 84 years, in which they remain active, but the majority needs a range of supportive health and social services. (c) 'Oldest-Old' are 85 years or older, generally dependent on the family and need a comprehensive programme of supportive health and social services.

34.3

Greying of nations

The demographic transition, commonly known as greying of nations reveals that the number of elderly is on the rise, which has intensified the concern for this vulnerable section of the population. Changes at both the lower and upper ends of the population distribution will give rise to an explosive growth of the elderly (persons aged 65 and above) and especially the oldest old (persons aged 80 and above) population. Figure 34.1 presents the population pyramid which indicates a significant projected increase in population in over 60 years age – infact almost double of the 1995 figures. United Nations Demographic Estimations has forecast that the number of people of 60 years and above worldwide is likely to go up from 427 million in 1985 to 1,171 million in 2025, an increase of over 174 per cent [3]. These percentages are and shall remain higher in the coming

934

Public health nutrition in developing countries

decades in the more developed regions of the world than in the less developed regions. However, unlike developed regions where decline in fertility began in the last century, the less developed regions have just started fertility decline and therefore currently account for most of the increase in the world's elderly population. In every region, however, the population over 75 years will increase at an even faster rate and those over 80 years will increase fastest of all. In most regions, the proportion in the oldest group will be more than double.

80+ 70–74 60-64 50–54 40–44 30–34 20–24 10–14 00–04

34.1 The world population is ageing. Population pyramid in 1995 and 2025.

34.4

Characteristic trends of ageing in India

India already ranks second population-wise, in the world, and has the largest proportion of the world's elderly population in absolute numbers. The Census of India, conducted every 10 years, has been the major (rather only) source of information on the age structure of the population. The last census report revealed the ageing population to be 76 million in 2001. The United Nations defines a country as 'ageing' where the proportion of people over 60 years reaches 7 per cent. With 7.5 per cent of the total population being over 60 years old India has progressed from being a mature society (elderly population between 4 to 7%) to becoming an ageing society (ageing population more than 7%). Fast growth rate – The number of persons aged 60 years and above in India has increased at a faster rate as compared to the growth rate of the population of all ages (total population) both in rural and urban areas. It has increased from 12 million in 1901 to 19.6 million in 1951 to 76 million in 2001, constituting 7.5 percent of the total population [4]. Further, the total number of elderly persons is projected to be around 300 million by

Nutrition for the aged

935

2051, comprising 17.3 percent of the population (Table 34.1). Table 34.1 Size of ageing population in India (Census, 2001) [4] Size 1961 1971 1981 1991 2001

25 33 43 57 76

% 5.6 5.9 6.5 6.8 7.5

This demographic shift in the ageing population amounts to a revolution in both demographic and cultural terms and have been brought about partly by socio-economic factors like better nutrition and living conditions and partly by improvement in health care. Life expectancy – As a result of improved health care facilities and standard of living, life expectancy of Indians is going up. The average Indian, who lived for 32 years in 1947, today has longevity of 62 years which may further go up to 75 years by the year 2015. At 60 years, males can expect to live up to 76 years while females have 18 years more after 60 years [5]. Age structure of the population – The number of elderly persons declines with increase in the age. According to Census data (2001), about 7.5 percent of the elderly population belongs to the age group 60+ and about 2.9 percent of them were in the 70+ age group. Less than 1 percent of the elderly persons were 80 years and above. In comparison, the respective figures for 1961 stood at 5.6 percent for 60+, 2.0 percent for 70+ and 0.5 percent for 80+ age groups (Table 34.2) [4]. Thus, the young old have been increasing at a much faster pace than the old-old in India, whereas globally maximum growth is recorded in the latter and not in the former category of elderly. Table 34.2 Age structure of ageing population – millions (%). [5] Age Structure 60+ 70+ 80+ 90+ 100+

1961 24.7 8.6 2.4 0.5 0.09

(5.6) (2.0) (0.5) (0.1) (0.02)

2001 76.6 29.3 8.0 1.2 0.2

(7.5) (2.9) (0.8) (0.2) (0.02)

In India, in the next several years, the old-old will represent a notable segment exerting their own influence on morbidity, disability and mortality in the aged. The population of old-old will produce great stresses on the basic communities, especially within families. Among the likely consequences of an increase in the old-old category, two should be mentioned. First, the probable increase in the number of frail or dependent persons due to increased frequency of handicaps and disabilities in later life and second, the increased difficulties to be overcome by families who are eager to play their traditional caring role.

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Female 34.2 Age Pyramid for India, 2001.

34.3 Age Pyramid for India, 2051.

Feminization of old age – Another feature of the demographic transition with serious, long-term implications is the increasing number of elderly females. Women make up the majority of the older population in virtually all countries. The “feminization” of old age is already advanced in the developed world and is growing even faster in the developing countries. India is one of the few countries in the world where men outnumber women at all ages till about 70 years. Only in the very old age group, 80 and over, are there more women in the population than men. This

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phenomenon among the older people is of importance as female life expectancy is higher than that of males. It also gives an indication of

34.4 Regional difference in the proportion of elderly (60+), 2001–2051 (Census 2001) [5].

widowhood or widowerhood. More than 54 percent of Indian women over 60 years of age live without a spouse as compared to 15.5 percent of older men [5]. As women have a longer life expectancy than that of men and in most cases, their husbands are several years older, a large proportion experience a prolonged period of widowhood, social isolation and declining health coupled with financial difficulties and dependence on others, i.e. family members, community, charitable and philanthropic organizations.

34.5 Percentage of elderly 60 and above by sex, 1901–2051.

Socio-economic transition in India – Along with the changes in the demographic profile, the country is also undergoing a changing social, cultural and economic milieu. Urbanization, accompanied with a breakdown of joint family system, increased migration from rural to urban

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areas to abroad, and loss of traditional values have left the elderly alone and lonely, often economically helpless. Increasing economic burden on the young family is resulting in greater desolation for the elderly. More and more young women are joining jobs, leaving the elderly to fend for themselves. Job competition poses further demands on the young couple, leaving still less time for social interactions with the elderly. Family structure – Industrialization and urbanization have brought great changes to family structure in this century. The extended family that existed in feudal society has changed to the nuclear family. This has affected the position of the elderly in the family as well as the family's capacity to take care of the aged. The traditional Indian family structure used to provide the required environment for comfortable living of the elderly. The extended family usually consisted of two generations living together wherein the elderly used to have a different status in the household. In recent years, there has been a significant shift from the patriarchal family towards a nuclear family. Again, with rapid urbanization and industrialization and increasing frequency of full time and part time paid work by both spouses, traditional family support systems for the elderly are also considerably strained. Various survey findings in this direction conclude on the deteriorating status of the elderly in the transient Indian family structure [6]. They observed that change in living arrangements, family structure and mode of sudden retirement adversely affects the old, and further, that the old people are in increasing proportions losing the status and security which they enjoyed in the traditional Indian family structure. Economic situation – Inadequate financial resources have been reported to be a major problem facing the elderly. Financial problems are more common among widows and among elderly in nuclear families. They also indicated economic insecurity to be having some bearing with the social strata of class and caste. In India, older people have to depend mostly on their own earnings/savings or on their own family. People employed in the agriculture sector continue to work as long as they are physically capable. In urban areas, retired men, i.e. after 60 years of age, may take up part time jobs to supplement their income. A vast majority of women are housewives, and depend on their families. Women's work is hardly quantified and monetized. In contemporary Indian society, the position and status of the old have been undermined by several factors such as: (a) Decline in the institution of the joint family; (b) Changing values as reflected in growing individualism arising from urbanisation, westernisation and according high priority to the needs of the immediately family;

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(c) Fewer children due to acceptance of small family norms by the middle and upper classes; (d) Participation of women in employment in cities, leaving the old unattended during the day; (e) Migration of younger members for alternative sources of livelihood; (f) Acute paucity of accommodation in urban areas, exorbitant rents and high cost of living which act as a strong disincentive to bring old parents to live with the children; (g) Complexities of modern life and fast pace of social change; (h) Economic dependency status of old people in the absence of old age social security benefits [7].

34.5

Physiological ageing

Ageing is a normal biological process. The human growth period terminates at around 30 years of age, when senescence begins. Senescence is the organic process of growing older and displaying the effects of increased age. Advancing age is accompanied by progressive physiological changes in functions of most organs; the rate of change varies among individuals and among organ systems. As people age, there also tends to be a concomitant increase in the presence and number of chronic conditions such as hypertension, cardiovascular disease, osteoporosis, diabetes and dementia among others. These further compromise the quality of life in old age. Ageing is associated with a decline in many body functions, an accompanying change in structure, loss of lean mass and a relative increase in fat mass over time. While earlier these changes were considered to be intrinsically due to ageing, research over the past several decades has increasingly ascribed them to age-related disuse, inactivity and degenerative diseases. Changes in body composition – Some of the most dramatic changes seen with age are in body composition. Lean body mass declines over the adult age span and the decline accelerates beyond 80 years. Sarcopenia, a deficiency of flesh or muscle, strongly influences muscle strength, gait and balance, contributing to the increased risk of falls and frailty in older persons. Sarcopenia develops even in healthy, successfully ageing adults and does not depend on the onset of disease. Its multifactorial etiology includes biological changes of ageing, disuse atrophy secondary to declining physical activities and in some cases, protein or energy undernutrition or catabolic disease processes such as congestive heart failure, rheumatoid arthritis, hyperthyroidism, Parkinson disease, and chronic infection.

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Fat mass increases twofold between 20 and 60 years of age, followed by progressive decline. High fat mass is a risk factor for many diseases affecting older persons, including coronary heart disease, high blood pressure, diabetes, gallstones, osteoarthritis, and cancers of the breast and prostate. Increased obesity, especially distributed in the abdominal area, is associated with insulin resistance, which in turn causes diabetes and may also play a role in hypertension and hyperlipidaemia. A positive energy balance, i.e. energy intakes exceeding energy expenditure, can explain the increase in body fat mass through middle age. Conversely, negative energy balance is the primary cause of loss of body fat in old age. Since protein balance is closely linked to energy balance, this negative energy balance may also be the cause of loss of body protein in old age even when a protein-adequate diet is consumed. Consequent to these changes in body composition, alterations in body weight are also observed. Body weight increases during adult life until 50–59 years, after which it is seen to decline, particularly in the next two decades. Further, a reduction in lean body mass and decline in body weight leads to a decrease in basal metabolic rate, as age increases. Coupled with a decrease in physical activity, it leads to a reduction in energy requirements and consequently in the quantum of the food to be eaten. Changes in bone health – Ageing is typically associated with a loss of bone and total body calcium. Women at all ages have lower total bone mass or total body calcium than men. Over a lifetime, women lose about 40 percent of their skeletal calcium, approximately one half in the first five years after menopause and the remainder at a slower rate thereafter. The implications of poor bone health in older persons are related to an increased fracture risk and the effect on their functional ability and quality of life. In most cases hip fractures result from an injurious fall in persons with osteopenia. Prevention of hip fracture thus requires attention to both fall-related risk factors and bone density. Nutritional factors associated with traumatic hip fractures include protein-calorie malnutrition, alcohol abuse, osteomalaecia, low BMI, low muscle mass and strength, low levels of body fat, and low amounts of soft-tissue padding over the greater trochanteric region [8]. Immune function – Considerable evidence indicates that ageing is associated with altered regulation of the immune system which contributes to the increased incidence of infectious, inflammatory and neoplastic diseases observed in older persons and to their prolonged post-illness recovery periods. The illness patterns in the elderly reflect both a deterioration of immune function and increased incidence of upper respiratory infections, tuberculosis and cancer. Several investigators have suggested that the nutritional status of older persons may be less than optimal, thereby contributing to immunological changes. Many macroand micronutrients such as protein, zinc and vitamins E, C, and B6, have

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been shown to play a regulatory role in immune system maintenance. Neurological and cognitive function – On an average the brain loses 5–10 percent of its weight between the ages of 20 and 90, besides undergoing other changes like decrease in surface area and increase in number of plaques and neurofibrillary tangles. Neurological functions most commonly affected are cognition, gait, coordination, sensations and daily living tasks. Mental impairment and dementia a result of chronic degenerative brain disease, have a particularly severe impact on autonomy and independence. Depression, not an inevitable consequence of ageing, is fairly common in older adults. It may be associated with failing health, loss of independence, social isolation, financial concerns, grief over death of near and dear ones etc. Depression can affect appetite, dietary intake, digestion, weight status, fatigue and the overall sense of well being. It is generally accepted that dementing illnesses and depression have a strong genetic background. Nevertheless, nutrients can have either a disease-accelerating or protective effect. Also, nutrition can have an impact on brain function by impairing energy supply; affecting neurotransmitter synthesis and intermediary metabolism; enhancing, or protecting from oxidative stress; and influencing cytokines. Mental symptoms such as cognitive impairment, emotional irritability or other neurological signs are well known in case of vitamin deficiencies. Sensory losses – Sensory losses affect people to varying degrees and at different ages. Age related alterations to the sense of taste, smell and touch can lead to poor appetite, inappropriate food choices and lower nutrient intakes. While decreased sensitivity to taste (dysgeusia) and smell (hyposmia) are commonly attributable to old age, other causes include medications, diabetes, liver and kidney disease, hypertension, dementias or zinc or niacin deficiency. Approximately 25 percent of adults over 65 years of age have a reduced ability to detect one or more of the four basic tastes (sweet, sour, salty and bitter) due to a reduction in the number and function of the taste buds in the tongue. Sensitivity to bitter and sour taste lasts longer than to sweet or salty taste. Furthermore, the olfactory bulbs in the brain begin to shrivel which reduces the ability to smell. This further makes food taste even blander.

34.5.1 Hearing loss and vision loss is also seen in old people to varying degrees. Oral health – Diet and nutrition can be compromised by poor oral health. Loss of teeth, dry mouth (xerostomia), faulty dentures or even no dentures significantly alters the type of food eaten. The diet may be soft and mashy

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and raw vegetable and fruits, hard to chew foods are avoided. Consequently, a deficiency of vitamins and minerals as well as fibre may arise. Gastrointestinal tract changes – After the age of 50, there is a reduction in salivary secretion and a reduction in ptyalin content. Hence the digestion of complex carbohydrates is affected. Dysphagia or difficulty in swallowing may also increase the risk of aspiration pneumonia. Gastric pepsin secretion as well as acid secretion decreases, gastric volume is reduced. Delayed emptying of the stomach is seen in elderly. Intestinal motility is reduced due to atrophy of gastrointestinal tract musculature. Such changes in the alimentary tract lead to altered food intake and avoidance of many foods. Constipation and flatulence are common complaints among the elderly.

34.6

Pathological ageing

Coupled with the age related physiological decline is the imposition of chronic degenerative diseases in old age e.g. hypertension, cardiovascular disorders, diabetes and cancers. In fact, multiple morbidities are very commonly found in this age. Furthermore, "clustering" of these diseases towards the terminal part of life is a common phenomenon. Coronary heart disease and stroke – Coronary heart disease and stroke have become the major causes of death and disability among both ageing women and men. CVD age related changes are highly variable and impacted by environmental influences such as smoking, exercise and diet. Proper food intake, particularly reduced intake of total and saturated fat and increased intake of plant food, is a cornerstone in preventing and managing coronary risk factors protecting against arterial damage. Cancer – The five most deadly cancers worldwide are also the most common in terms of their incidence. Together they account for about 50 percent of all cancer cases and deaths. Among men, the leading eight killer sites are lung, stomach, liver, colonrectum, oesophagus, mouth/pharynx, prostate and lymph nodes. In women, the leading killer sites are breast, stomach, colon-rectum, cervix, lung, ovary, oesophagus and liver. Analysis of the risk factors involved in the development of major cancers shows that a few factors dominate-tobacco, diet, alcohol, infections and hormones; fortunately, all lend themselves to preventive action [8]. Osteoporosis and bone fractures – Osteoporosis and associated bone fractures are one of the major causes of disability and death that result in enormous medical expense the world over. The number of osteoporotic fractures increases exponentially with age. In India, unlike the senile osteoporotic fractures of the West, the high fluoride, low calcium dietaries and post-menopausal loss of bone density may be contributing factors for developing osteoporosis [9].

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Women are more prone because their bone loss accelerates after menopause. While estrogen deficiency is the primary cause, especially in elderly women, factors such as diet, physical activity and smoking are closely associated with osteoporosis. Lifestyle modifications, particularly increased calcium intake and physical activity, could over time have an important preventive impact on fracture rates. In order to live longer and healthier lives, it would therefore not only be necessary to delay the process of physiological ageing but also to prevent/delay the imposition of pathological ageing (in the form of chronic degenerative diseases) on an individual, while maintaining a good quality of life. While lower morbidity would reduce mortality, compression of morbidity into a lesser time frame would ensure a life with minimum disability and frailty, a life of dignity and independence.

34.7

Nutrition and ageing

Nutrition fits into the two ageing domains of gerontology and geriatrics. Gerontology, the study of normal ageing, derives from science, psychology and sociology. Gerontologic nutrition focuses on health promotion, risk reduction and disease prevention in older persons. Geriatrics is the study of chronic diseases frequently associated with ageing, including their diagnosis and treatment. Medical nutrition therapy for older adults is often called geriatric nutrition. In ageing, nutrition may play multiple roles. Firstly, as a primary prevention, role of nutrition should be emphasized in health promotion and disease prevention. It is a good strategy to combine healthy eating with physical activity. As secondary prevention, nutrition involves risk reduction and slowing the progression of chronic nutrition related diseases like hypertension, cardiovascular disorders, diabetes, osteoporosis and cancer to maintain functionality and quality of life. Tertiary prevention includes medical nutrition therapy of various diseases, often in a hospital setting. Nutrition is coming to the fore as a major modifiable determinant of chronic disease and age-related decline. Scientific evidence increasingly supports the view that alterations in the diet have strong effects, both positive and negative, on health throughout life. Most importantly, dietary adjustments may not only influence present health but may determine whether or not an individual will develop diseases like cancer, cardiovascular disease and diabetes much later in life. Researchers have evaluated the influence of various diet patterns on ageing changes and length of life in both experimental animals and human epidemiological studies. Several concepts have emerged from these studies.

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Energy – Studies on experimental animals have established that calorie restriction is an important measure for prolonging life span. Animals fed diets restricted in kilocalories yet adequate in protein, vitamins and minerals beginning at weaning and continuing through adulthood live 40 percent longer than those given unlimited access to food. Chronic diseases such as heart and kidney disease also appear at a later age in energy restricted animals. However, such studies have not been replicated in human subjects. Basal metabolic rates decrease linearly with age due to the changes in body composition. Energy requirements generally decrease with age because of changes in body composition, decrease in basal metabolic rate (BMR) and a reduction in physical activity. Energy needs decrease approximately 3 percent per decade. WHO (2002) has recommended that since low levels of physical activity and unchanged levels of energy absorption typically accompany older age, lower energy intakes are required to prevent obesity. The energy requirements of old age appear to be 1.4 to 1.8 multiples of the BMR to maintain body weight at different levels of physical activity [8]. Levels of physical activity that result in energy requirements in the higher end of the range are desirable for reducing morbidity and mortality. Translated into quantitative estimates, an intake less than 1500 kcals daily may result in micronutrient deficiencies and also give rise to health problems in the elderly. Box 34.1 Recommended daily nutrient intakes (WHO, 2002) [8] Energy – 1.4–1.8 multiples of BMR to maintain body weight at different levels of physical activity. Protein – 0.9–1.1 g/kg Fat – 30 en% in sedentary older persons and 35 en% for active older persons. Saturated fats should not exceed 8 en%. Riboflavin – 1.3 mg for men and for 1.1 mg for women. Folate – 400 μg Vitamin B 12 – 2.5 μg Vitamin C – 60–100 mg Vitamin A – 600–700 μg retinol equivalents Vitamin D – 10–15 μg Vitamin E – 100–400 IU Vitamin K – 60–90 μg Calcium – 800–1200 mg (in the presence of adequate vitamin D nutrition) Iron – 10 mg assuming there are no excessive iron losses Selenium – 50–70 μg Zinc – High Zn availability (50+%) men 4.2 mg; women 3.0 mg Moderate Zn availability (30%) men 7.0 mg; women 4.9 mg Low Zn availability (15%) men 14.0 mg; women 9.8 mg

In India, ICMR (1990) have also given lower energy requirements for elderly as compared to young adults, based on their age and activity levels [10]. Requirements of other nutrients have not been specifically outlined for older persons even in the Proposed Recommendations (2008-09) [11].

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Proteins – As people age and experience a loss of skeletal tissue mass, stores of protein in skeletal muscle may be inadequate to meet the body's needs, making dietary protein intake more important. Decreased food intake and sedentary lifestyle along with reduced energy expenditure become critical risk factors for malnutrition especially for insufficient intake of protein and micronutrients. WHO (2002) has therefore suggested that protein intakes of 0.9–1.1 g/kg body weight per day may be considered beneficial for healthy older persons. Lower intakes would, however, result in depletion of muscle mass and sarcopenia and excess amounts could unnecessarily stress the kidneys [8]. Carbohydrates – An abundant intake of carbohydrates is needed to protect protein from being used as a source of energy. Current dietary guidelines [12] recommend that approximately 45–65 percent of total daily calories should come from carbohydrates. Emphasis should be placed on increasing the intake of complex carbohydrate sources such as legumes, whole grains, vegetables and fruits to provide fibre, phytochemicals and essential minerals and vitamins. Since constipation is a serious concern for many older adults, increasing dietary fibre intakes is essential. Lipids – In relation to this aspect, one can relate a high fat intake, particularly saturated fat and cholesterol to increased morbidity and mortality risk. Besides obesity, a high fat consumption has been linked to CHD, stroke, certain cancers and even Alzheimer's disease. Hence reduction in fat and energy intake from a younger age will contribute immensely to healthy ageing. Current dietary recommendations propose 25–35 percent energy to come from fats with most from polyunsaturated and monounsaturated sources and intakes of cholesterol should be less than 300 mg/day [8, 12]. To meet the total fat recommendation of 20 to 35 percent of calories, most dietary fats should come from sources of polyunsaturated and monounsaturated fatty acids. The consumption of saturated fats should be minimized and not exceed 8 percent of total energy. Sources of omega-6 polyunsaturated fatty acids are liquid vegetable oils, including soybean oil, corn oil, and safflower oil. Plant sources of omega-3 polyunsaturated fatty acids (linolenic acid) include soybean oil, canola oil, walnuts, and flaxseed. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are omega3 fatty acids that are contained in fish and shellfish. An optimal ratio of n6 to n-3 fatty acids in the diet is believed to be ≈4:1. Plant sources that are rich in monounsaturated fatty acids include vegetable oils (e.g., canola, olive, high oleic safflower, and sunflower oils) that are liquid at room temperature and nuts. A relatively new concern with respect to monounsaturated fatty acid consumption involves the concentration of trans-fatty acids in the diet. Elaidic acid (trans 18:1n-9) is the principal trans fatty acid in the diet.

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Trans-fatty acids are formed during the hydrogenation process, a process that converts vegetable oils to a semisolid state. Major sources of transfatty acids in the diet are baked products, processed foods, and margarines rich in hydrogenated fat or oil. There is evidence that increased trans-fatty acid consumption, in contrast with consumption of saturated fat, increases plasma concentrations of lipoprotein (a), an independent risk factor for CHD. They also have a deleterious effect on the plasma lipoprotein profile, elevating LDL-cholesterol and reducing HDL-cholesterol concentrations. Minerals – Whereas overt mineral deficiencies are less common in healthy adults, sub-clinical nutrient deficiencies can develop. Poor mineral status in older persons may be attributed to inadequate intake, physiological changes that may affect the need of such nutrients and medications. Ageing is typically associated with a loss of bone and total body calcium more so in women. It has been suggested that in the presence of adequate vitamin D nutrition, calcium intakes in the range of 800–1200 mg/day will result in both a beneficial effect on bone mineral density of the femur, neck and lumbar spine and a reduction in fracture rates. Potential benefits of high calcium intakes and various other health-related measures, e.g. reduced blood pressure and decreased risk of a colon cancer, may also be important, although data are insufficient to know for certain [8]. Iron requirements in women decrease after menopause, while those of men remain similar. Iron deficiency anaemia in old age is most likely to be related to blood loss from disease and medications or decreased absorption caused by medications or hypochlorhydria rather than inadequate intakes. Zinc status is especially important for older persons, who need to maintain their full immunocompetence. Intakes of zinc in older adults decrease in relation to decrease in energy intake and maybe much below the required levels. Zinc deficiency is associated with impaired immune function, anorexia, loss of sense of taste, delayed wound healing and pressure ulcers has given the recommended intakes for dietary zinc for people over 65 years of age as 4.2 mg/day for men and 3.0 mg/day for women (high Zn availability (> 50%); 7.0 mg/day for men and 4.9 mg/day for women (moderate Zn availability – 30%); 14.0 mg/day for men and 9.8 mg/day for women (low Zn availability – 15%)[8]. Sodium intakes are often associated with hypertension. Therefore it is prudent to limit dietary sodium to approximately 2–4 g/day. Vitamins – Several vitamins have been ascribed with significant anti ageing contributions. Antioxidant vitamins like vitamin E, C and carotenoids are known to display disease prevention properties for a number of diseases ranging from cardiovascular disease and cancer to cataracts and macular degeneration. B group vitamins play an important role in maintaining cognitive ability and neuromuscular integrity as age advances. It is thought that requirements of vitamin A are high in old age due to

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the possible role of provitamin carotenoids in disease prevention, e.g. cancer, cardiovascular disease. However, concern has also been expressed about a low margin of safety for preformed dietary vitamin A in older persons. Based on these considerations, it appears that 600–700 μg RE/ day represents an adequate intake for older men and women. Inadequate vitamin D intake can also lead to bone loss and increased risk of osteoporosis. There are many reasons for vitamin D malnutrition in older persons including low exposure to sunlight, poor skin response to sunlight, and decreased absorption or decreased hydroxylation of vitamin D. Studies have shown that 1.2 g of elemental calcium and 20 μg of vitamin D/day significantly reduced the risk of hip fractures in older women [13]. According to US dietary recommendations, it appears that older persons need 10–15 μg vitamin D per day to ensure optimal bone health [14]. Vitamin E is of interest as a protective antioxidant and membrane stabilizer. In addition, vitamin E intakes have been associated with a protective effect against cataract and cancer, Alzheimer's disease and cardiovascular disorders. However, further research is needed to determine the adequacy of current vitamin E recommendations for older persons. Most of the interest in vitamin E requirements has centred on the possible beneficial effects of pharmacological doses (60–400 IU/day) of the vitamin, which could not be achieved through an otherwise healthy diet. High vitamin C blood levels and/or intakes have been associated with a lower prevalence of senile cataract, higher high-density lipoprotein cholesterol concentrations and lower incidences of coronary artery disease [15]. However, it appears that older persons do not have different vitamin C requirements to younger people and that an intake level of 60–100 mg/ day is adequate [8]. Recently, a new marker of folate status-homocysteine levels-has come into widespread use. There is great interest in the role of homocysteine as an atherogenic agent and the possibility that tissue folate deficiency could play an indirect role in atheromatous disease. Data from the Framingham Heart Study among older people demonstrated that serum homocysteine levels are correlated with dietary folate levels, and that serum homocysteine levels are high at dietary folate intakes of <400 μg/day [16]. Large-scale intervention studies will be needed to show that administration of folate at this level or above will in fact diminish the risk of vascular disease. Antioxidant nutrients – The role of antioxidant nutrients in preventing free radical damage has been well documented. Although a wide variety of antioxidants in foods contribute to disease prevention, the bulk of research has focussed on antioxidant nutrients like vitamin E, vitamin C, carotenoids and selenium. Green leafy vegetables and fruits are rich in these nutrients and hence most nutritionists emphasize a liberal intake of these foods in old age.

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Besides its anti–ageing properties, vitamin E is known to afford protection against cancer ischemia, cataract, arthritis and certain neurological disorders. The protective effects of vitamin C extend to cancer, coronary artery disease, arthritis and ageing. Carotenoids, including B carotene, and selenium are associated with reduced risk of certain cancers. However, the general consensus is that liberal servings of fruits and vegetables are more beneficial than antioxidant pills or medication [17, 18]. Phytochemicals – In addition to the recognized essential nutrients, there are many other food components-collectively known as phytochemicalsabout which little is known but whose biological effects can lower the risk of major health problems such as cancer and heart disease. Their effects may be hormonal, anti-inflammatory, anti-microbial, anti-oxidant, antimutagenic or anti-angiogenic (Table 34.4). Phytochemicals, mostly phenolic acids and flavonoids, are found in garlic, onion, ginger, oats, soyabean, tea, certain herbs and spice and red wine. The presence of these anti-oxidants in such foods may be the reason for the anti ageing properties associated with them. Box 34.2 Phytochemicals in foods ●

●

● ● ● ●

● ●

Carotenoids in orange/green vegetables, red wine: antimutagen antioxidant, anti-carcinogen, immuno-enhancing. Flavonoids in green/yellow vegetables, soy: antioxidant, anticarcinogen, estrogen, immuno-modulating. Polyphenolics in berries, oregano: antioxidant, antibacterial. Catechins in green tea: antimutagen, anticarcinogen. Isothiocyanates and indoles in cruciferous vegetables: antimutagen. Allyl sulphides in garlic, onions: cholesterol lowering, anticarcinogen, antibacterial. Curcumin in turmeric: anti-inflammatory. Non-digestible carbohydrates in vegetables and fruits: cholesterol lowering, stimulates growth of microbial flora

Water – Maintenance of fluid balance is essential for normal physiologic functions at all ages. Dehydration in older adults can be caused by impaired sense of thirst, decreased fluid intake, decreased kidney function or increased losses due to increased urine output from medicines like diuretics. It often goes undetected but can present itself as falls, confusion, and decline in consciousness, weakness, fatigue etc. It is important to obtain essential nutrients through a food-based approach and not be dependent on vitamin and mineral supplements. The traditional nutrient based approach is limited in that it does not take into account the environmental, socioeconomic and lifestyle context of eating, nor does it adequately address the chemical

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complexity of foods and the interactions and synergies, whether between different foods or individual food components. On the other hand, the food-based approach extends beyond nutrients and food groups; they include the way foods are produced (agriculture), prepared (cuisine), processed and developed (industry). They are therefore culture sensitive.

34.8

Dietary guidelines for older persons

In view of the increasing older population worldwide, many agencies including the WHO [8] and US Departments of Agriculture and Health and Human Services [12] have outlined dietary guidelines for older persons. WHO (2002) has emphasized the inclusion of healthy traditional vegetable and legume-based dishes where meat and nuts may be used only as condiments. The use of herbs and spices is encouraged but the consumption of traditional dishes/foods that are heavily preserved/ pickled in salt is to be limited. The guidelines recommend a prudent selection of nutrient-dense foods such as fish, lean meat, liver, eggs, soy products (e.g. tofu and tempeh) and low-fat dairy products, yeast-based products, fruits and vegetables, herbs and spices, whole grain cereals, nuts and seeds. Moreover, nuts, seeds, beans, olives and fatty fish would also cater to the fat intake. Where refined fats are necessary for cooking, selection from a variety of liquid oils including those high in n-3 and n-6 fats (canola, soyabean and olive oil) is desirable. There is also a strong focus on increasing variety in foods to be eaten as well as preserving healthy traditional food related practices. As the dependence on easily available ready to eat foods in increasing, the rapidly growing processed food industry and fast food chains should make concerted efforts to shift from the ready availability of high fat convenience foods to meals which are low in animal fat and high in nutrients and phytochemicals. Box 34.3 presents WHO (2002) foodbased dietary guidelines for older persons. The key recommendations for Older Adults as part of the Dietary Guidelines for Americans (2005) include consumption of vitamin B12 and vitamin D through fortified foods or supplements. Consumption of sodium should be restricted to 1500 mg, while potassium intakes should be minimum 4700 mg/day [12]. Besides regular physical activity, recommendations also caution against starting a weight loss programme without medical consultation. It also warns against eating or drinking raw or unpasteurised milk, egg or meats.

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Box 34.3 Food-based dietary guidelines for older persons (WHO, 2002) [8] ●

●

●

●

●

●

●

●

●

●

●

Emphasize healthy traditional vegetable- and legume-based dishes with meat and nuts to be used as condiments. Limit consumption of traditional dishes/foods that are heavily preserved/pickled in salt and encourage the use of herbs and spices. Introduce healthy traditional foods or dishes from other cuisines (e.g. tofu in Europe and the tomato in Asia) to increase the variety of foods consumed. Select nutrient-dense foods such as fish, lean meat, liver, eggs, soy products (e.g. tofu) and low-fat dairy products, yeast-based products (e.g. spreads), fruits and vegetables, herbs and spices, whole-grain cereals, nuts and seeds. Consume fat from whole foods such as nuts, seeds, beans, olives and fatty fish. Where refined fats are necessary for cooking, select from a variety of liquid oils, including those high in n-3 and n-6 fats. Avoid fatty spreads. Enjoy food and eating in the company of others. Avoid the regular use of celebratory foods (e.g. ice cream, cakes and pastries, mithai and confectioneries) Encourage the processed food industry and fast-food chains to produce readymade meals that are low in animal fats and high in nutrients and phytochemicals. Eat several (5-6) small non-fatty meals. This pattern appears to be associated with greater food variety and lower body fat and blood glucose and lipid levels, especially if larger meals are eaten early in the day. Transfer as much as possible of one's food culture, health knowledge and related skills to one's children, grandchildren and the wider community. Be physically active on a regular basis and include exercises that strengthen muscles and improve balance. Avoid dehydration by regularly consuming, especially in warm climates, fluids and foods with high water content.

!".9

Ageing in the development agenda

Till a decade ago, ageing did not figure as a priority in the development agenda. With the increasing numbers of older persons, planners and policy makers have woken up to the fact that suitable initiatives need to be undertaken to deal with this group. A time line of these key events is outlined below (Box 34.4). The Vienna International Plan of Action on Ageing, adopted by nearly 125 countries of the world at the First World Assembly on Ageing held in Vienna in 1982 was the first formal commitment towards concern for the elderly. This plan identified particular areas of concern for ageing persons and provided a starting point for approaching the subject in a systematic manner by recognizing the multiple dimensions of ageing. The primary aim of this plan was to strengthen the capacities of countries to deal effectively with the ageing of their populations and with the special concerns and needs of their elderly. It also aimed to promote an appropriate international response to the issues of ageing through action for the establishment of the new economic order and increased international technical cooperation, particularly among the developing countries themselves [19].

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Box 34.4 Key events, 1982–2002 1982 First World Assembly on Ageing, Vienna - International Plan of Action on Ageing 1991 United Nations Principles for Older Persons 1993 World Conference on Human Rights, Vienna Assembly 1994 United Nations International Conference on Population And Development, Cairo 1995 United Nations Social Development Conference, Copenhagen 1997 Fourth International Conference on Health Promotion, Delhi 1999 United Nations International Year of the Older Persons 1999 Macao Plan of Action on Ageing for Asia and the Pacific 1999 National Policy of Older Persons, Govt. of India 1999 National Council for Older Persons, India 2000 Year of the Older Persons, India 2002 Valencia Forum - Research Agenda on Ageing for the 21st Century 2002 Second World Assembly on Ageing, Madrid - Madrid International Plan of Action on Ageing, 2002 2002 Asia Pacific Seminar on Regional Follow-up to the Second World Assembly on Ageing, Shanghai - Regional Implementation Strategy for the Madrid International Plan of Action on Ageing, 2002 2007 The Maintenance and Welfare of Parents and Senior Citizens Act, Govt. of India

The UN International Year of the Older Persons in 1999 ensured that continuing attention was focussed on the elderly. The Macao Declaration and Plan of Action on Ageing for Asia and the Pacific endorsed by Governments in the region, in 1999, addressed seven areas of concern relating to ageing and older persons - a significant one being health and nutrition. The Research Agenda on Ageing for the 21st Century, a joint project of the United Nations Office on Ageing and the International Association of Gerontology, was submitted to the Second World Assembly on Ageing through the Valencia Forum in April 2002. It identified major priorities and critical arenas for research exploration. Salient among the priorities was research on healthy ageing and quality of life issues. Focus on older persons continued even at the Second World Assembly on Ageing held in Madrid in April 2002. A life course approach to deal with ageing issues was recommended. The Shanghai Regional Implementation Strategy for the Madrid International Plan of Action on Ageing and the Macao Plan of Action on Ageing for Asia and the Pacific [20] also reiterated the need to ensure quality of life at all ages for a healthy old age by promoting a life course perspective on health and ageing, through such measures as promoting good nutrition, healthy lifestyle and avoidance of risk factors. National Policy for Older Persons – In India, the concern for senior citizens has gained momentum only recently. The year 2000 was declared as the Year of the Older Persons in India, soon after the UN International Year of Older Persons in 1999. After several years of deliberation, the

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Ministry of Social Justice and Empowerment released A National Policy for Older Persons in the year 1999. The policy provides a broad framework for inter sectoral collaboration and cooperation both within the government as well as between governmental and non-governmental agencies. The policy has identified a number of areas of intervention: financial security, health care and nutrition, shelter, education, welfare, protection of life and property etc. for the wellbeing of older persons in the country. Amongst others, the policy also recognizes the role of the NGO sector in providing user friendly affordable services to complement the endeavors of the State. The policy also emphasizes the importance of family in providing vital non-formal social security for older persons. To facilitate implementation of this policy, the participation of Panchayati Raj institutions, State Governments and different Departments of the Government is envisaged with the coordinating responsibility resting with the Ministry of Social Justice and Empowerment, Government of India [21]. National Council for Older Persons (NCOP) has been constituted by the Ministry of Social Justice and Empowerment in May 1999 to operationalise the National Policy on Older Persons. The objectives of the NCOP are as follows: ● ●

● ●

●

● ● ●

●

Advice the government on policies and programmes for older persons. Provide feedback to the government on the implementation of the National Policy as well as on specific programme initiatives for older persons. Advocate the best interests of older persons. Provide a nodal point at the national level for redressing the grievances of older persons at an individual level. Provide a lobby for concessions, rebates and discounts for older persons both with the Government and private sector. Represent the collective opinion of older persons to the Government. Suggest steps to make old age productive and interesting. Suggest measures to enhance the quality of inter-generational relationships. Undertake any other work or activity in the best interest of older persons.

The Maintenance and Welfare of Parents and Senior Citizens Act was passed by the Parliament in 2007. The bill has a clause for punishment to those who abandon their parents or relatives whose property they have inherited or would get as their legal heirs. The bill provides for setting up of a tribunal in each district for helping the old in distress. It also has a provision for establishment of old age homes which should be the last resort for the poor and the childless [22].

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!".10 Initiatives in old age care Other initiatives taken by the nodal Ministry, the Ministry of Social Justice and Empowerment, Government of India, include getting the instructions issued from the Ministry of Health to all State Governments to ensure separate queues for older persons at all stages, getting the instructions issued from the Hon'ble Chief Justice of High Courts and Lower Courts for expeditious disposal of cases involving older persons and setting up of a telephone help line with the help of an NGO, Agewell Foundation, in Delhi. Certain ongoing schemes of the Ministry were revised during 1998–99 to facilitate implementation of the National Policy. The one-time construction grant for old age homes/multiservice centres for older persons under the Scheme of Assistance to Panchayati Raj Institutions/Voluntary Organizations/ Self-help Groups has been enhanced from Rs 5 lakhs to Rs 30 lakhs for eligible organizations. An Integrated Programme for Older Persons has been formulated by revising the earlier scheme of assistance to voluntary organizations for programmes relating to the welfare of the aged. The strategy involved in this scheme includes awareness creation and sensitization of children and youth towards older persons, reinforcing the Indian family tradition of providing special care and attention to the elderly, organizing the older persons into coherent self help groups and making productive use of older persons. Under this scheme, financial assistance upto 90% of the project cost is provided to the NGO for establishing and maintaining old age homes, day care centres, mobile medicare units and for providing non institutional services to older people [22].

!".11 Initiatives by the voluntary sector HelpAge India is the biggest NGO working for the benefit of older persons. Some of their initiatives include formulating a plan of action for implementation of the policy. Key features of the plan included pension for all poor aged especially widows, microcredit schemes to reach all villages, financial security for daily wage earners, healthcare at doorstep of all elderly, promotion of healthy ageing, home care services for all aged persons, incentives to elderly to pursue education, media to play a more positive and expanded role. Several Governmental and non-governmental agencies have established day care centres and old age homes, some free of charge and some on a pay and stay basis. More than half of the 1000 old age homes nationwide and over 125 day care centres have been supported by HelpAge India. The Mobile Medicare Unit Programme is directly implemented by HelpAge India to provide basic essential at the doorsteps of needy and underprivileged elderly.

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Way forward With a growing number of individuals surviving to enjoy their "renaissance years", there has been considerable interest in ensuring a good quality of life in healthy old age. In our efforts to provide a better quality of life to the elderly it is imperative to strengthen their economic security. Provision of old age pension or other social security benefits may be a step in this direction. To promote the concept of productive ageing, policies and programmes should be planned to utilize the expertise and skills of the elderly and maximise their contribution to the family and community at large. Special efforts need to be directed towards provision of health and nutrition support for the elderly. Assistance to elderly persons living alone or disabled with regard to food, medical aid, banking, paying bills etc. should be considered. Facilities like home catering services, meals on wheels etc. may be encouraged for elderly unable to prepare meals for themselves. Access to medical care for the elderly should be ensured. Setting up of geriatric units/special clinics/mobile medical units/health camps in the area should be given priority. Dieticians and doctors who are sensitized about the special needs of the elderly would prove more effective in elderly care. An integrated approach may be adopted by opening day-care centres for the elderly. Such centres could be located in each colony and provide facilities of recreation (TV, newspapers, magazines), religious activities (satsangs, discourses, group tours), basic medical care and referral as well as health and nutrition counselling services to the elderly women. Income generating activities, training programs, awareness creation campaigns etc. could also be initiated at these centres.

References 1. 2. 3. 4.

5. 6. 7.

(2001). Biological Changes in Ageing. New Delhi: Public Lecture. and ANDERSON SL (1993). Nutritional Assessment and Therapy in Patient Care 7th ed. St Louis: Mosby, p. 457. VIJAYAKUMAR S. (1999). Population ageing in India. Research and Development Journal, 5(2), p. 3. Registrar General of India (2001). Census of India. Ministry of Home Affairs, Government of India. www.censusindia.net/results/resultsmain.html. Accessed 12 May 2008. IRUDAYARAJAN S (2006). Personal Communication. IRUDUYARAJAN S, MISHRA US, SARMA PS (1999). India’s elderly burden or challenge. New Delhi: Sage Publications India, 19, p. 211. BOSE AB (1994). Policies and programmes for the ageing in India. In: Department for Economic and Social Information and Policy Analysis. The Ageing of Asian Populations. New York: United Nations. BAGCHI K

WILLIAMS SR

Nutrition for the aged 8. 9. 10.

11.

12.

13.

14. 15.

16.

17.

18. 19. 20.

21. 22.

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(2002). Keep fit for life. Meeting the nutritional needs of older persons. Geneva: WHO and Tufts University. PURI S (2001). Nutritional concerns of older persons. In: Chaudhary A, ed. Active Ageing in the New Millenium. New Delhi: Anugraha India, p. 110. Indian Council of Medical Research (ICMR) (1990). Nutrient requirements and recommended dietary allowances for Indians. A report of the expert group of the ICMR. Hyderabad: NIN. N ARASINGHA RAO BS and SIVAKUMAR B (2009). Nutrient Requirements and Recommended Dietary Allowances. In: Textbook of Human Nutrition 3rd edition, Bamji M, Krishnaswamy K, Brahmam GNV (eds.), Oxford and IBH Publishing Co. U.S. Department of Health and Human Services and U.S. Department of Agriculture (2005). Dietary Guidelines for Americans, www.healthierus.gov/ dietaryguidelines Accessed 15 December 2009. DAWSON -HUGHES B et al (1991). Effect of vitamin D supplementation on wintertime overall bone loss in healthy postmenopausal women. Annals of Internal Medicine, 115, pp. 505–512. Institute of Medicine (1997). Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. pp. 250–287. FREI B (1991). Ascorbic acid protects lipids in human plasma and low-density lipoprotein against oxidative damage. American Journal of Clinical Nutrition, 54, pp. S1113–S1118. SELHUB J et al. (1993). Vitamin status and intake as primary determinants of homocysteinemia in an elderly population. Journal of the American Medical Association, 270, pp. 2693–2698. PURI S (1999). Dietary Antioxidants and Ageing – A Review. In: Diet and Ageing – Exploring Some Facets. Bagchi K, Puri S, (eds.). New Delhi: Society for Gerontological Research and HelpAge India, p. 95. BAGCHI K and PURI S (1998). Free radicals and antioxidants in health and disease. East Med J WHO, 4(2), p. 253. WORLD HEALTH ORGANISATION (1998). Women, Ageing and Health – Achieving health across the life span. Geneva: WHO. UNESCAP. Shanghai Regional Implementation Strategy for the Madrid International Plan of Action on Ageing and the Macao Plan of Action on Ageing for Asia and the Pacific http://www.unescap.org/esid/psis/ageing/strategy/toc.asp Accessed 15 December 2009. Ministry of Social Justice and Empowerment (1999). Govt of India. National Policy for Older Persons. Helpage India (2008). Senior Citizens Guide. WORLD HEALTH ORGANISATION

35 Nutrition related non-communicable chronic disorders Kamala Krishnaswamy and Avula Laxmaiah

Kamala Krishnaswamy, MD, is the former Director of the National Institute of Nutrition, India and former President of the Nutrition Society of India. Dr. Krishnaswamy is currently on governing and advisory boards of several institutes and chairperson of project advisory committees. She has carried out a number of research studies in the fields of diet-cancer interactions, nutrient-drug interactions, environmental toxicology, non-communicable chronic diseases and vitamin B complex deficiencies. Avula Laxmaiah MBBS, MPH, is Deputy Director (Scientist ‘E’) at the National Institute of Nutrition, India. Dr. Laxmaiah is an epidemiologist and is involved in national nutrition monitoring through the National Nutrition Monitoring Bureau (NNMB).

35.1

Introduction

The current concerns in nutrition include not only undernutrition and its consequences but also many chronic diet related problems. Such disorders may have their origins in fetal (prenatal) and child malnutrition as well as intake of energy dense foods and physical inactivity in later life. The diet related chronic disorders are of global concern and contributing to rising health care costs [1]. In India, underweight and stunting due to number of macro and micronutrient deficiencies are common among children, adolescents and pregnant women [2]. These disorders have a cascading effect on diet related non-communicable diseases. In most nutrition circles, therefore, the need for a common agenda is often reiterated particularly in terms of lifestyle changes and physical activities to prevent disorders at both ends of the spectrum. Of this, diet, physical inactivity, personal risk behaviours are of prime importance [3]. The rising epidemic of obesity and insulin resistance, particularly in developing countries is the forerunner of almost all chronic non-communicable diseases and calls for an integrated package of interventions [4]. The metabolic programming of undernutrition in utero directly influences the development of diseases such as diabetes,

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coronary artery disease, hypertension, stroke and cancer [5]. Intrauterine undernutrition permanently alters structure, physiology, metabolism and function leading to enhanced risk of chronic non-communicable diseases in later life. The ageing phenomena as well as ailments such as arthritis, gallstones and cataract are also related to obesity and dietary intake of nutrients and phytonutrients. In fact, the origins of most of these disorders may be related to our genes as they are programmed to palaeolithic/hungergather society diets and activity patterns. The current diets and activities are not matched to our genes.

35.2

Prevalence of non-communicable diseases at global and national level

Non-communicable diseases (NCD) are not infectious or contagious. NCD may result mainly from lifestyle factors including risk behaviours of individuals and genetics. The important diseases are obesity, diabetes, hypertension, coronary artery diseases, chronic obstructive pulmonary diseases (COPD), mental problems, cancer etc. As per the World Health Organization (WHO) estimates, non-communicable diseases account for nearly 59% of the 57 million persons, who died in 2002 [6]. In the same year, deaths due to non-communicable diseases also outstripped deaths due to both communicable diseases and injuries, and were the leading cause of chronic illnesses world wide, accounting for nearly 47% of the 1.49 billion years of healthy life years ‘lost’ due to illness, as measured in disability adjusted life years (DALY) and to 46% global burden of disease. It is further said that the burden of NCDs is expected to increase to 57% by 2020, of which 50% will be due to cardiovascular problems and 79% of all deaths worldwide will be attributable to chronic diseases in developing countries. In India, chronic diseases contribute to 53% of deaths and 44% of DALYs [7] (Table 35.1). It is evident that NCDs, particularly cardiovascular diseases, diabetes and hypertension are increasing through out the country particularly in urban India.

35.3

Cardiovascular diseases

Compared to all other ethnic groups, South Asians have an excess risk of coronary artery disease. The burden of cardiovascular diseases is 3–4% in rural and 8–10% in urban India. The prevalence of stroke in India is considered to be 203 per 100000 populations above the age of 20 years [7]. In 2001, heart disease and stroke were the leading cause of death in both high and low middle-income countries, accounting for 19% and 21%

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Table 35.1 Deaths and DALYs (Estimated) by cause in India [7] Cause Cardiovascular diseases Cancer Chronic respiratory diseases Diabetes Other chronic diseases Communicable diseases pre-natal and maternal conditions and nutritional deficiencies Injuries

Deaths

DALYs

29 7 7 2 8 36

11 4 3 1 25 42

11

14

respectively and cardiovascular diseases are the major contributors to mortality and morbidity in the South Asia region [8]. WHO estimates the cause specific mortality rate due to cardiovascular diseases will be the highest by 2020 in India. About 2.6 million Indians are predicted to die due to coronary heart diseases, which constitute 54.1% of all cardiovascular deaths. Nearly half of these deaths are likely to occur in young and middle aged individuals (30–39 years) [9]. The Global Burden of Disease (GBD) study has revealed that about 52% of the cardiovascular deaths occur below the age of 70 years in India as compared to 23% in developed countries [10].

35.3.1 Hypertension A meta-analysis of data available shows a prevalence rate of 16.5% in urban and 15.7% in rural India [11]. Indian Council Medical Research study (1994) [12] reported that the prevalence of hypertension among men and women in urban areas of New Delhi was 25% and 29%, while it was only 13% and 10% among men and women respectively in rural areas. It ranges between 20% and 40% in urban and 12–17% in rural India [13]. The prevalence of hypertension worldwide was 972 millions in 2000 and will be 1.56 billion in 2025, with equal numbers in men and women [14]. According to National Nutrition Monitoring Bureau (NNMB) surveys carried out in 9 States during 2005–06 in India [15], the prevalence of hypertension (≥140 mm of Hg systolic blood pressure (SBP) and/or ≥90 mm of diastolic blood pressure (DBP)) was 25% and 24% among rural men and women, respectively. However, it was highest in the State of Kerala (men: 50.9%; women: 46.8%) Orissa (men: 40.9%; women: 42.4%), Maharashtra (men: 31.4%; women: 13.7%) and lowest in Gujarat (men: 14.2%; women: 10.4%) and Tamil Nadu (men: 17.8%; women: 46.8%).

35.3.2 Obesity and overweight Recent estimates suggest that there are one billion overweight/obese people in the world. The problem is of a serious nature even among

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children and adolescents. The rates are far higher in middle and lowincome countries. In South Asia, one-third of the urban adult population is classified as overweight and obese and is also increasing among South Asian children. The prevalence of overweight and obesity as per the National Nutrition Monitoring Bureau has doubled among men from 2.3% to 4.1% and women from 3.4% to 6% [16] over a period of two decades in rural areas (1975–79 to 1996–97). The prevalence of overweight/ obesity among adolescents in urban areas ranged from 6% to 25% in various urban cities of India [17]. The Sentinel Surveillance system for cardiovascular diseases in Industrial populations in North Indian cities like Delhi, Lucknow, Ludhiana, the prevalence of overweight and obesity was 41%, 37% and 15% respectively [18], while in central Indian cities, it was 20% and 36% in Nagpur and Pune, respectively. In South Indian cities such as Bangalore, Trivandrum and Coimbatore, it was 48%, 38% and 27%, respectively. Serial epidemiological surveys in Rajasthan have shown the prevalence as 60% during 1994 [7], 63% during 2001, and 79% during 2003 using the criteria (waist–hip ratio (WHR): Men >0.9, females: >0.8). Several studies also revealed that Indians in general, have higher body fat percent even at lower body mass index (≤25) [19, 20].

35.3.3 Diabetes The prevalence of diabetes has risen more rapidly in South Asia than in any other region of the world. By the year 2030, India will have the highest number of persons with diabetes (79.4 millions) [21]. All community-based studies have documented rising prevalence of diabetes in all parts of India. Both diabetes and impaired glucose tolerance (IGT) increases with age. The sentinel surveillance project [18] documented 10% overall prevalence of diabetes from 10 regions of the country among 20–69 years. The Indian Council of Medical Research documented 58.3 million cases in 1998 and by 2004 it could have accounted for 1.15 million years lost due to disease and 2.26 million DALYs [11]. The prevalence of metabolic syndrome as reported by various workers varies from 10 to 40%, which is strongly associated with diabetes. Diabetes, if it is untreated or not well-controlled results in CVD, hypertension, kidney damage, eye disorders, gangrene, peripheral neuropathy and vascular disorders.

35.3.4 Cancer The patterns of cancer vary greatly across the globe. In 2002, there were about 11 million cases worldwide of which 7 million died and it is estimated

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that this number will escalate to more than 16 million, with 10 million deaths by the year 2020 [22]. Almost 70% of these may be in developing countries with 5% of global resources. The overall incidence of cancer though low, is higher in urban India as compared to rural India. The calculated figures from ICMR (2001) registries show that in urban males the incidence rate is 113 per 100,000 and in urban females 123 per 100,000 while, in rural areas it is 46 and 58 per 100,000 in males and females, respectively [23]. The major cancers are tobacco related (lung, oral cavity, larynx, pharynx and oesophagus) in men while oral, oesophagus, lung (related to tobacco), breast and cervix in women. The prevalence of oral cancers are the highest and in recent times colon and prostate cancers are also increasing. The breast cancers in women are higher in urban India, while cervical cancers predominate in rural India.

35.4

Nutrition transition and NCDs

Several developing countries have conflicting goals of preventing undernutrition, obesity and diet related disorders [3]. Due to diverse public health control measures adopted, high rates of fertility, mortality and famines leading to undernutrition in vulnerable segments are now being replaced by low fertility, reduced mortality and increased life span [24] (Figure 35.1). The demographic transition is resulting an increase in young adults as well as a substantial increase in the proportion of elderly population. However, the quality of life has not improved in all segments. The demographic changes accompanied by urbanisation, economic growth, technological innovations, mechanisation coupled with reduced physical activity and higher leisure time of sedentary nature have compounded the scenario. Migration from rural and tribal to urban agglomeration exposes people to adverse nutritional environment, inactivity and stresses, which are responsible for epidemiological and nutritional transition [25, 26].

35.5

Macronutrients

Dietary changes create an altered energy balance. The starchy foods of low calorie value with high fibre and micronutrient poor diets are being replaced with calorie dense, fatty, salty and low fibre and micronutrient/ phytonutrients poor diets with more animal foods, which are loaded with saturated fats. The children in urban areas are becoming obese due to both lack of physical activity as well as easy availability and access of junk food, which consists high energy, fat, sugar and salt and carbonated beverages, which promote fat deposition.The dangerous triad of stunting

35.1 Nutrition transition and NCDs.

Longevity/ Healthy ageing

Starchy, low fat, high fibre, micronutrient poor diet Labor-intensive work Infectious diseases

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due to malnutrition in early ages, availability of energy dense foods at a later date and sedentary habits escalate the problems of obesity and changes in body composition with specific reference to fat deposition promoting insulin resistance and diet related non-communicable diseases. Trace elements such as Mg and Ca were significantly lower for Asian Indian vegetarians than for the white Caucasians vegetarians [27]. Nearly 95% of ethnic South Asians in the UK, whose random blood glucose level indicated high risk of diabetes had vitamin D deficiency. However, the clear cut implications of micronutrient deficiencies on the metabolic syndrome and cardiovascular diseases are not clear, especially for South Asians and further studies may be required with sufficient duration. The latent predisposition to chronic disorders appears to be related to our ancestral diet of Palaeolithic or Hunter-gatherer society [28]. The principal defect appears to be related to a quick insulin response based on the low glycemic index for the current foods. This response earlier conferred survival benefits in “Fasting and Famine” situations of our ancestors and favoured lipogenesis and glucose conversion to storage lipids. The gatherer foods are more bulky while the hunted foods are high in animal protein (lean mass). The foods were rich in complex carbohydrates, mono and polyunsaturated fatty acids (MUFA and PUFA), micro and phytonutrients, fibre and low in cholesterol, saturated fats and sodium. The quality of fat was apparently better with a lower omega 6/ omega 3 ratio than the current fats which are more saturated and relatively higher in omega 6 fats. The foods were also minimally processed. Potassium in the diets was invariably high due to plant foods of diverse nature. The high protein (19–35% energy) would have reduced the lipids. The carbohydrate content was around 22–40%, which are much lower than current intakes of 60–70%. Further, their physical activity was much higher. Thus our genes are sculpted or programmed to Palaeolithic diets. The modern diets are more refined and are high in glycemic index (insulinogenic), are low in fibre and micronutrients as they are more refined. The diets are energy dense foods (high in sugar, fat) and salt. Such diets coupled with sedentary habits promote insulin resistance and adiposity. Further the intake of animal foods apparently is more dense in saturated fats and cholesterol due to the nature of animal feeds and are diametrically opposite to our ancestral dietary pattern of high intake of lean protein from forest animals. The rapid escalations of obesity in tribes indicate acculturation to modern diets and life styles which are detrimental to human health and result in several chronic diseases. Nutritional studies in hunter-gatherers indicate that they would have had better folic acid and vitamin B12 status. Vascular problems such as coronary artery disease, stroke and peripheral vascular disease can be mitigated by folate and Vitamin B12 found in plant foods such as vegetables, fruits and beans and

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milk respectively. The wild plants grown in natural soils rich in micronutrients is a nature’s gift for mankind to provide the necessary vitamins and minerals as against the current practices of intensive agriculture, usage of artificial fertilisers and pesticides. Industrial effluents further complicate the problems (Table 35.2). Table 35.2 Hunter-Gatherer diets

Current diets

Bulky Low energy density Slowly digested Protein

Palatable Energy dense Rapidly digested Protein Fat Saturated fats

Fat Unsaturated fats Complex carbohydrates-fibre Vitamins / minerals Glycemic index Na/K ratio Calcium

35.6

↑ ↓ ↑ ↑ ↑ ↓ ↓ ↑

Refined foods Fibre vitamins/minerals Glycemic index Na/K Ratio Calcium

↑ ↑ ↓ ↑ ↑

↓

↓

Risk factors for diet related NCDs

Diet and lifestyles (modifiable factors) are important determinants of NCD. While age, sex and genetic factors cannot be altered (non modifiable factors), it is possible to change the risk profile by altering the diet and physical activities. Equal priority should be given to the control of nutritional deficiency diseases as well as NCDs. The risk factors for chronic disorders (Box 35.1) are high blood pressure, high concentrations of blood cholesterol and triglycerides, overweight and obesity, physical inactivity and tobacco use. These lead to metabolic abnormalities of insulin resistance and inflammatory state, which are further perpetuated by high intake of energy dense foods and high salt intake. Poor nutrition during pregnancy, infancy and early childhood further deteriorate the situation. High plasma concentrations of the amino acid homocysteine have been associated with atherothrombotic disease. High homocysteine concentrations are thought to impair endothelial function, increase oxidative stress, impair methylation reactions, and alter protein structure. Although some studies have shown improvement of vascular surrogate end points, homocysteine-lowering treatment has not yet been associated with a significant reduction of cardiovascular events. Studies that have examined the relationship between plasma homocysteine and arterial stiffness parameters have shown heterogenous results. There were ethnic differences for plasma folate and

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Box 35.1 NCDs – important risk factors High blood pressure High blood concentrations of lipids – ↑ cholesterol / Triglycerides (TG) / ↓ High Density Lipoprotein (HDL) ● Overweight / obesity – Truncal / central distribution ● Inadequate intake – low micro & phyto nutrients, fibre present in fruit and vegetables ● High intakes of energy dense foods – fat / sugar ● High intake of salt ● Reduced physical activity – home, school, work, transport, recreation ● Excess use of tobacco & alcohol ● Poor maternal / fetal / early infant / child nutrition (altered structure / physiology / metabolism) ● Glucose intolerance (Insulin resistance) ● ●

vitamin B12 (in particular lower levels in Indians); there was no evidence that homocysteine plays a role in different ethnic groups differently for ischemic heart disease (CHD) in Singapore and in particular to the Indians [29].

35.7

Overweight and obesity and dietary factors

The rising trend in obesity and overweight is part of the global epidemiological transition and is a public health threat and a serious burden on the public health expenditure. Though short-term measures are available for treatment, none of them are sustainable and it is essential to prevent the disorder. Obesity is simply defined as a condition of abnormal or excess fat or adipose mass, which impairs health and productivity. World over data clearly indicates that body mass index and abdominal obesity is increasing in epidemic proportions, which are important risk factors for type 2 diabetes, the metabolic syndrome and cardiovascular disease (CAD) [30–31]. WHO’s expert consultation has also agreed that Asian Indians have higher health risks even at lower BMI, and consists more body fat and health risks, than the European populations. The obesity epidemic appears to be more in developing countries and especially in poor socioeconomic groups. The levels of BMI are the indicators for risk of morbidity, mortality and suggest priorities for interventions. The abdominal fat is a greater risk for development of metabolic syndrome. Overweight and obesity are independent risk factors for insulin resistance, type 2 diabetes, cardio-vascular diseases and some cancers of gastrointestinal tract, breast and ovary, arthritis, gall stones as well as psychosocial consequences (Table 35.3). Morbidity due to obesity is universal with several systems being affected. Thus obesity demands the attention of all health care workers and there is a drain on health care costs. It needs preventive care as the consequences are cost prohibitive.

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Table 35.3 Health consequences of overweight and obesity Cardiovascular problems

Cancers

Ischemic heart disease (CHD) Stroke Hypertension Cardiomyopathy Deep vein thrombosis

Breast (post menopausal) Endometrial Ovary Colon Oesophagus, Stomach Kidney

Endocrine

Metabolic disorders

Type 2 diabetes(NIDDM) Infertility Polycystic ovarian syndrome Reproductive hormone disturbances

Dyslipidaemia Insulin resistance Metabolic syndrome Inflammation Hyperuricaemia Gout Gastrointestinal Gastro-oesophageal reflux Gall stones Non alcoholic fatty liver

Pulmonary Sleep Apnoea Breathlessness Asthma Pulmonary embolus Others Osteoarthritis Low back pain

Increased anaesthetic risk Fetal defects

Though there are certain endocrine and metabolic disorders, which result in obesity, the major aetiological factor appears to be a positive energy balance. Energy dense foods or excess energy intake per se with very little physical activity and energy expenditure results in increased body weight and body composition changes with accumulation of fat in abdominal region and truncal areas. In recent times, the food intake appears to be more or less stable while the physical activity levels are reducing at all levels from childhood to adults. Energy cannot be created or destroyed, but can be converted to different forms. A small increase in food intake over a period of time results in gain in weight. There is convincing evidence that sedentary living coupled with energy dense foods, sugary drinks and fast foods promote obesity in all sections of populations. With added disadvantage of being under nourished at an earlier age the problems multiply. Sedentary behaviours, such as television viewing and working on computers or leisure time activity, which do not involve any physical activity, contribute to positive energy balance. Apart from CVDs and diabetes the serious consequences of obesity are certain types of cancers (Table 35.3). The origins of obesity can be traced back to fetal undernutrition, which programs the individual to higher risks of obesity in a later life. There is enough evidence now to suggest that exclusive breastfeeding and longer duration of breastfeeding prevent obesity and

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related disorders later [22]. Human milk is a natural source of all nutrients. The bioactive constituents of human milk (leptin) could modulate energy metabolism.

35.8

Blood lipids (Dyslipedaemia)

Cardiovascular diseases are caused by narrowing of blood vessels due to atherosclerotic fatty deposits and plaque formation associated with inflammatory deposits. Immune cells and their inflammatory activity and smooth muscle cell proliferation of arterial walls following endothelial damage resulting in platelet adhesions and reactivity and monocyte/ macrophage infiltration are the major events in the process of atherosclerosis. The oxidised lipids formed in the lesion perpetuate the process. Micro thrombi and plaque instability lead to obstruction, haemorrhage and rupture. Epidemiological, clinical, metabolic and experimental studies consistently indicate that high intake of saturated fats, trans in hydrogenated fats and dietary cholesterol enhance blood cholesterol, triglycerides including low and very low density lipoproteins and insulin resistance which in turn damage the endothelium leading to arterial lesions and higher blood pressure. Various investigations have shown that the intake of saturated fatty acids (SFA) is a significant independent predictor of fasting and post-prandial insulin concentrations [32]. The protection provided by HDL cholesterol is also an important factor and has emerged as a predictor. Refined carbohydrates increase triglycerides and decrease HDL. Among fatty acids, the saturated fats are harmful, while mono and polyunsaturated are protective [33]. The long chain omega 3 fats as in fish (EPA & DHA) have several beneficial effects (decrease lipids, blood pressure, inflammation and stabilizes plaque) [34]. Evidence from experimental studies has also indicated the benefit of long chain n-3 PUFA (fish oil) over n-6 PUFA (safflower-seed oil) in preventing insulin resistance, but convincing evidence from human studies is lacking. Supplementation with long chain n-3 PUFA appears to improve insulin sensitivity in subjects with impaired glucose tolerance [35]. It has been shown that an imbalance in dietary n-6 and n-3 PUFA may be important for the development of insulin resistance and dyslipidaemia in South Asians [36]. In vegetarian Asian Indians, a higher intake of n-3 PUFA could be obtained by the addition of several low cost vegetarian dietary items containing n-3 PUFA (GLV, rajmah, bajra, black gram). The bioactive components in fruits and vegetables lower atherosclerotic process to reduce cardiovascular accidents and also have some anti-tumour activities to prevent some of the tumours [37].

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Metabolic syndrome

The metabolic syndrome is a group of conditions that put one at risk of developing heart disease and diabetes mellitus (Box 35.2). Metabolic syndrome is widely prevalent in Asia and India (30%) in particular and is associated with a higher risk of CVD and diabetes [38]. Insulin resistance is central to the syndrome and it may also be associated with fetal and childhood malnutrition and subsequent changes in growth pattern and fat accumulation which begins as early as two years or even at birth [39]. Genetic factors may also operate at different levels. High waist/hip ratio (WHR), elevated triglycerides, reduced HDL, high blood pressure and elevated fasting glucose levels are typical of this syndrome (Table 35.4). Dietary aberrations and poor physical activity are the determinants of the syndrome. Box 35.2 Criteria for clinical diagnosis of metabolic* syndrome 1. Abdominal obesity (Excessive fat tissue in and around the abdomen) 2. Atherogenic dyslipidemia (high triglycerides, low HDL cholesterol and high LDL cholesterol) 3. Elevated blood pressure 4. Insulin resistance and glucose intolerance (the body can't properly use insulin or blood sugar)

* Presence of any 3 factors considered diagnostic for metabolic syndrome

Glucose intolerance (Insulin resistance) Glucose Intolerance (Insulin resistance) occurs when the body’s ability to process glucose becomes impaired. The rise in the blood glucose levels in the fed state (after meal) stimulates the pancreas to produce more insulin that is necessary in the metabolism process to assimilate and store the available glucose. Impaired glucose tolerance occurs when the pancreas either does not release enough insulin or the cells become resistant to the insulin. Insulin resistance (or impaired glucose tolerance) is classified as a fasting glucose level of 110 mg/dl to <126 mg/dl.

35.10 Hypertension High blood pressure is a risk factor for CVDs and strokes. Several studies have related high sodium intake and blood pressure (BP). In tribals who do not take salt, even age associated increase in blood pressure is not observed. In many populations sodium excretion in urine and blood pressure are related [45]. Increased potassium intake in the diet lowers the blood pressure levels. Vegetables and fruits supply adequate amounts

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Table 35.4 Cut-off levels for risk factors of non-communicable diseases Indicators

Level (mg/dL)

Interpretation

References

Total cholesterol (mg/dl)

<200 200–239 >240

Desirable/Normal Borderline high High

40

Low density lipoprotein (LDL) (mg/dl)

<100 100–129 130–159 160–189 >190

Optimal LDL cholesterol Near optimal LDL level Borderline high LDL level High LDL level Very high LDL level

HDL cholesterol (mg/dl)

<40 40–60 >60

Low Normal High

Serum triglycerides (mg/dl)

<150 150–199 200–499

Normal Borderline High

Waist circumference for Asians Indian (cms)

≥ 90 cm ≥80 cm

Men Women

41

Body mass index (BMI) = [Weight (kg)/Height (m)2]

<16.0 16.0–17.0 17.0–18.5 18.5–20.0 20.0–25.0 25.0–30.0 ≥30

III degree CED II degree CED I degree CED Low Normal Normal Over weight Obesity

42

Body mass index (BMI) = [Weight (kg)/Height (m)2]

<18.5 18.5–<23.0 ≥23.0–<27.5 ≥27.5

Underweight Normal Increased risk High risk

43

Diabetes mellitus

<110 mg/dl Normal ≥ 110 to <126 Impaired glucose tolerance ≥126 Diabetes Mellitus

44

of potassium and can counteract the effects of sodium, if consumed in smaller amounts. A balanced diet also provides calcium and magnesium, which lowers blood pressure. From a health point of view vegetables and fruits with dairy products minus the fats would provide the much needed minerals. The dietary approaches to stop hypertension (DASH) [46] diet of reduced salt, weight reduction diets high in fruits and vegetables, low in dairy fat, high in whole grains, poultry, fish, nuts and low in fats, sugar and sugary beverages are comparable with antihypertensive drug effects. Urbanisation is one of the important factors for nutrition transition and emergence of obesity, the metabolic syndrome

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and cardiovascular diseases. Urbanisation is variable within the developing regions; almost three fourths of the population in Latin America and Caribbean, and 38% in Africa and Asia [47]. The rural to urban migration in many of the developing countries exposes migrants to urbanized diets and life styles. Studies done in Brazil and India have shown that many of these migrants living in urban slums have become obese and are affected by non-communicable diseases [48].

35.11 Fetal and childhood malnutrition According to Barker’s hypothesis [5], intra uterine growth retardation (IUGR), premature delivery and subsequent rapid postnatal catch up growth is associated with higher risk of coronary heart disease, stroke, diabetes and hypertension. A thrifty phenotype hypothesis that emphasises fetal undernutrition leading to altered metabolic programming is perhaps a better explanation in resource poor developing countries because abundant food supply later in life leads to maladaptive increase in weight and increases the risk of non-communicable diseases [49]. Several studies have shown that Asian Indian babies born small and with low birth weight had higher systolic blood pressure and adiposity at 8 years of age [50]. Box 35.3 David Barker's hypothesis Professor David Barker and his colleagues working in Southampton have shown that fetal nourishment before birth and nutrition in infancy determine the patterns of fetal and infant growth, programme the development of risk factors such as raised blood pressure, fibrinogen concentration, and factor VIII concentration and glucose intolerance and hence are key determinants of coronary heart disease.

Even cancer mortality due to breast, uterus, and colon is higher in stunted children with accelerated growth [51]. Underweight and stunting can lead to tracking of risk factors for NCDs which are associated with an increased risk of chronic heart disease, stroke, diabetes etc. There are evidences to show that the risk of adult obesity increases if the individual suffered from undernutrition during the childhood [52]. In many countries, the urban poor and illiterates have high prevalence rates of overweight [53]. Unhealthy dietary practices worsen the situation. The factors that influence the incidence of non-communicable diseases are presented in Table 35.5.

35.12 Vegetables and fruits in the diet Urged by scientific evidence, dietary guidelines of all countries strongly recommend that vegetables and fruits be consumed daily in sufficient

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Table 35.5 Risk for non-communicable diseases Diseases

Increased risk

Obesity

● ● ● ●

●

Cardiovascular diseases

● ●

● ● ●

Energy dense foods Sugar sweetened soft drinks Physical inactivity Adverse socio-economic conditions Heavy marketing strategies Abdominal obesity and obesity Saturated and trans fatty acids/ Dietary cholesterol/ Myristic acid High sodium Unfiltered boiled coffee High alcohol

Decreased risk ● ● ● ●

●

● ● ● ● ● ● ●

Cancer

● ● ● ● ● ● ●

Type 2 Diabetes

●

● ● ●

Obesity/Overweight Salt preserved food (fish) Preserved red meat Very hot drinks High intake of alcohol Aflatoxins Tobacco consumption Overweight/Obesity/ abdominal obesity IUGR Maternal diabetes Physical inactivity

● ●

● ● ●

High intake of fibre Fruits and vegetables Physical activity Exclusive breast feeding

Linoleic and alpha linoleic fatty acids / fish (EPA-DHA), Oleic acid Plant sterols, nuts, Dietary fibre Whole grains cereals Potassium Fruits and vegetables Low intake of alcohol Physical activity Vegetables and fruits Physical activity

Dietary fibre Vegetables and fruits Physical activity

quantities to provide micronutrients and phytonutrients that are thought to promote human health and combat both micronutrient deficiencies as well as pathogenesis of several chronic disorders (Box 35.4). Fruits, vegetables, grains, legumes, nuts, and tea are rich sources of phytonutrients. Vegetables and fruits are widely recognised as miracle foods for promotion of health and prevention of chronic diseases due to their bioactive constituents by varied mechanisms. The Joint FAO/WHO Expert Consultation (2004) on Diet, Nutrition and the Prevention of Chronic Diseases recommends the intake of a minimum of 400 grams of fruit and vegetables per day, excluding starchy tubers such as potatoes, for the prevention of chronic diseases including heart disease, cancer, type 2 diabetes and obesity. World Health Report 2002 indicates that 2.7 million lives could potentially be saved each year if fruit and vegetable consumption could be sufficiently increased.

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Vegetables and fruits are low in calories, bulky with fibre, with a high satiety factor and therefore are of great value to reduce calorie intake and prevent obesity, a forerunner of all diet related chronic disorders. Some of these reduce lipids and glucose absorption due to their fibre content. The active constituents influence the aetiopathogenis of cardiovascular diseases, cancer, cataract, osteoporosis, diabetes, chronic obstructive pulmonary diseases, arthritis and diverticulosis. Non-starchy vegetables, complex carbohydrates probably decrease mouth, pharynx, larynx, oesophagus and stomach cancers [54]. Allium vegetables with organosulfur compounds modulate the activity of several metabolizing enzymes that activate or detoxify (glutathione S-transferases) carcinogens and inhibit the formation of DNA in several target tissues. Red meat contains high saturated fat and collagen, which leads to collagen sensitization and consequent production of anti-collagen antibodies in susceptible individuals leading to inflammatory arthritis. Alcohol consumption causes cancers of the oral cavity, pharynx, oesophagus and liver, and a small increase in the risk for breast cancer. Chinese style salted fish, salt preserved foods and high salt increases the risk for nasopharyngeal cancer and stomach cancer [54]. In the developing world, tobacco consumption is rising by 3.4% per year. Major health effects of smoking, the most common use of tobacco, include an increased risk in hypertension, lung cancer and cardiovascular diseases [55]. Box 35.4 Commonly available phytonutrients ● ● ● ● ● ● ●

Flavonoids (Polyphenols) Carotenoids Isoflavones (Phytoestrogens) Lignans (Phytoestrogens) Inositol Phosphates (Phytates) Isothiocyanates, Indoles and Saponins Phenols, Cyclic Compounds and Sulfides

35.13 Prevention and control of NCDs The epidemiological transition in India from infections to chronic, noncommunicable diseases has created different challenges for our public health system. It is therefore essential to encourage health-promoting behaviours, which include healthy diets and physical activity as well as avoidance of tobacco and stress management to impact NCDs. A population-based strategy of healthy diets across the life span has to be adopted in primordial and primary prevention for those at risk. Complementary to this, measures have to be taken to detect chronic conditions through early screening and initiate optimal treatment of the

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disease (secondary and tertiary prevention). These diseases are lifestyle related, have a long latent period and need specialized infrastructure and human resource for treatment.

35.13.1Policies Developing countries like India are facing a double burden of diseases, namely chronic energy/protein deficiency and obesity, leading to several non-communicable diseases. Therefore, a comprehensive policy addressing all risk factors including fetal/child malnutrition is crucial. A multi-sectoral, multi-pronged and multidisciplinary approach with a strong public/private partnership will provide an enabling environment and reduce the risks by improving morbidity, mortality, and impact healthcare costs. A life course approach is needed for successful primordial and primary prevention. There should be concordant policies on health, food, agriculture, nutrition, education, industry and commerce, urban rural development, social welfare and information technology. The food label is one of the most important and direct means of communication of product information between buyers and sellers. It is the primary means by which consumers differentiate between individual foods and branded to make informed purchasing choices. In the Indian context, where overweight, obesity and the resultant non-communicable diseases are assuming epidemic proportions, consumption of unhealthy foods can be discouraged to a large extent by effective food labelling practices, which give ample scope for the consumers to make informed choices. The government needs to work along with private sector and civic societies to make available, affordable and accessible healthy choices and options for physical activity. A good leadership and functional alliances will provide an enabling environment to upgrade education, knowledge and skills among all sectors (Figure 35.2). The community should be empowered to actively participate. A public health cadre with carrier opportunities and restructuring of health care system for effective functioning are required. The Government of India and many other countries have already launched several National programmes to prevent and control noncommunicable diseases. In India the important programmes are; the National Cancer Control Programme (1984), National Program for the Prevention and Control of Diabetes (1987), National Program for the Prevention and Control of Cardiovascular Diseases, and Stroke (2006).

35.13.2Strategies Diet Strategies to promote health mostly focus on production, preservation,

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35.2 Public health interventions.

processing, value addition and making available, accessible and affordable healthy choices. Therefore, focus should be on the availability of the healthy foods with mandatory labelling patterns on every food product released to the market for sale. It is evident that integrated approaches to both undernutrition and overnutrition can reduce the burden of non-communicable diseases to a greater extent. Integrated multi-sectoral, multifaceted and multidisciplinary approaches have to be evolved to prevent and control the already escalating obesity and related morbidities. Active measures to promote physical activity both at individual, community and at group level (schools, industries and offices) must be encouraged. Recreational activities, which promote physical activities, must receive more attention. More walking and cycling paths to promote safe activities are required. The strategy is to promote physical activity at workplaces and schools where people spend a lot of their time daily. The school children act as change agents. Trim and Fit programmes for students have to be initiated to reduce obesity and improve physical fitness. Greater involvement of parents in this programme is needed, as the home environment contributes largely to the moulding of habits of the children. Comprehensive workplace health promotion programmes are effective in improving the health status and productivity of employees. Therefore, ‘National Workplace Health Promotion Programme’ has to be initiated to encourage organizations to conduct and sustain workplace health promotion programmes that will achieve desired health outcomes. Training courses and education initiatives have to be carried out to equip management with the knowledge and skills to conduct and promote a healthy lifestyle at their workplaces. Tobacco in all its forms must be censured and tobacco farms should be diversified to other commercial crops as one of the important control strategies.

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Maternal and fetal nutrition Maternal nutrition is an important determinant of birth weight. In India almost one in three babies are of low birth weight and therefore it is essential to build the nutrition of adolescent and pregnant mothers with healthy diets consisting of macro and micronutrients particularly of iron, folate, iodine, vitamin A, zinc, calcium, magnesium and vitamin B12. During pregnancy, attention is required to fulfil calorie, protein and micronutrient requirements to promote 10–12 kg body weight gain and lactation to support the growth of the foetus and infant. The type of fatty acid (oleic acid/ DHA being beneficial) in the diet during pregnancy and lactation are known to influence the plasma cholesterol and cognition in infancy and childhood. Exclusive breast-feeding and prolonged breast-feeding can reduce the risk of obesity and related disorders later. Energy dense and micronutrient rich complementary foods to promote growth and development must be ensured to prevent dual burden of diseases and to avoid irreversible changes in brain growth, prevent stunting and obesity in adult life.

35.14 Actions Greater political commitment and strong leadership in the public health sector is required to ensure the prevention and control of noncommunicable diseases. Advocacy can be broadened to raise awareness and encourage the policy and institutional changes necessary for creation and strengthening of existing health infrastructure for tackling of noncommunicable diseases. The health care providers need to lobby and accord high priority to the following: All the interventions must be culture and region specific and utilize local resources 1. Define national goals and objectives and target populations for advocacy to control non-communicable diseases, including health as well as non-health sectors. 2. Establish and strengthen existing policies for the prevention and control of non-communicable diseases 3. Ensure reduction of risk factors as an integral part of National health development plans, paying special attention to the needy population. 4. Establish national multisectoral body or mechanism for planning, guiding, monitoring activities for prevention and control of noncommunicable diseases.

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Box 35.3 Healthy practices ● ● ●

●

●

●

● ● ● ● ● ●

●

Achieve energy balance and appropriate weight for height. Achieve good nutrition during pregnancy and lactation. Exclusive breastfeeding for 6 months and introduction of complementary foods at 6 months. Prevent stunting and promote growth in children and adolescents (linear growth and muscle mass) by ensuring consumption of adequate good quality proteins and micronutrients. Increase consumption of fruits and vegetables, legumes, whole grains and nuts. Limit energy intake from total fat, shift fat consumption from saturated to unsaturated Consume unsaturated fats with appropriate fatty acids. Eliminate trans fatty acids (bakery products and sweets). Limit intake of free sugars and salt. Restrict alcohol and avoid tobacco. Encourage physical activity. Be aware of fattening trajectory (adiposity rebound in malnourished children) Promote complex carbohydrates and fibre rich diets.

5. Build capacity for intersectoral collaboration involving all government sectors and other stakeholders, such as professional association, community representatives, and non-governmental organisations. 6. Establish separate units for tackling of non-communicable diseases in the Ministry of Health and Family Welfare and different levels of health systems. 7. Develop and implement an evidence based plan for health promotion and prevention of non-communicable diseases. 8. Establish mechanisms for early detection and screening for common non-communicable diseases such as hypertension, diabetes, and certain cancers. 9. Develop training programmes to strengthen capacity for building health systems State governments, regional and local institutes have the responsibility and specific role to convert the above mentioned strategies into action. Persons at several levels need to be empowered with knowledge and skills. Village Panchayats, NGOs, self-help groups, women working groups, labour unions, teachers and health and para-health professionals must be involved for proper implementation of appropriate actions. Canteens, restaurants, and other public catering establishments must be encouraged to serve healthy foods. The healthier choice symbol on packed food should be encouraged for easy consumer recognition. Restaurants, food courts, and fast food centres have to be encouraged to offer more vegetables and fruits and less salt, sugar and fats to their customers.

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35.15 Childhood and adolescent nutrition Nutritious diet is essential to achieve full genetic potentials of growth and development during these periods. Adolescents need appropriate health education and supplementary nutrition for micronutrient deficiencies and healthy pregnancy outcomes to prevent intrauterine growth retardation and low birth babies. In order to avoid adiposity, linear growth, muscle and bone mass have to be built up during childhood and adolescence. Tracking of risk behaviours and unhealthy dietary practices in time and providing appropriate education to them may be useful for prevention of NCDs. Faulty dietary habits have to specially receive due attention. Thus, a life cycle approach prevents an obesogenic environment including regulation of inactive TV viewing, long hours of computer work and sedentary leisure time activities to prevent clustering of risk factors of metabolic syndrome. Adulthood Diet, physical activity, avoidance of tobacco and alcohol are major issues for prevention and control of NCDs. It is important to practice relaxation technique (yoga etc) to avoid stress. It is evident that the way we are born and grow and the food we eat, the drinks we take, the way we play, move around, the work we do and the stress of life, all have an important role to play in the initiation, promotion and progression of NCDs. Education Public awareness programmes must target all age groups and simple messages on diet and physical activity and harmful effects of tobacco must receive great attention. Both dietary and physical activity guidelines should be widely published through mass media approach and information technology (web-based guidelines). Media has a strong impact especially on children and adolescents, and hence unhealthy foods should not be advertised. Education can play a critical role in awareness building and policy implementation. A wide reach and an active partnership of media can go a long way in promoting health and wellbeing of the individuals.

35.16 Community-based programmes for primary prevention A National Healthy Lifestyle Campaign programme should be under taken to educate the people on the importance of healthy lifestyles to provide a supportive environment for healthier eating. Health education and promotion will provide information to the public on the benefits

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of a healthier lifestyle. Measures have to be taken to provide an environment conducive for the adoption of healthy habits. As the population becomes more educated, they are more aware and better informed on health choices resulting in higher interest in adoption of correct preventive practices.

35.17 Health education and role of mass media It is necessary to provide skills and environmental cues for the public to effect the appropriate behaviour changes by establishing health promotion cells. Social marketing strategies have a strong place in information, education and communication. The primary tool for control of noncommunicable diseases is comprehensive and active awareness of the population about the risk factors and practicing the preventive measures. Research studies evaluating the effectiveness of health education in India and elsewhere have shown successful results among the youth and adults [56, 57].

35.18 Secondary and tertiary prevention Diabetes and hypertension are major risk factors for cardiovascular diseases. To improve early detection of the chronic conditions of diabetes, hypertension and hypercholesterolemia, a ‘community health screening’ programme targeted at >35 years population needs to be developed. The population based strategy aims at relatively modest reductions in the risk for each individual, but the cumulative benefits to the community are large since there are many more persons in the mild or moderate risk category factor than in the higher risk category. The two strategies are not mutually exclusive but should be synergistically complementary to each other. Lowcost case-management strategies are also required for persons who manifest disease. Such technologies are already available but await widespread dissemination and application.

35.19 Conclusions The global epidemic of NCDs due to faulty lifestyles is a serious matter of concern and warrants immediate attention of all concerned. The rapidly increasing incidence of these diseases is affecting the poor and disadvantaged populations disproportionately, contributing to widening health gaps between and within countries. Developmental, demographic, economic, health and nutritional transitions result in altered dietary habits and sedentary life styles. The risk factors require to be addressed in totality by comprehensive policies and well-structured programs involving multiple

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sectors through multifaceted strategies. The plans should focus on overall mapping of the epidemics of non-communicable diseases and analysing their technical, social, economic, and behavioural determinants as basis for providing guidance on policy, programme, legislative and financial allocation that are needed to support the prevention and control of communicable diseases. Exposure of individuals and populations to the common risk behaviours for non-communicable diseases, such as tobacco consumption, unhealthy diet, physical inactivity, and alcohol should be reduced. Health care for non-communicable diseases should be strengthened by developing appropriate guidelines and healthy diets on cost effective basis [58]. It is also essential to prioritise research issues for prevention and control of non-communicable chronic diseases.

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Public health nutrition in developing countries GIACCO R, CUOMO V , VESSBY B, UUSITUPA M , HERMANSEN K , MEYER BJ , RICCARDI G ,

(2007). Fish oil, insulin sensitivity, insulin secretion and glucose tolerance in healthy people: is there any effect of fish oil supplementation in relation to the type of background diet and habitual dietary intake of n-6 and n-3 fatty acids? Nutr Metab Cardiovasc Dis, 17, pp. 572–580. GHAFOORUNSS A (1998). Requirements of dietary fats to meet nutritional needs and prevent the risk of atherosclerosis – an Indian perspective, Ind J Med Res, 10(8), pp. 191–102. KRISHNASWAMY K (2004). Newer roles of vegetables in the prevention and control of problem of over nutrition and chronic degenerative diseases. In: Nutrition and Vegetables. Nath P, Gaddagimath PB and Dutta OP (eds). Dr. Prem Nath Agricultural Science Foundation, Bangalore, pp. 162–180. MISRA A , MISRA R , WIJESURIYA M, BANERJEE D (2007). The metabolic syndrome in South Asians: Continuing escalation & possible solutions, Indian J Med Res 12(5), pp. 345–354. YAJNIK CS (2002). The life cycle effects of nutrition and body size on adult adiposity, diabetes and cardiovascular disease. Obes Rev., 3, pp. 217–224. FEEMAN et al (2001). Guidelines for diagnosis and treatment of high cholesterol, JAMA 28(6), pp. 2400–2402. MISRA A , VIKRAM NK , GUPTA R , PANDEY RM , WASIR JS , GUPTA VP (2006). Waist circumference cutoff points and action levels for Asian Indians for identification of abdominal obesity, International Journal of Obesity, pp. 106–111. JAMES WP , FERRO -LUZZI A , WATERLOW JC (1988). Definition of chronic energy. Eur. J. Clin. Nutr., 42, pp. 969–981. WHO Expert Consultation (2004). Appropriate body mass index for Asian populations and its implications for policy and intervention strategies The Lancet, 36(3), pp. 157–163. The Expert Committee on the diagnosis and classification of diabetes mellitus. Report of the Expert Committee on the diagnosis and classification of diabetes mellitus. Diabetes Care Suppl, 25(1), pp. 5–20. REDDY KS and KATAN MB (2004).Diet, nutrition and prevention of hypertension and cardiovascular disease. Pub Health Nut, 7(1), pp. 167–186. SACKS FM et al (2001). Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. New Engl J Med. 34(4), pp. 3–10. FOOD AND AGRICULTURAL ORGANISATION (2004). Globalisation of food systems in developing countries impact on food security and nutrition. Food and nutrition paper. United Nations; FAO. SAWAYA AL , DALLAL G , SOLYMOS G , DE SOUSA MH , VENTURA ML , ROBERTS SB , SIGULEM DM (1995). Obesity and malnutrition in a shantytown population in the city of Sao Paulo, Brazil. Obes Res, 3(2), pp. S107–S115. PRENTICE AM (2003). Intrauterine factors, adiposity, and hyperinsulinemia, BMJ, 32(7), pp. 880–881. BAVDEKAR A, YAJNIK CS , FALL CH , BAPAT S, PANDIT AN, DESPANDE V , BHAVE S , KELLINGRAY SD , JOGLEKAR C (1999). Insulin resistance Syndrome in 8 year old Indian Children: small at birth, big at 8 years, or both? Diabetes, 48, pp. 2422–2429. WHO/ FAO (2002). Diet, nutrition and the prevention of chronic diseases. Report of a joint WHO/FAO Export consultation. WHO Technical Report series 916, WHO/FAO, United Nations. RIVELLESE AA

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36 Planning result-oriented public health nutrition programs: theory and practice Ashi K. Kathuria

Ashi Kohli Kathuria, MSc (Food and Nutrition), is the senior nutrition specialist at the World Bank, New Delhi. She has extensively provided strategic and technical leadership to large public health and nutrition programmes in India. Her areas of interest include programme development, monitoring and evaluation, policy and advocacy work, and sector assessment and analyses. Prior to her position at the World Bank, Ms. Kathuria was deputy director at USAID, New Delhi, office of social development, and among other guided USAID (India) work in the maternal and child health and nutrition, education, women’s empowerment, workforce development, and disaster preparedness and response.

!$.1

Introduction

Public health program planning in its early days related largely to the planning of public health infrastructure and systems. It was undertaken almost exclusively by public health professionals. Today, it has evolved into a notably specialized and comprehensive field that integrates cutting edge public health science, social science theories, principles of management, and social dynamics and interactions. It engages a range of stakeholders in the process, including the program participants1 and incorporates their perspectives during each stage of program planning. Two major advances in international development over the past decade have had significant directional implications for public health program planning and management. One is the focus on development results and their effective measurement; the other is the emphasis on collaboration within the development community for policy coherence, technical cooperation and aid harmonization. Several international initiatives have 1. The term program participant refers to the people who benefit from the services and is distinct from program person. It is synonymous with the often used term, ‘beneficiaries’, but is the preferred term used throughout this chapter. This is in recognition of, and to highlight, the fact that no program would be possible without the participation of the people who are expected to benefit from the program.

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led to these directions. The Millennium Declaration marked the beginning of an unprecedented era of collaboration for development; and the Millennium Development Goals (MDGs) are probably the best known and most ambitious global commitments to results-based development. The agreed MDGs, targets, and indicators provide the basis for measuring progress and the effectiveness of aid. The Monterrey Consensus (2002), the Rome Declaration (2003), the Paris Declaration (2005) and the Managing for Development Results global initiative further underscored the shared responsibility of all stakeholders in achieving development results[1]. To improve the effectiveness of international aid and to better demonstrate development results, many international agencies, donors and countries adopted practices referred to as Managing for Development Results (MfDR) or Results Based Management (RBM). MfDR or RBM makes results central to all phases of the development process. It aligns program development, implementation, monitoring and evaluation with results, and uses results as the basis of learning and decision-making [2, 3]. All public health nutrition program planning efforts must be responsive to this context. They should ensure a strong result focus during all stages of planning and seek to build partnerships and foster collaboration. In the specific context of public health nutrition, several events have underscored the need to invest in, and to accelerate action, to improve nutrition. Starting with the MDGs, the critical role of nutrition in human development has been highlighted. Improving nutrition will contribute to the achievement of six MDGs – directly to MDG 1, 4 and 5 and indirectly to MDG 2, 3, 6 (see Box 36.1 for the contribution of nutrition to each of these MDGs). The 2008 Lancet special series “Maternal and Child Undernutrition” highlighted the significant contribution of undernutrition to mortality and disease. It demonstrated that interventions to address maternal and child undernutrition and save millions of lives are available. The Lancet also pointed out the low priority accorded to nutrition by donors and developing countries [4]. The “Copenhagen Consensus 2008”2 ranked five nutrition interventions amongst the top ten most cost-effective development interventions [5]. This is far higher than interventions in any other sector, and demonstrates the highly costeffective nature of nutrition interventions. Following these events, higher commitment to improve nutrition is emerging from the international agencies, bilateral agencies, private foundations, civil society and the private sector. Consensus is also emerging on a global “Framework of Action” to scale-up action to address malnutrition. This framework outlines key considerations, principles, and priorities for action to address malnutrition [6]. 2. The Copenhagen consensus summarizes the views of a panel of leading economists, including five Nobel Laureates, on the top ten development investments.

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Box 36.1 Nutrition’s contributions to the attainment of MDGs [19] Goal 1 – Eradicate extreme poverty and hunger • Malnutrition erodes human capital, reduces resilience to shocks and reduces productivity (impaired physical and mental capacity). Goal 2 – Achieve universal primary education • Malnutrition reduces mental capacity. • Malnourished children are less likely to enroll in school or more likely to drop out. • Current hunger and malnutrition reduces school performance. Goal 3 – Promote gender equality and empower women • Better-nourished girls are more likely to stay in school and to have more control over future choices. Goal 4 – Reduce child mortality • Malnutrition is directly or indirectly associated with more than 35% of all child mortality. • Malnutrition is the main contributor to the burden of disease in the developing world . Goal 5 – Improve maternal health • Maternal health is compromised by an anti-female bias in allocation of food, health and care. • Malnutrition is associated with most major risk factors for maternal mortality. Goal 6 – Combat HIV/AIDS, malaria, and other diseases • Malnutrition weakens resistance to infections. • Undernutrition reduces malaria and diarrhoea survival rates.

The aforementioned developments have important implications for public health nutrition program planning. One, program planning for public health nutrition programs must focus on the most cost-effective, proven interventions; they must include robust monitoring and evaluation systems to measure and document results. Two, it must build in mechanisms to test effectiveness of the delivery approaches. This will contribute to a better understanding of the ‘how’ of the delivery of nutrition interventions, an area less understood than the ‘what’ of nutrition interventions. Finally, it must incorporate strategies to advocate for and build commitment for nutrition, within the organization as well as amongst a range of external audience, including leaders and opinion makers, policy makers, and programmers. This chapter attempts to bring to the reader a comprehensive discussion of the key elements of program planning, some prominent theories and conceptual frameworks used in planning public health programs, and guide them through the various steps in a program planning cycle. It does not offer a blue-print or prescription for program planning, since program planning can happen in many different ways and there is no ‘one best way” to plan public health nutrition programs. Instead, by bringing together the academic and the practitioner perspectives on program planning, the

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chapter hopes to help the reader understand and apply the theories, concepts and tools of program planning to develop nutrition programs that have a higher potential for achieving their intended results. The chapter is organized into five sections. The first section provides the background; the second provides an overview of program planning and its nature; the third discusses some of the widely used frameworks, concepts, theories and tools for program planning including two frameworks specifically applicable to nutrition program planning. The fourth section takes the reader through the steps involved in program planning. Illustrations and practical examples from nutrition programs are used across all sections to make the connections between theory and practice. The last section concludes with a few points for further reading, thought and discussion.

36.2

Program planning – an overview

36.2.1 Definitions Planning has been defined in several ways. It refers to the management function that involves envisioning the change desired to improve a situation or to resolve a problem, setting goals and objectives, and after examining several options in a rational manner, making choices about the best route for achieving the intended change, laying out the course of action, planning to proceed with these in a logical, preset manner and establish a means to measure the attainment of those desired improvements [7]. The term ‘program’ refers to an organized and structured set of strategies and actions to deliver some prioritized services or interventions to address a problem, improve a specified situation, bring about the intended change, or achieve the desired result. Program planning serves as a bridge between and among theories, measurement sciences, substantive content and actual practice of public health [8]. It often involves working backwards through the entire chain starting with the intended result that the plan is to achieve. After having identified the result, planners identify the actions and processes required to be undertaken to produce that result, and thereafter the inputs or resources needed to carry out those actions. Although some texts draw distinctions between a program and a project (generally programs being more complex and large with respect to geographical coverage and reach, duration, planned results and resource levels, as compared to projects), throughout this chapter (unless specified otherwise) the term ‘program planning’ encompasses project planning, as the principles, concepts and steps discussed are applicable to both. Of the many approaches to planning, the one that is almost universally applied to the planning of public health programs is ‘rational planning’. Rational planning is based on a cause and effect relationship and involves an analysis of the problem to be addressed (including the full set of

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conditions and associated factors that cause, enhance or limit it); the use of scientific knowledge and theories to find the most effective intervention or mix of interventions to address the problem; and the application of systematic, logical sequence of thoughts and actions to improve the problem of concern. Planners set goals, consider alternatives, implement programs, monitor results and evaluate the program [9].

36.2.2 The nature of planning Program planning involves many steps but it is not a linear process and the steps may not be sequenced. It is an iterative process involving to and fro between various steps. These steps are sequenced in the diagrammatic representation in Fig. 36.1 for ease of exposition, but it is important to remember that these steps may not be linear.

The Program Cycle The phases of planning are shaded

36.1 Steps in program planning

The starting point for the program planning process may differ depending on the need and context of the planning effort, particularly the circumstances that triggered the planning. For example, if program

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planning is initiated in response to a community needs assessment during which health problems to be addressed have been prioritized, then a number of steps related to the problem identification that would otherwise be necessary, would not need to be undertaken. Similarly, if planning for a new national nutrition program is initiated in response to a national strategic priority or a policy to address a nutrition problem highlighted by a large survey, then again problem identification has already taken place. If planning is related to an ongoing program, the first step would then be to review the learnings from the earlier implementation experience and the findings of any evaluation that might have been conducted. Program planning is also a continuous process and does not necessarily end when a program gets into the implementation phase. Good planning is, in fact, cognizant of, and responsive to, events, situations, and new learnings that occur during the life of a program that might trigger a reconsideration of options. A change in policy, an increase or decrease in the resources available to the program, a change in its context, implementation experience, availability of new knowledge and so on are examples of situation that may require a change of course, or a revision of targets or the intervention mix or the manner of service delivery. Good planning also factors in the information flowing back to the program through various feedback loops such as program monitoring data or through feedback received from the program personnel and participants, or findings and recommendations of the evaluation. Planning, program implementation and evaluation have a cyclical relationship [9]. Good program planning not only draws up the program implementation plans but also builds in plans and resources for evaluation, and is informed by evaluation findings. Similarly, evaluation should focus on how to improve the effectiveness of programs and should, during the evaluation process, consider the program planners’ perspectives. The program cycle (Figure 36.1) shows the cyclical nature of planning and evaluation.

36.2.3 Factors that prompt nutrition program planning The need for program planning may be prompted by several factors that result in highlighting a nutrition problem of concern, an opportunity to address a known nutrition problem, a policy or governmental mandate, or a combination of all of these. A nutrition problem could be highlighted through the findings of nutrition and health surveys, such as the national Demographic Health Surveys (DHS) conducted periodically in several countries, the District Level Household Surveys (DLHS) in India, or other sub-national or even local surveys. Routinely collected hospital/other health system statistics may also be indicative of a nutritional problem, e.g., number of cases of diabetes, night blindness during pregnancy, low birth weight and underweight children. It is also possible that an existing and known nutrition problem

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might find a strong champion to take up the cause and become the advocate for developing a program to address the issue [9]. Governmental priorities and mandates, policy recommendations and budgetary allocations are important triggers for program planning [9]. Further, international commitments – for example the adoption of the MDGs, donor priorities, the announcements of grants and requests for proposals, civil society interest and so on – could provide the impetus for program planning. Public health nutritionists must be alert to situations that may offer the opportunity to address a nutritional problem, and take leadership in actively pursuing options and resources for programs to improve nutrition, build champions to advocate for evidence-based policies and programs. Against this backdrop, the next section discusses the basic concepts underlying rational planning and introduces some planning tools and frameworks used in the planning of public health programs.

36.3

Theory, concepts, frameworks

The purpose of this section is to provide the reader an understanding of the theory and concepts fundamental to developing results-oriented programs and familiarize them with some program planning tools that help the planner to keep the focus on results during the planning process. The section includes a description of the ‘program theory’; two generic program planning frameworks widely used in public health program planning, the ‘logical framework’ and the ‘results framework’; and two nutrition-specific conceptual frameworks – ‘the nutrition cause and intervention framework’; and ‘the life cycle framework’. While the theoretical concepts are covered in this section, the development of the program theory through an example is discussed in Section 36.4, entitled ‘Steps in Program Planning’.

36.3.1 Program theory The program theory is the conceptual framework that shows how a program intends to address the problem and bring about the desired change [10]. It hypothesizes the relationship between the nutrition problem (in the instance of a nutrition program) and the proposed set of actions to address it, identifies the various causal factors, and describes how the program actions interact with the causal variables to produce the desired change. Thus, it forms the backbone of ‘theory-driven’ program planning and program evaluation efforts. However, program development is often undertaken on the basis of broad cause-effect relationships, and does not make explicit the detailed program theory. There are compelling reasons to develop and articulate the program theory during the development phase of the program. During the planning stage, it provides a rigorous conceptual framework to assess

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logic and plausibility of the full chain of events that begins with the problem and its causes, the assumptions and the feasibility of the interventions and program action and ends with the intended change that the program expects to achieve. A well-articulated program theory serves as a simple, yet comprehensive tool, for communicating the program’s logic, intentions and desired results with different stakeholders [9], seeking their inputs for verifying the planners’ understanding of the problem, assessing the feasibility of interventions, and finally in strengthening their belief in the program. It puts the program plan on a firmer footing, thereby strengthening the support base for the program [9] which is necessary for program implementation and resource mobilization. During implementation, it is a good communication tool to develop a shared understanding of the program logic amongst the program staff, contributing to better implementation [9]. During evaluation, the articulated program theory presents to the evaluators an accurate view of the program from the planners’ perspectives. The program theory has been described in several ways, e.g., the ‘logic model’, ‘program model’, ‘outcome line’, ‘theory of change’ and ‘action theory’ [11]. The common feature underlying all of these descriptions is that they map and describe the model of how a program is supposed to work and the process through which program components are presumed to produce the desired effect [10]. Two models of the program theory are described here: (a) the Rossi, Lipsey and Freeman program theory; and (b) the Logical Model. The Rossi, Lipsey and Freeman program theory The Rossi, Lipsey and Freeman model of program theory has three interrelated components – the impact theory, the program’s organizational plan, and the service utilization plan [11]. The organizational plan and the service utilization plan are together referred to as the process theory (Figure 36.2).

36.2 Overview of program (Source: Adapted from P.H. Rossi et al [11]).

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The impact theory explains the causal and effect relationship between the program’s activities and its intended results. It describes the assumptions around this cause–effect relationship and how the program activities will result in improved conditions to address the problem. The cause–effect relationship could be direct, e.g. when a certain program activity can affect some intermediate condition and lead to the improved outcome [11]. It could also involve a sequence of outcomes leading to the intended change. In this chain of events, direct outcomes are referred to as proximal or immediate outcomes and the outcomes that follow later are the intermediate outcomes and the distal outcomes. The achievement of distal outcomes is dependent on the successful attainment of the proximal outcomes [11]. The cause–effect relationship, in its simplest form has a single pathway. However, in practice, often this relationship is complex and there are multiple pathways leading to the intended change [10]. The cause–effect relationship is often influenced by certain factors, referred to as moderating factors or moderators – influencing either the program-proximal outcome relationship, or the proximal-distal outcome relationship, or both – which could either enhance or constrain the causal linkage [10]. Moderators could be qualitative variables, such as gender, motivation, socio-economic status, or quantitative variables, such as program coverage, the number of contacts [10]. Given the significant influence that moderators could exert on the achievement of a program’s intended outcomes, during program development it is crucial to identify the various moderators and the possible influence of these on outcomes, so that these could be addressed to the extent possible. To illustrate the impact theory, let us assume that a program for pregnant women intends to reduce the prevalence of anemia during pregnancy. It delivers three interventions: (1) dietary counseling; (2) counseling regarding the benefits of iron–folate supplements during pregnancy; (3) distribution of the prescribed number of iron–folate tablets, including treatment dose for anemic women. Assuming that the program is implemented well, the counseling is expected to lead to an increase in the knowledge of pregnant women regarding consumption of iron rich foods and the benefits of iron-folate supplementation, the proximal or immediate outcomes. These immediate outcomes in turn will motivate women to consume improved diets and the prescribed dosage of iron–folate supplements, the intermediate outcome, which is expected to bring about a reduction in the prevalence of anemia, the distal outcome. The pre-conception iron status of women is a moderator. Improving the iron status of adolescent girls through counseling for dietary improvements and iron supplements could significantly reduce the prevalence of anemia in pregnancy (distal outcome). Figure 36.3 diagrams the path to outcomes in this example.

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36.3 Impact theory of the "prevention of anemia in pregnancy" example showing sequence of outcomes and moderator

The Rossi, Lipsey and Freeman theory has been further nuanced by Issel. Issel describes three sets of inter-related relationships – the causal theory (describing the causal linkages), the intervention theory (describing the intervention–causal linkages) and the effect theory (describing the linkages to outcomes) [9]. The effect theory is akin to the impact theory described above. This model is helpful in a step-by-step construction of the impact theory, and is used in Section 36.3 to take the reader through a systematic development of the program theory. The process theory describes the transactions that take place between the program and the participants to actuate the cause–effect relationship – on the program side by the organizational plan and on the participants’ side by the service utilization plan. The organizational plan describes the functions, activities, resources (human, financial, and physical) of the program and their organization to deliver the program services [11]. The service utilization plan focuses on the program’s service delivery aspects that relate to the program participants – their perspectives, motivation, experiences, socio-cultural background, and so on [11]. The process theory is a good framework to guide the planning of program processes in a manner that integrates the perspectives of the program organization and that of the program beneficiaries or participants. The logical model of program theory The ‘logical model’ or the ‘logic model’ is another popular tool used to represent the program theory or the logic on which the program produces its presumed effect. It links outcomes (both, short and long term) with program activities and the theoretical assumptions of the program. It is a systematic, visual depiction of the relationship among the resources to

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deliver the program, the planned activities and the changes or results that are expected to be achieved [12]. The basic logic model consists of five elements – inputs or resources, activities, outputs, outcomes, and impact. Resources include the human, financial, organizational and community resources available to a program to dedicate to performing the activities that will help achieve the intended results. The program activities are the processes, tools, events, technology and actions needed to deliver the program interventions to achieve the intended results. Outputs are the direct products of program activities and may include, for example, the targets for the services to be delivered by the program (e.g., the number of counseling sessions to be held) or the targets for the program coverage (e.g., the number or percent of participants to be enrolled). Outcomes are the specific changes in program participants’ behavior, knowledge, skills, status and level of functioning [12] (e.g., increase in numbers or percent of mothers exclusively breast feeding their babies for six months]. These five elements are linked through a chain of reasoning or ‘if–then’ statements or assumptions (Figure 36.4).

.

36.4 The logical model

Outcomes could be short-term, generally those that can be attained within a 1–3 year timeframe, and long-term, those that are attainable in 4– 6 years. Impact is the fundamental intended change that the program hopes to achieve as a result of the program activities, and is generally expected over a 7–10 year period [12]. Although there are differences in the logic model representation of the program framework and the program theory described earlier, there are overlaps and consistencies. The logical model’s inputs and activities overlap with the process theory; and the outputs, outcomes and impact of the logic

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model overlap with the impact theory. The prominent difference is that in the logic model all program activities are drawn together without differentiating between the interventions and the activities that will lead to the outcome and other supportive activities, whereas this distinction is clearly made in the process theory [9]. Some believe that because the logic model lays a relatively higher emphasis on inputs and activities, the program rationale may not receive the due attention [9]. In the program theory, on the other hand because of the distinct process and impact theory, both aspects get strong emphasis. Program planners and evaluators must view the above approaches as tools that help to think through and develop plausible programs that have a strong scientific rationale, assess needs and gaps, and develop the entire program and select the one that best suits them. Program planning frameworks (a) Logical framework The logical framework (also referred to as ‘logframe’) is one of the core techniques used widely during the entire project cycle from program planning, through implementation and monitoring to eventually, the evaluation. It is a “cause and effect” model of the program’s interventions to bring about the intended results and draws together all key components of the planned project or program into a clear set of statements and communicates in a simple and concise manner, the essential elements of a complex program. At the same time it helps to organize thinking, relate activities and investments to expected results, set a framework for monitoring and evaluation, performance indicators, allocate responsibilities and communicate concisely and unambiguously with all key stakeholders as well as achieve stakeholder consensus [13]. A logframe is a 4 × 4 matrix with a hierarchy of objectives — the project structure, indicators of performance, means of verifying the indicator and important risks and assumptions along the horizontal axis and the goal, purpose, outputs and activities along the vertical’ axis (Figure 36.5). The framework uses the if-then logic to work through the matrix and check the logic. Starting at the activities level, the ifthen logic means that if we undertake the activities and the assumptions hold true, this will lead to the outputs. If the outputs are produced, and if the assumptions hold true, then the purpose will be achieved. If the purpose is achieved and the assumptions hold true, then the program will contribute to the goals [14].

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36.5 The Logical Framework – The 'If'/ 'And'/ 'Then'/ Logic that underlies the logframe approach [14].

Developing the logframe is a collaborative process and a participatory ‘team approach’ involving program management, staff and all key and primary stakeholders is critical in the development of a good logframe. Stakeholder’s commitment and ownership are as important as the technical design, quality and intended results. A logframe is a living document and can be modified during the program implementation as required following a team process [14]. (b) Results framework The Results framework is a conceptual tool for planning and performance measurement that has been adopted by many development organizations in response to the focus on RBM and the heightened emphasis on development results [15]. The Results framework is a generic term to describe a strategic planning, management and results measurement tool [16]. It is based along the lines of the logical model and is used in many contexts – at the program level, organizational level, country level and the global level. It is used not only to define the results to be achieved but to also describe the context in which results are planned to be achieved, measured and monitored [17]. At a program or project level, the results framework displays the program logic that explains how the development objective is to be achieved, including causal relationships and assumptions underlying these [18]. It diagrams the logical cause-effect relationships between various activity outputs at the bottom, intermediate results or outcomes in the middle, and the strategic development objective at the top [3]. In a results framework, the logical sequence through which a development intervention transforms a set of inputs into specific outputs, outcomes and impacts is depicted through a ‘results chain’. The results chain is a plausible causal relationship

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that described how certain inputs will likely lead to intended outcomes. They form the ‘storyline’ underlying the program and explains visually the problem(s) that the intervention is trying to address, the desired objective(s) to be achieved, the intermediate results that are critical for achieving the objective(s), and the required arrangements to measure progress towards these objectives. The results framework, thus, facilitates planning, execution, monitoring and evaluation of a development intervention [17]. The distinctive feature of the results framework is that it puts the higher order development objective and intermediate outcomes centre-stage, and is less concerned about defining and measuring the inputs, processes and outputs; whereas in the traditional project approach there is equal emphasis on monitoring all elements of the log-frame hierarchy. A potential danger with this approach is that by concentrating on the higher-order results, their linkages with project activities may become overly vague or disconnected and might compromise activity implementation monitoring. To mitigate this risk, it is suggested that programmer’s devote time and attention to also align individual program activities into the overall results framework [3]. Nutrition-specific planning frameworks Nutrition is a complex interplay of many factors, and the determinants of nutrition often lie across many sectors. Many of the nutrition problems seen in a particular target or age group might have their origin in another phase of life. Thus, any nutrition program planning efforts must take into account the various inter-related causes leading to the problem at hand and examine the problem from the perspective of its origin. This is essential to make rational decisions and to identify the most appropriate and effective interventions to address the problem. Two widely accepted frameworks that most public health nutritionists will be familiar with, are presented here as possible frameworks to guide the analysis of the key determinants of the problem and the influencing factors, select the critical intervention points and identify the most appropriate mix of interventions to address the problem. (a) The nutrition conceptual framework The conceptual framework presented in Fig. 36.6 (adapted from the UNICEF nutrition framework) is a good tool for the analysis of the causes of child undernutrition, and to select suitable interventions. The framework shows that the immediate causes of undernutrition are inadequate ‘food and nutrient intake’ and ‘infections/disease’. These are

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influenced by three underlying causes – access to food, maternal and child care practices, and lack of sanitation, hygiene and health services. Income, poverty and its various contributors and the social, political and economic contexts are the major basic causes that contribute to malnutrition. The framework also lays out effective nutrition interventions at each of the levels. Direct nutrition interventions such as infant and young child feeding and caring practices, micronutrient interventions and household hygiene and sanitation address the immediate causes of malnutrition (these are also the short routes to improving nutrition). Agricultural interventions, poverty reduction, education , women’s empowerment, health systems improvement are interventions to address the underlying causes (these are the longer routes to improve nutrition but are by no means less important).

36.6 Conceptual framework for analysis

While using the malnutrition causal framework, an analysis of the immediate causes (the direct determinants) and the factors at the underlying and basic levels, in the specific context of the particular community is important. There is increasing evidence of the strong association between the poor status of women and higher rates of child malnutrition; this is understood to be one of the key contributors to the high levels of

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malnutrition in South Asia [19]. Therefore, issues that relate to power equations, gender inequality, low female literacy, and social exclusion are important factors to consider, especially since they constrain the abilities of households, mothers and caregivers to access services and practice appropriate behaviors important to achieving optimum nutrition. It is likely that they strongly moderate the program-outcome pathway and must be fully explored during the community needs assessment. (b) Nutrition life cycle framework Examining the nutritional problems through the life cycle approach during planning of public health nutrition programs provides many benefits. First, it highlights the specific nutrition needs, problems and vulnerabilities unique to each of the life cycle stages, thus helping design suitable ways and means to promote good nutrition throughout the life course, taking into consideration the specific nutritional issues and vulnerabilities of that stage [20]. For example, for optimum nutrition during infancy, early and exclusive breast feeding, timely and appropriate complementary feeding, prevention and treatment of infections, continued breast feeding during illnesses, micronutrient supplementation, growth monitoring and promotion are essential for optimum nutrition. Second, health and nutritional problems that manifest during a particular life cycle stage may not wholly depend on the nutritional intakes and status during that particular phase, although nutrition during the specific period may also be compromised or may have also its own unique problems. Nutrition status during an earlier life stage may continue to interact with and affect the nutrition outcomes of the present life stage [20]. For example, better nutrition during pregnancy improves intra-uterine growth, improve birth outcomes, and results in better nutrition for the newborn. Similarly appropriate nutrition during the first two years of life improves physical growth and development, including cognition and brain functions and affects adult height and improved cognitive function. The life cycle approach helps one analyze and consider the relative benefits of intervening in a life stage earlier to the one which presents the nutritional problem, or in both, to achieve the maximum nutrition benefit. It thus helps weigh the criticality of extending the intervention to include another life cycle phase, and select appropriate intervention and approach mix against the consideration of benefits, costs, resource levels, the program time period and so on.

36.4

Steps in program planning

This section guides the reader through the preparation for planning, the phases of program planning and the key elements to be considered by the planning team in each phase. For this purpose, the planning process has

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been organized into six phases – problem identification, envisioning and defining results, selecting interventions, implementation planning, monitoring and evaluation planning and finally planning for program ending. While the phases are distinct, it does not mean that planning would move in a linear manner from one phase to the next. As highlighted earlier, planning is an iterative process that involves going back and forth between the various steps and phases. The development of the program theory is taken up through the example of a hypothetical public health nutrition program, a program to reduce the prevalence of anemia in pregnant women living in a remote tribal area.

36.4.1 Getting ready for program planning Prior to initiating active program planning phases, some preparatory actions are required. These include, putting together a planning team, identifying stakeholders and partners, outlining the planning approach and process, establishing timeline and so on. The planning team Program planning is best done as a team effort. For nutrition program planning, a team of planners could include the public health nutritionist, health and social science professionals/experts, government representatives, civil society representatives, community members, communication experts, members of the business community, advocates for nutrition. While the decision on who to have on the planning team, how large a planning team to have, and what kind of structure to adopt for the team is very contextual, criteria such as the type of skill mix and expertise needed, engagement of other partners, agencies, and stakeholders – the scope and boundaries for their engagement, the mix of external and internal members on the planning team need to be very carefully considered. Many of these considerations will depend on the internal expertise, experience and capacity of the organization undertaking the planning, the budget allocated or that could potentially be mobilized for the planning effort. The choice of the team leader is another critical consideration. Because many critical technical decisions will need to be made during the planning process, ideally the team leader should bring strong technical skills and leadership qualities to steer the process [9]. Partnerships The program planning phase is the most appropriate phase for forming partnerships, engaging stakeholders, and building ownership towards the

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program [14]. The exploration and mapping of who is doing what in terms of public health nutrition, or who is interested in doing something to improve the nutrition problem is important. Actively seeking partnerships or ways in which other existing or upcoming programs can complement the program being planned is crucial for coordinated efforts, synergy of purpose, harmonization of strategies and optimal utilization of resources. It is also worthwhile to identify and involve a champion or advocate who will lend weight to the planning team, influence decision makers within an organization or in the larger arena [9]. Program planning plan and the guiding principles Before initiating the planning, the planning team should draw up the program planning plan. This includes, outlining the approach and the process to be followed, establishing timelines, assigning roles and responsibilities, and estimating and securing resources required for the planning effort. Making choices and decisions will be required throughout the planning process, including situations where consensus may not emerge and hard choices would need to be made. Therefore, it is a good practice for the planning team to agree on some key principles to guide decision making. Examples of possible guiding principles are, involving stakeholders in all stages of planning and decision making, the option that is of the maximum benefit to the participants will be preferred over other options all other things being equal, and so on. Such a decision making framework with pre-agreed criteria is a very helpful tool during the planning process. With these basics in place, the planning team is ready to initiate the planning process outlined in Fig. 36.1 and discussed below.

36.4.2 The planning process Problem identification and statement An accurate understanding of the health problem to be addressed, its dimensions, the causal chain leading to the problem, including the contributing or protective factors, forms the basis for the need of the program, and the foundation upon which the program is built. The problem forms the basis for envisioning the intended change or result for determining the interventions and mechanisms for their delivery, and for measuring the change in the situation as a result of the program. Three key elements of the problem identification phase are information gathering and exploration, prioritization, and articulation of the problem.

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Information gathering and exploration One of the key elements of identifying the problem is to collect as much information as possible about the nutrition-related issues in the setting of the proposed program. This involves, first and foremost, searching for the existing data, both qualitative and quantitative from all possible sources, such as literature, survey reports, medical records, data from existing programs and projects – large and small, public and others (NGO, donorsupported, public–private partnership programs) [9] . Planners should carefully review the existing information to identify critical gaps in information that need to be filled through primary data collection and to inform the decision about the type and scope of the community health/ nutrition assessment – frequently referred to as community needs assessment – to be undertaken. Community Needs Assessment (CNA) The CNA could serve as the starting point for program planning. If the problem is already well understood, then it is a means to verify the problem and assess community needs. In the context of public health nutrition, CNA provides a realistic measure of the situation of nutrition in the particular community, the key problems and their causes, including the factors (moderators) that enhance or limit the problem [21]. For example, the community members’ initial awareness about nutrition, what they think and feel about a particular situation, prevalent feeding and caring practices, infant feeding practices are important determinants or contributing factors to the situation of nutrition in the community. In addition, the CNA provides valuable insights in to the health and social aspects that could add to, or undermine the success of the program, e.g., factors like preventive health services, socio-economic conditions, gender and power relations, and motivation to participate. Not only is the information from a CNA valuable, the process is itself of great value. It provides the opportunity for communities, or their representatives, to get engaged in identifying problems and needs, prioritizing the most important ones, setting goals and objectives and finding solutions to the problem [21]. It also provides the community groups or sponsor agencies the opportunity to assess current programs and policies, the resources available and to identify what may be further required of the programmer and the communities to change things. For the planning team, the CNA serves as an opportunity to identify the different stakeholders and understand their interests. A CNA can be conducted in many different ways (Box 36.2 for some possible approaches to conducting a CNA). It is important to remember

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that the CNA may not be a one-time effort and it may be necessary to go back to the community to get stakeholder involvement, and to ensure that the program as being planning is indeed responsive to the problem and the community needs [9]. Box 36.2 Possible approaches for conducting a Community Needs Assessment A CNA may be conducted using different approaches and processes. For example, existing data can be used, surveys can be designed and conducted, key informants can be interviewed, community foray can be organized, and focus group discussions can be held. Observational data is a relatively inexpensive and unobtrusive manner of gathering information, especially to understand community characteristics, their organization, traditions, and so on. For example, walking through a village weekly market may provide a good sense of who does the food shopping and makes decision about what is to be bought – the men or the women? Do men and women interact freely with each other? This information, for instance, will inform decisions about the critical target audience for a nutrition education program and whether to conduct joint or separate sessions for men and women. Depending upon the time and resources available to the planning team, any of these approaches or a combination of sorts can be used. A series of 2-3 stakeholder workshops that bring together representatives from across the relevant community constituencies, e.g., men and women, community leaders, opinion makers are often used as an efficient way of determining community needs. No matter whichever approach is followed, it is important to have information on the magnitude of the problem, the causative factors specifically as they pertain to the problem in that context, population characteristics, attitudes and behaviors.

Problem analysis and prioritization The process of prioritization and decision making to select the problem(s) to be addressed can be both overwhelming and challenging - overwhelming, because it requires organizing, analyzing large amounts of information collected from multiple sources, which may not always be consistent with each other; challenging, because of the potential for lack of consensus arising from the varied interests of the different stakeholders and possible biases of particular team members, especially towards their area of expertise. It is usually helpful to first, involve as many stakeholders as possible and involve communities in the prioritization of the problem, and second, to adopt a framework of rational criteria for decision making. Some criteria, such as the magnitude of the problem, its severity, the availability of effective interventions and so on, are useful to consider during prioritization (Box 36.3 for a description of some of the criteria to consider during prioritization).

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Box 36.3 Possible criteria for prioritization of public health nutrition problems Magnitude of the problem From the public health nutritionist’s view, the magnitude or the size of the problem is its relative deviation from a normally acceptable level or norm (the normative need), reflected through measures such as mortality rates, prevalence rates, relative risks, or through quality measures such as QALYs and DALYs. From the community’s perspective, the expressed need coming out of the CNA reflects the magnitude in terms of the relative demand for or utilization of services. It is possible that the normative need and the expressed need are not consistent and it may be challenging to give full consideration to both during prioritization. Severity or the importance of the problem: This should be carefully considered, since at times the most severe problem may affect only a small proportion of the population. It is possible, as is generally the case with nutritional problems that the problem is silent until the damage is done. For instance, underweight and stunting in children might not be noticed unless very severe but results in permanent damage to physical and mental growth; micronutrient deficiencies such as anemia, iodine deficiency disorders are not visible until very late. Potential effectiveness of the interventions Problems with causes that have a higher potential to being modified through an intervention might receive a relatively higher priority over others on this criteria. Technically effective nutrition interventions for most of the public health nutrition problems, especially undernutrition are known. The Lancet series on Maternal and Child Undernutrition (2008) has laid out a comprehensive set of efficacious solutions that have been shown to work under all contexts. Potential availability of resources The approximate estimated costs of addressing the different problems and how these match with the available or potentially available resources is another consideration. This criterion could determine the number of problems that would be feasible for the program to address. Yet other criteria related to costs of the program and the program’s potential to address the problem are costeffectiveness, cost- benefit ratios and costs per program participant. Organizational priorities and comparative advantages The prioritized problems and actions to address them must be aligned to the strategic priorities of the organization undertaking the planning and should preferably be able to capitalize on its comparative advantages.

It is helpful to develop a prioritization matrix with the prioritizing criteria against the X-axis and the problem against the Y-axis. Scoring each of the identified problems against the criteria in the matrix (which can be assigned weights according to their relative importance in the given context), or simply assigning a high/low value and then prioritizing on the basis of the scores is one rational way to prioritize problems [8]. It is important to remember that such a matrix serves only as a framework for decisionmaking and is not a mathematical calculation tool. Planning teams can design their own prioritization tools or mechanism to suit their needs. Problem analysis and prioritization is not a linear process, and the need to re-prioritize may emerge as analysis progresses. It is possible that a problem initially thought to be of high priority might either not be amenable

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to change, or might not be within the program’s scope, or that it is not politically or culturally feasible, or that verification with stakeholders or through the CNA indicates differently [9]. Developing the causal theory The first step in developing the causal theory is to get an accurate understanding of the health problem, its dimensions, the causal chain leading to the problem, including the main causative factors and influencing factors contributing to or limiting the problem. This is essential to clarify the causal links and determine vital pathways that can be modified with known interventions. One helpful way is to diagram the problem and the full causal chain, including the influencing factors. The chain diagram provides the framework to link the causative factors to the program’s interventions. It is in fact, a good idea to diagram several of the top ranked problems [9]. Doing so will expose the problems for which one or more causal factors that may exist are not within the scope or manageable interest of the program, thus helping further prioritization. While developing the causal chain it is important to draw upon the scientific evidence base, at the same time draw upon the CNA and the specific context and environment of the problem. In the instance of public health nutrition, while there is a good evidence base for a large number of the problems, it is imperative to verify the operating causative factors in the context in which the problem is situated, and identify the socio-cultural and other factors that either contribute to the known causes or offer a protective effect. It is also important to examine the causes of the nutrition problem, particularly in the instance of maternal and child undernutrition, from the malnutrition causal framework and the life-cycle framework described earlier in Section 36.2. The former will help explore which particular aspect(s) of the immediate causes of nutrition – food insecurity, lack of appropriate care, lack of health services, are the most pervasive, which ones might be affecting specific socio-economic groups and so on. The life-cycle framework will help understand the origin of the problem and examine the relative effectiveness and benefits of the intervention points. Once the casual diagram is completed, it must be shared with different stakeholders and the program population for a reality check. This is a crucial step. If the diagnosis of the problem and its causal chain is not accurate, no matter how good the interventions and their implementation, the program will not produce the intended effect [9]. The development of the causal chain for problem in our example of the high prevalence of anemia is illustrated in Fig. 36.7. The causal chain shows the causes for the high prevalence of anemia, the influencing factors and moderators.

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36.7 Causal chain of the anemia in pregnancy example

Formulating the problem statement There is no one prescribed way to state the problem. This can be done in innumerable ways, as long as it explains the causes of the problem with all the linkage such that it facilitates choosing the appropriate intervention and intervention point. Issel provides a very comprehensive template for the problem statement that facilitates directly linking causal statement to the different elements of program design and evaluation [9]. Using a slightly modified version3 of this template, the problem statement for the high prevalence rates of anemia in pregnancy example could be articulated as follows: The high prevalence of (anemia) among (pregnant women in tribal villages of India), indicated by (the low hemoglobin concentrations of < 12 g), is caused by (low intake of dietary iron, lack of access to ante-natal services and to iron-folate supplements), and is influenced by (poor pre-pregnancy iron status, lack of knowledge about benefits of iron-folate supplementation). Issel’s template helps to provide the framework that link each aspect of the problem statement to the program development and to the program evaluation. For example,in the above problem statement, the high prevalence of (Health problem) part of the problem statement directly relates to the goal for the program to be kept in mind during program development and to the outcome evaluation; the among (population/community) part defines the ‘targeted participants’ for program development purposes and the ‘intervention group’ during evaluation; the indicated in (health outcome indicators) part of the statement are the ‘outcome indicator/s’ selected during program development and their achievement is assessed during evaluation; 3

This modified template uses the term ‘influencing factors’ to collectively reflect the terms ‘mediating factors’ and ‘antecedents’ used by Issel in the context of the causal theory, since this text uses the terms ‘moderating’ and ‘mediating’ factors as described in the Rossi, Lipsey, Freeman model as factors operating between the proximal and distal outcomes.

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the is caused by (causative factors) and is influenced by (influencing factors) part of the statement helps determine the interventions during program development and represent the outcomes during evaluation. Once the problem statement is defined, the next step is to envision the change in respect of the problem that the program intends to bring about, and set concrete goals and objectives for the program.

36.4.3 Envisioning and defining results Setting goals and objectives This step of program planning focuses on envisioning and defining the results that the program intends to achieve, setting goals and objectives, selecting indicators, and setting targets. In many texts, setting goals and objectives is suggested as a step that follows selection of interventions and the development of the logical model or the program impact theory. However, given the centrality of results to program planning, beginning with the desired vision of change and articulation of the goals and objectives is useful. This approach aids in the selection of interventions and the further development of the program with an eye on the planned results. However, just as in other aspects of planning, setting goals and objectives is a non-linear and iterative process. Goals and objectives flow from the health problem, and are linked to the interventions and program activities. Therefore, on one hand while objectives and targets may drive the choice of interventions, on the other they may need to be adjusted or revised based on the interventions, e.g. their feasibility, dosage, intensity, and such other factors. Goals are broad statements of the desired status of nutrition or health to which the program results contribute. In terms of the results framework and the results chain order, goals correspond to the highest order of results at the top of the chain and are expected to be achieved over a long term horizon. Objectives correspond to the outcomes; and several objectives may contribute to the achievement of a goal [17]. For example, improved maternal nutrition (objective) and child nutrition (another objective) and several others such as those related to prevention and timely treatment of infections, improving sanitation and hygiene contribute to reducing child mortality (goal). Goal statements are not necessarily made in measurable terms. Objectives are specific measurable statements of desired change, generally in an outcome such as the knowledge, behavior, biochemical parameter or another intermediate outcome such as policy, but could at times be related to process changes that the program intends to bring about. Well-defined objectives clearly state what will change, by how much or to what extent, and by when [9]. They guide the further development of the program, serve as the programmer’s framework for decision making and resource allocation, and provide a structure for program evaluation [22].

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Program objectives are derived from the analysis of the problem and can be stated in many different ways. It could be stated in terms of increasing or decreasing, improving or reducing a certain outcome, or it could be stated in terms of maintaining current levels, if a deteriorating trend calls for maintaining current levels, or in terms of a level of achievement (e.g. reducing by 10 percent). No matter how the objective is stated, it must address the what, by when, and by how much of the intended change in relation to the problem [9]. Selecting indicators Indicators are measurable parameters that directly or indirectly measure program outcomes, outputs and processes. They are used to track program performance and determine the success or failure of a program. Given their importance in measuring and judging program performance, indicators must be selected with great care. An indicator must be relevant and meaningful, i.e., it must be closely related to the effect or to the key process that it measures and must also be meaningful to program personnel; it must be sensitive to showing change within the timeframe of the objective or outcome, else it could dilute or not capture the intended change; it should be feasible to collect data on the indicator at a reasonable cost; standardized tools must either exist (or be developed and standardized) for data collection; and finally certain indicators might be mandated by some donors/funding agencies [9, 14]. Objectively Verifiable Indicators (OVIs) are standards against which change can be measured. They set targets in terms of Quantity, Quality and Time (QQT). Indicators should be specific, usable, measurable, sensitive, cost-effective, and available. Two acronyms are widely used to characterize good indicators – SMARTER which refers to Specific Measurable Achievable Realistic Time-Bound + Enjoyable Rewarding, and SPICED which refers to Subjective, Participatory, Indirect, Cross-Checked, Empowering, Diverse [14]. Box 36.4 Types of indicators [14] Direct and proxy indicators Direct indicators are those that relate to directly observable change. These are simply a more precise, comprehensive and operational restatement of the respective objective. Indirect or proxy indicators are used when the expected changes are not directly observable like the quality of life, organizational development; or if the costs of measuring direct indicators is not justified; or if they are measurable beyond the life span of the activity. Proxy indicators may be used instead of, or in addition to direct indicators. Cross-Sector indicators Sector-based or technical indicators must be balanced by the inclusion of other more cross-sector indicators; for example relating to social issues, gender, the environment, and capacity building.

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Formative and summative indicators Formative indicators are set with a time-frame to be measured during part of, or across the whole of, an activity; hence, they are really synonymous with milestones. Summative indicators are used to measure performance at the end. Qualitative and quantitative indicators Quantitative indicators measure magnitude of change in quantitative terms. These are not able to capture change that is difficult to quantify. Qualitative indicators capture qualitative data and may not be straightforward. Process indicators are usually qualitative and assess the how of activities or processes. For example, how technologies were developed and adopted, how income was generated, and who was involved. These may at times be subjective and can be verified with end-users and participants, but may still be less than fully objective. It is best to have a mix of quantitative and qualitative indicators.

Setting targets Targets are numerical values that depict the level of desirable change in an objective or an indicator as a result of the program. A target normally has two parts. One part states the magnitude of change and the other states the date or time period by which the change will be achieved [9]. Estimating and assigning numerical values to the magnitude of expected change is a complex task and informed judgments are required to set realistic and achievable targets. Estimations should be based on a rational basis, such as, trend analysis that can be undertaken through literature review, drawing upon experience from similar programs, examining the magnitude of the effect of the intervention from efficacy or effectiveness trials, using objectives set by a state or national plan or a combination of some of these bases. Some possible ways to make rational decisions pertaining to target setting are briefly discussed below. When the current state of health or nutrition is to be maintained, then it is best to use the current baseline as the target. Another method is to use prescribed norms or targets, e.g., those prescribed by national goals or planning documents. Depending upon where the existing parameter value of the target population lies in relation to the national value, this method can also be nuanced to better suit the program. For example, if the target population lies far below the national target, then a reasonable percentage of the national target (chosen against considerations of intervention intensity, its efficacy and the other parameters discussed earlier) could be used. If disaggregated data for the national value is available, then many other options could be used, such as 50 percent of the best or the target of the middle ranking, and so on depending on where the target population lies in relation to the national or sub-national values. For setting multiyear program targets, the cumulative value of estimated annual change (based on some of the above parameters) may be used to determine the program targets. Another option is to calculate the target that would be

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required to demonstrate a statistically significant magnitude of change, although this method could lead to selecting highly ambitious targets [23, 9]. A set of options for setting targets for objectives suggested by the Public Health Foundation, USA in Box 36.5 can be helpful in selecting an appropriate method for setting targets. Box 36.5 Possible methods to use in setting targets for objectives l

Use an absolute percentage to indicate a “reasonable” change over the period. For example, an absolute decline of 1% of the current level adds to 10% over the decade. Be careful to calculate the % for the numbers from the beginning of the decade or it will be a compounded percentage achieved (as below).

l

Use a compounded percentage to both indicate a “reasonable” change over the period but one which becomes less than the absolute. For instance, a decline of 1% each year from the previous year over the period of a decade is actually 9.6% (1-(.99)9) and not 10% as above. Reverse this calculation to obtain the annual percentage change if you have a total that you’d like to achieve by the end of the decade.

l

Use the current U.S. rate as the challenge point. This works when the state or community rate is worse than the U.S. rate and within a distance achievable. This works when the jurisdiction is deemed “like the U.S.” or average in some way.

l

Use the median values of one’s peers. The Community Health Status Indicators (CHSI) Project has generated 88 peer groupings of counties that share similar characteristics. These characteristics include factors that are thought to influence communitylevel health. This target works when the U.S. rate is too high or too low for the type of jurisdiction. For instance, southern states tend to have more poverty and so to compare health outcomes to the U.S. rate is too much of a challenge.

l

Adopt the Healthy People 2010 targets for the indicators. When the jurisdiction cannot decide and when its current levels are similar to the U.S., the actual Healthy People targets may be very appropriate as well as ready and easy to use.

l

Calculate the “better than the best” (used in Healthy People 2010) - setting a target better than the current status of the best population group in the state.

l

Calculate the “best of the best” (Allison 1999) - benchmarking against the top 10% in any area of the U.S.

l

Calculate what’s achievable based on clinical or community trials. For instance, breast and colon cancer deaths can be reduced by 30-40% of the peak in breast cancer in the mid 1980’s and by the same amount in colon cancer today. Consideration needs to be made in how quickly intervention (in this case, screening) will affect the death rate and how effectively the intervention will be launched in the community.

Source: Public Health Foundation (11/00), Setting Target Levels for Objectives.

It is important to involve the stakeholder in setting objectives and targets. This builds ownership, creates a better understanding of the program, and gets their commitment. If it is not possible to develop these with the stakeholders, a final reality check with them is essential.

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36.4.4 Selecting interventions The intervention package Interventions are the actions that are undertaken to alter the causal pathway to effect the desired change. These may exert their effect by either directly acting on the cause, by altering the influencing or moderating factors. The causal statement provides the starting point for selection of interventions. For each problem with all its causes, influencing factors and moderating factors, there will be several interventions to choose from [9]. Therefore, selecting the most feasible, and the most cost-effective intervention or set of interventions, usually referred to as intervention package, is required. Several criteria useful in making the right choice of interventions include: the efficacy of the intervention which indicates the strength of the cause–effect relationship; the feasibility of the intervention and its delivery (technical, administrative, social, geographical and political); its adaptability, e.g., to be tailored to the specific target age groups, cultural and linguistic settings; the cost as assessed by cost–benefit ratios, cost-effectiveness, or costs and benefits [9, 24]. The efficacy and effectiveness of several nutrition interventions is known. A list of effective nutrition interventions to address the major public health nutrition problems for which a strong evidence base exists have been presented in the 2008 Lancet Series on Maternal and Child Nutrition [4]. Box 36.6 presents a list of these interventions. Another set of prioritized interventions, the short routes and the long routes to improving nutrition from “Repositioning Nutrition: a Call for Reform and Action” is presented in Box 36.7 [25]. Nutrition program planners can select the most appropriate interventions package in the specific context of their program and the problem. The intervention dosage The term intervention dosage refers to the amount, strength and duration of the intervention [9]. As related to nutrition interventions, dosage could be measured in terms of milligrams or micrograms of a specific nutrient or micronutrient administered over a specified number of days, or it could be specified in terms of the number of days, or hours of nutrition education, or weeks of counseling and so on. The dose-response can influence outcome, therefore the dosage of the intervention exposure needs to be carefully considered. For some interventions, such as vitamin A or iron supplementation, well established protocols specify the intervention dosage. However, for interventions such as nutrition education or counseling, a critical component of most nutrition program intervention packages, the knowledge base on dose-response is not yet conclusive and requires more research [26]. Given this situation selecting the dosage may be a difficult task. Nevertheless, decisions will need to be made regarding

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Box 36.6 Interventions that effect maternal and child undernutrition. [4] Sufficient evidence for implementation in all 36 countries Maternal and birth outcomes Iron folate supplementation Maternal supplements micronutrients

of

Evidence for implementation specific, situational contexts

in

Maternal supplements of balanced energy and protein multiple

Maternal iodine supplements

Maternal iodine through lodisation of salt

Maternal deworming in pregnancy

Maternal calcium supplementation

Intermittent preventive treatment for malaria

Interventions to reduce tobacco consumption or indoor air pollution

Insecticide-treated bednets

Newborn babies Promotion of breastfeeding (individual and group counselling)

Neonatal vitamin A supplementation Delayed cord clamping

Infants and children Promotion of breastfeeding (individual and group counselling)

Conditional cash transfer programmmes (with nutritional education)

Behaviour change communication for improved complementary feeding* Zinc supplementation

Deworming

Zinc in management of diarrhea

Iron fortification and supplementation programmes

Vitamin A fortification or supplementation

Insecticide-treated bednets

Universal salt iodisation Handwashing or hygiene interventions Treatment of severe acute malnutri-tion * Additional food supplements in food-insecure populations.

the number of educational contacts, activities, length of contact, duration of the intervention, type of communication channels to be used and so on. Review of prior nutrition education program experience, advice from social science, especially behavior change experts, identifying a suitable theory are some of the ways that can inform the decision making regarding intervention dosage. Further developing the program impact theory/effect theory This section builds upon the causal theory developed in the previous section to further develop the intervention and the impact theory. The intervention theory explains how the interventions affect the causal

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Box 36.7 Routes to better nutrition [25]

Source: Repositioning Nutrition as Central to Development: A strategy for Large Scale Action, World Bank, 2006

factors, including the influencing factors and how they interact with them, and includes a description of the relationship between the intervention and the outcome [9]. The articulation of the intervention theory enables planners to fully understand the relative ability of interventions to significantly alter the key causal factors in the specific context of the program situation, identify any factors that may be outside the manageable interest or the

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purview of the program and prioritize, and refine the intervention or the intervention package. It helps program staff to understand the rationale for the intervention; and during evaluation it presents to the evaluators the planners’ view of the cause–effect framework [9]. Given the multiple cause–effect linkages and cross-cutting relationships that exist in real-life situations, developing the cause–effect theory can be a complex task [11]. It requires drawing on the literature and existing knowledge, using intuition, creativity with logical thinking and reasoning to contextualize the established causal relationships to the program situation, and realistically assess the risks and assumptions [11, 9]. Stakeholder engagement is particularly valuable – it brings to the table new ideas, exposes perspectives and experiences that might otherwise be missed, and provides the necessary logic and reality check. It could be helpful to get some expertise and experience in developing program theory, e.g. a researcher or evaluator to help develop a valid, plausible and well-articulated program theory. In order to develop the intervention theory, planners need to identify and transpose next to the causes and/or influencing factors, one or more interventions (selected on the basis discussed earlier) that will interact with and alter that specific causal pathway. This exposes the points of interventions, their relative effects, and the points at which weak or no causal linkages exist and forms the basis of selecting the most appropriate and effective interventions that the program will undertake. Taking the earlier example of reducing anemia prevalence in pregnant women, the intervention theory transposed against the causal theory developed earlier is diagrammed in Fig. 36.8.

36.8 Intervention theory showing points of altering of causal chain and influencing factors

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The next step is to articulate the impact theory. The impact theory specifies the relationship between proximal, intermediate and distal outcomes or the expected impact. This requires identifying the operating moderating factors that influence the relationship between the proximal and distal outcomes, and the actions that the program will take directly, or leverage from existing program to positively impact the relationship. The impact theory for the prevention of anemia in pregnancy example is diagrammed in Fig. 36.3. As developing the three sets of relationships is an iterative process, the articulation of the impact theory may require going back to the causal theory or even to the CNA to theorize which of the interventions will be effective in the specific context of the particular community or program. Once the program theory is articulated, it must be reviewed and validated with stakeholders. At this point goals, objectives and targets must be reviewed to better judge if these are attainable or to consider any revisions that might seem necessary [11]. The strength and the validity of the program intervention can be only as strong and valid as the impact theory. If the cause and effect relationship is not valid or very weak, no matter how well and careful planned and implemented, the program will not lead to the anticipated result [10]. A valid impact theory must be supported by evidence that the cause and effect relationship assumed actually exists. This evidence can come from research, prior program experiences, efficacy or effectiveness trials. If none of these is available, then a smaller operations research could be considered prior to developing a large-scale program. Planning for program implementation The best and most effective interventions, if not delivered as conceived, in the planned dosage, in the right manner, at the right time, in the right sequence, at the right place will not lead to the desired results. The strongest of the cause–effect relationship might theoretically exist, yet if that interaction is constrained in the actual transaction that will put the theory into practice, expected results will not be achieved. Thus robust plans for program implementation are crucial to develop and test prior to the fullscale implementation of the program. Planning for program implementation essentially means detailing the ‘process theory’ of the program. The section below describes key aspects of developing the service utilization and the organisation plan – the two key elements of the ‘process theory’. (i) Developing process theory A useful starting point is to use the program process theory framework to define the various aspects of the service utilization plan and the organizational

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plan [9]. Implementation planning includes planning for implementation structures, arrangements, resources – human, physical, financial, the logistics, and so on (components of the organizational plan) that will deliver the planned interventions in the planned dosage and manner to the program participants in a way that recognizes and responds to their needs, motivates them to participate in the program and utilize the services for the duration required for the effect to be produced (components of the service utilization plan). (a) Service utilization plan – Developing elements of the service utilization plan to feed into the development of the organizational plan is a logical good practice, although much back-and-forth between the two is to be expected. For example, human resources – a key element of the organizational plan – can only be appropriately assessed once the program’s participants or target clients, place of delivery, ways of reaching out to them and the activities have been finalized, which are all elements of the service utilization plan. Taking the example of reduction of the prevalence of anemia in pregnant women, the service utilization plan will delve into questions such as: What will motivate pregnant women in the particular community setting that the program is expected to target to enroll in and attend ante-natal clinics? What are the barriers and constraints to their participation or in taking iron–folate tablets? It will outline appropriate measures that respond to these issues and factor these into program development. For example, the constraints identified are distance to clinics and resistance by family elders and men. The responses could be either provision of services nearer home or provision of transport/transport costs to address the distance issue, and counseling of family elders and men about the importance of antenatal care for the health and well being of the mother and the baby. One of the first and foremost aspects of the service utilization plan is defining the target population, setting eligibility criteria for participation (if it is not targeted to the entire population), determine ways to maximize the inclusion of those who are eligible for services (e.g., through outreach communication, enrollment drives and so on), and minimize the inclusion of those who do not need the services (e.g., through screening methods) [9]. Both, inclusion into the program of those who do not need the program services and will not benefit from them, and under-inclusion of those who need the program services and would benefit from them, amount to sub-optimal provision services to the target group and could undermine the effect of the program. There are also implications for resource use and any further economic analysis undertaken during evaluation or otherwise [9]. The social marketing theory and its ‘four Ps’ – product, place, price and promotion, is one useful way to apply to developing aspects of the program participant perspectives of their interaction with the program

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[9]. As applicable to nutrition programs, the ‘product’ is the service to be delivered, the ‘place’ is the most appropriate place for service delivery from the participants’ viewpoint, the ‘price’ relates to the constraints and barriers of the participants in accessing the program services (just as the price of a product would take into account the purchasing power constraints of the buyer), the ‘promotion’ is about creating awareness of the services, and motivation and incentives to utilize the services until the duration of the program [9]. Analysis of social dynamics and cultural aspects such as power equations, women’s status, literacy levels, gender, linguistic preferences, and environmental issues need to be considered during the development of the service utilization plan. It is possible that while developing the service utilization plan, one might need to revisit the CNA findings or consult program participants or community representatives. (b) Organizational plan – Having determined these aspects, an organizational plan that is responsive to the service utilization plan can be developed. Again taking the example of the reducing the prevalence of anemia in pregnant women program, the organizational plan will delve into questions such as the kind of personnel, their organization, skills and capacities required to perform the program functions and deliver services, e.g., enrolling pregnant women into the program, counseling them, questions about when, where, which screening tests and by whom will be undertaken to screen anemic women. What will be the protocols for iron-folate distribution? What are the follow-up mechanisms needed? Will the program be delivered at clinics or at outreach centers? Some of the key components of the organizational plan that are important to consider during planning include the organization and delivery of the program interventions and activities, the organization and management of program resources – human, physical, financial and time, policies and systems including management, administrative, financial, logistics systems, monitoring and information systems. While estimating the financial resource requirement and planning for monitoring and management information systems is discussed in subsequent sections, the salient points pertaining to the other aspects are discussed here. (i) Activity implementation plan – Planning for the delivery of program interventions and carrying out the program activities in an organized timely manner should take into account the information obtained from the service utilization plan. The terms intervention and activities are sometimes used interchangeably, but here they are used as distinct from each other. For example, nutrition education is the selected intervention in a certain program However, in order to conduct nutrition education successfully, several activities will need to be performed –

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activities not only to deliver the education session but activities that will motivate the participants to come for the sessions. Listing the key activities that need to be performed, their sequencing and frequency, the responsible person, the timing and the timeline for their being undertaken and completed are critical aspects of planning related to activities. A detailed implementation plan that shows the activities, when these will be initiated and concluded, who will be responsible for the activity is a good planning tool. A separate timeline or a PERT chart could also be useful tools to plan, manage and monitor activities as well as timelines. (ii) Physical and material resources – These include the physical infrastructure or the facilities to house the program offices, the office furniture, equipment, supplies, including computer software, required to run the program offices. On the program delivery side, it includes facilities such as the centers from which services are to be delivered, their location, furniture and equipment including equipment associated with service delivery or screening (e.g., for nutrition programs these may include weighing scales, height boards, mid-upper arm circumference tapes), the supplies, including registers and records and the supplies to be delivered to the participant (e.g., micronutrient supplements, supplemental food), communication material (e.g., videos, print material, flip charts), and the logistics and supply chain to ensure an uninterrupted supply. Planning for physical resource planning, especially the aspects that relate to the program’s interface with the participants, should take account of the information from the service utilization plan. (iii) Human resources – Human resources are the most critical of all program resources and usually forms the largest proportion of the program cost. Planning for human resources includes anticipating and planning for need for the number and type of personnel, types of expertise, skills, experience and capacities required, organization and location of personnel, associated teams and/or hierarchies, their recruitment and retention, training, performance, accountability, motivation, incentives and rewards. If the program has a role for volunteers, the specific roles for them, their recruitment and training, incentives, their motivations should be planned for separately as these are likely to be different from the regular program staff. Similarly, if the program plans to associate personnel from an existing program, its rationale and feasibility should be carefully assessed, in terms of how much can be realistically expected from them, their skill sets, and whether it potentially creates competing priorities. Personnel needs should also be thought of in terms of the

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program leadership and management functions, as well as the support functions for the program – technical support, and administrative support including financial and procurement. An organizational chart is a good tool to depict how personnel are organized into work groups or teams, the relationship of these work groups, the chains of authority and responsibilities, the reporting relationships, and so on. It also shows how the program is located within the organization as the cross support from other programs and the like can be depicted in the organization chart. (iv) Policies, protocols and systems – Integral to good implementation is the development and adoption of sound policies, systems, operations manuals that will guide program personnel and operations. Some of the key policies and systems pertain to human resources – their recruitment, remuneration and benefits, performance, training, incentives; administration, finance management and procurement; communication and information systems. It is very likely that the organization doing the planning or to implement the program already has the necessary policies and systems in place and new ones do not need to be developed for the program. However, these should be reviewed in term of the program’s need. For example, the organization’s policy might be to have all staff located at determined centralized levels. The service utilization plan demands that service providers deliver services at the community level, thereby making it impossible for some service providers to be located at centralized locations. Under circumstances such as the one arising in this example, existing policies might need to be modified or special exceptions will be required. The need to develop specific protocols and operations manuals for the program must be examined in earnest. These are necessary to ensure that the program maintains fidelity to its design and is delivered in a standardized manner as conceptualized. Assessing and testing the organizational and service utilization plan is important. Are these appropriate to not only operationalize the impact theory but relate appropriately to the actual situation and circumstances of the program and the participants it serves? Are the procedures and functions well defined and adequate for the purpose, viewed both from the perspectives of the program managers as well as the program participants? Such questions are helpful to assess the implementation plan. If the program being planned is large and complex and, especially if it is trying new approaches for implementation, it is wise to run a pilot-test for implementation at a small scale before implementing the program at full scale. The learning from the piloting should be

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used to revise or modify the implementation plan. Similarly any new material resources, protocols or operational guidelines must be pre-tested. Pre-testing can be done in several ways – having focus group reviews, testing in the community where the program will operate, seeking expert opinion and comments. Figure 36.9 shows a graphic display of the program theory – the impact and the process theory, including elements of the organizational plan and the service utilization plan, for the prevention of anemia in pregnancy example.

36.5

Estimating and securing financial resources

36.5.1 Developing budgets After having determined all the requirements of a program, the cost of each of the items has to be estimated. A budget is the tool to estimate the financial requirements of the program by translating all of the program’s activities and plans into monetary terms. Thus, a budget is like the program plan expressed in terms of money [27]. Budget formats or templates may vary by the type of budget, or the requirement of the program sponsors/ funding agencies. Budgets may be called for by line-items and cost categories, by program components or objectives, year-wise or for multiple years [27]. Regardless of the format required, in terms of developing budgets, it is useful for the planner to develop annual line item budgets for each program component. These can then be computed, transcribed and presented into the required format. A component wise budget offers the advantage of planning different scenarios and based on component priorities to trim or expand the budget as necessary. Similarly, annual budgets allow for tracking expenditures against the year’s budget. In terms of cost categories, there are at least two major categories – personnel and non-personnel. Personnel costs include salary, benefits and allowances of the staff, and consultant costs. Non-personnel costs generally include travel, equipment, supplies, rent, communication, transportation and other categories that may be specific to the program activities. A third category – indirect costs – is sometimes included by many funding agencies. Indirect costs cover a share of the cost of utilities, equipment, facilities that are shared across many programs. Different agencies have a different formula for calculating indirect costs, so this should be taken directly from the agency to be requested for funding [27]. To cost each item in the program, it is necessary to review each activity and the implementation plan against the timeline. This provides more realistic estimates since some costs are not required from the beginning of the program, and may be phased in later, or some activities may be planned only for certain duration of the program. Once all the items are outlined,

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36.9 Program Theory (Anemia in pregnancy program example).

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per unit costs should be estimated and multiplied by the number of units and number of months or years for recurring expenditures and once for one-time costs. When planning multi-year budgets, annual salary raises and cost escalation need to be factored in. The budget must also include the cost of evaluation and monitoring. Precision and specificity are important in budgeting. Thus, obtaining real estimates from the right source, e.g., from personnel department for personnel, distributors for equipment, supplies and so on contribute to developing more realistic budgets. Under-budgeting and over-budgeting should be avoided; the former may constrain program activities and the latter may lead to underspending. It is also important that costs be reasonable – this is generally an important criterion during the review of budgets by the funding agency or program sponsor. Calculating and presenting per participant cost is generally a good strategy with some justification if these are high.

36.5.2 Budget justification Budget justification or budget narrative is often required to be provided along with the budget. This explains the rationale for including the items and how they are necessary for the planned activities [27]. Because the budget is the financial summary of the program plan, it is important that there is consistency between objectives, activities, implementation plans and the budget. There should be no surprises in the budget, nor should any activities be left unbudgeted. Calculation errors can prove very costly; therefore it is prudent to have an appropriate review and clearance system in place. A plan to raise the required resources that identifies options and strategies for mobilizing resources, such as the funding agencies to contact, fund-raising events, partnerships, seeking internal resources should also be developed during the planning phase. This plan should also identify budget scale-down or trimming options, if the required resources cannot be mobilized. One of the ways of dealing with budget uncertainties is to plan budgets for two or three funding scenarios – high, medium, low – with prioritized components being retained in the low funding scenario.

36.6

Planning for program monitoring and evaluation

Result-orientation requires that program planning include the development of appropriate systems to assess and measure results. This includes two key aspects – monitoring and evaluation.

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36.6.1 Monitoring Monitoring, or to be more accurate, process monitoring, is the on-going, almost real-time activity of collecting data about the implementation of the program, its analysis, and use at different levels of the program to assess implementation and take timely corrective action when necessary [9]. A robust monitoring system that generates reliable, timely data on the right indicators serves as a critical managerial or oversight tool to ensure that during implementation, the program is delivered within the parameters established during the planning [9]. Program monitoring relates to the assessment of the organizational plan and the service utilization plan (the process theory). It provides the necessary information to alert program personnel about aspects of the organization plan or the service utilization plan that are not working as expected, and make decisions to modify or revise those aspects to make the program more effective [9]. Thus, the monitoring system forms an ongoing loop to feed into the implementation planning or re-planning necessary to make changes that might be required to improve the processes, outcomes and results, in addition to serving as a management tool to address issues of accountability. The monitoring process, ideally, is a two-way flow of information. This two-way flow requires that data collected at a particular level, in addition to being used at that level, flows upward (all of the data or at least some part of it), is collated and analyzed at designated levels to translate the data into meaningful information, and feedback on performance, specifically including aspects of follow-up or corrective actions to be undertaken flows back. In practice, many times the downward information flow, referred to as the feedback loop, is weak or at times non-existent. Often, in the absence of formalized systems for data analysis and use, data although collected and sent up is not adequately utilized. This is a huge lost opportunity to actually assess the program implementation, take corrective action to ensure that the program indeed functions to deliver the services as planned. In planning for a monitoring system, one of the first questions to be addressed is what all should be monitored? While there is no prescribed set of activities that are a must to be monitored, a general rule of the thumb is to map out critical activities and processes that relate to the expected outputs or process objectives [28] are closely associated with intervention delivery in the manner and dosage planned, and track coverage of target participants. Once the critical set of activities have been selected, the planning team must identify the set of outputs, inputs and processes that are critical to track, and select appropriate indicators or specific measures relating to these. In other words, the team should complete the results framework by working further down the results chain

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from the objectives and outcomes that were outlined in the section “setting goals and objectives”. Thereafter, one must consider how the data on these measures or indicators will be collected (e.g., the data source and quality, periodicity of its collection, the tools for data collection and recording) [14], how and where will the data flow, be processed and analyzed (e.g., when and where which set of data will be analyzed and processed to turn it into meaningful information), and finally how it will be used (e.g., data interpretation and corrective action). Developing these systems during planning will ensure that appropriate resources are allocated for monitoring and the system guides program managers and staff to effectively track implementation and take corrective action on a real-time basis to support the achievement of results. Program planners might want to consider incorporating other forms of monitoring such as participatory monitoring, community-based monitoring, social audits, community reviews. These offer great value in terms of stakeholder engagement, holding program providers accountable, self-correction, empowering communities, and building partnerships and capacity [14]. Depending on the decisions on the choice of the monitoring mechanisms selected, costs of monitoring must be budgeted for.

36.6.2 Evaluation Program evaluation is the systematic process planned to measure the program’s effect against its stated objectives; or to examine aspects of how the program was implemented in relation to what was planned; or both. Program planning and evaluation are inter-related and cyclical [9]. Evaluation planning will determine the purpose, scope, design, type of the evaluation to be conducted, and the quantum of resources required (human and financial). Evaluation provides the loop to feed learnings and insights from the program into the next planning cycle [9]. While it makes intuitive sense to give due consideration to evaluation planning and budgeting adequately for evaluation, in reality this is often not the case. Some of the reason that evaluation planning is an afterthought include competing priorities for resources (resources allocated for evaluation could mean those many resources less for implementation), lack of expertise, apprehensions in the minds of programmers and other stakeholders of evaluations, since these are often seen as judging a program’s performance, the rush to complete planning and begin implementation, and so on. With the focus on RBM and results management, several funding agencies and program sponsors now require evaluation plans as part of the proposals. It is suggested that the planning team build into the planning process time for and resources for key evaluation planning activities such developing

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the evaluation plan, the evaluation design, development of tools and their testing, and the conduct of the baseline (either prior to implementation or as soon as implementation begins). Some key aspects that should be considered by the planning team while thinking of the program’s evaluation plan include: the purpose of the evaluation (e.g., requirements of the program, needs of the different stakeholders), how the evaluation findings will be used (e.g., to improve the program, inform policy), what type of evaluation methods will be desirable (e.g., quantitative, qualitative, participatory or a mix), what kind of evaluation design to consider (e.g., pre-post, comparison against a counterfactual), the evaluation team (e.g., internal or external evaluators), the costs, and many others. It could be useful to involve a person with evaluation expertise on the team for a full consideration of these issues. Involving stakeholders in the consideration of, and decisions on these issues helps in making evaluation an integral part of planning, addressing to an extent apprehensions of ‘being evaluated’, feeding evaluation findings to be considered into future planning. Evaluation of the process theory as well as the impact theory is desirable to fully assess if a program was successful in bringing about the desired change. Impact or outcome evaluation measures the program impact. It is also important to understand how these impacts were achieved (or not achieved). For instance, if the impact evaluation determines that the program did not have the intended impact, it would be crucial to understand if indeed the program was delivered in the planned manner, the interventions delivered in the planned dosage for the planned duration, the coverage achieved. These aspects, the subject of the process evaluation, will help determine whether the effect theory was incorrect, or if implementation failure led to or contributed to the programs’ failure [9]. Program failure could have its roots either in the impact theory or in the process theory (see Fig. 36.10) [9]. Qualitative research will answer questions such as the quality of program transactions, capacity of program staff, and relevant social, institutional and governance issues. In order to enable evaluators to better understand issues, problems, what worked and so on from the perspectives of the different stakeholders qualitative methods complement quantitative evaluation techniques. A combination of quantitative and qualitative methods offers many advantages – it helps to explain, contradict or confirm findings from quantitative surveys, capture new unanticipated perspectives, enables data triangulation, and fully understand the range of factors (e.g., social, political, cultural institutional, governance) that help to explain the outcomes [29,30].

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36.10 Causes of program failure [9].

36.7

Planning for program ending or termination

All development programs have time limits dictated largely by the program funding cycle, and at the end of the cycle, the program must either end or, depending on funding availability, roll over to another funding cycle. Because program termination has consequences for the sustainability of the program impact, the program participants, it is imperative that program planners articulate an explicit strategy and plan for its withdrawal in an orderly and responsible manner. This is best done during the program design phase, or early in the life of a program, so that it allows time for proper preparation and deliberate actions over the life of the program to protect and sustain program gains and outcomes once it ends. Two key terms ‘Exit’ and ‘Graduation’ are used in the program withdrawal or ending context. ‘Exit’ refers to the withdrawal of all externally provided program resources from an entire project or program area. ‘Graduation’ refers to the withdrawal of program resources from specific program sites or activities that according to certain pre-determined criteria or benchmarks [31]. The exit strategy or graduation strategy, describes how the program intends to withdraw its resources while assuring that the outcomes achieved do not erode and that further progress towards the program goals continues. Ideally, the exit strategy sets in place a system whereby the benefits expand beyond the original beneficiaries and their communities [31]. Developing an exit strategy requires the following: Identifying approaches to be used for different program components; selecting criteria for graduation (of communities) and exit (of the program from the region); setting benchmarks for assessing progress toward meeting the criteria; establishing a time line, recognizing flexibility may be required; identifying action steps, dedicating resources; developing mechanisms for periodic review of the progress of and learnings from strategy implementation and for possible modification of the exit plan [31].

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Possible approaches for program exit include phase down, phase over and phase out. Phase down, the gradual reduction of program inputs, is the preliminary stage to both phase over and phase out. Phase over refers to the transfer of program responsibility to another entity that could either be an existing organization (community-based, civil society, NGO, governmental) or one especially formed by the program to take over its functions. This approach is appropriate when a core set of program activities will need to be continued beyond program exit. Phase out refers to the withdrawal of program inputs (service provision, other resources, technical assistance) without making explicit arrangements for the program’s continuation. This approach is generally considered when the change produced is of a selfsustaining nature, and once achieved outside inputs can be discontinued, but the impact of the program continues, e.g., behavior changes related to health, nutrition and child caring practices can become permanent without requiring continued efforts or activities, provided communities see the benefit of adopting these [31]. The choice of the most appropriate exit approach for a program will depend on the type of program activities, the program environment, the time-frame for exit, and the available human, institutional, financial and physical resources. It is important to identify the exit approach either during program planning or early in the life of the program for many reasons. If program responsibilities have to be phased over to community groups, communitybased organizations, governmental or quasi-governmental bodies, either existing ones or to be created during the life of the program, their engagement with the program early on will be critical. A realistic assessment of their capacities and systematic building up of these will need to be undertaken during the life of the program. In some cases, legal empowerment of the organization created might be needed. Another aspect to consider is the determination of the criteria to be used to trigger program exit. The criteria could be based on time limits (program exit to happen after a pre-determined time frame), achievement of program outcomes or impacts (as determined by achievement of predetermined targets), and progress toward the identified graduation process (as determined by achievement of graduation related milestones). Many program situations call for using a combination of criteria from each of the three groups [31]. Another important aspect of the exit plan, especially when a phaseover approach is adopted is the generation of resources through alternative means, such as establishing the organization or service as a business, using a revolving credit or business model, seeking community contributions if economic situation of households permit, establishing user fees or charges for services, and seeking alternative institutional (external) support from government or private donors, fund-raising events and so on.

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Conclusion

Several international initiatives over the past decade, the Millennium Declaration and the adoption of the MDGs, the Monterrey Consensus (2002), the Rome Declaration (2003), the Paris Declaration (2005) and the Managing for Development Results global initiative have underscored two points that are highly relevant for public health nutrition program planning. One is the imperative to demonstrate results, and the other is the focus on partnerships, collaboration, and harmonization of efforts to achieve development results. The discussion through the chapter situated program planning in this context and maintained a results-oriented approach with the engagement of stakeholders through its various sections. It also brought together the theory and practice of planning programs that focus on results – their measurement and achievement. The discussion of the theories, concepts, frameworks and tools for planning, built our understanding of the theoretical basis underlying results-oriented programs and their planning. The subsequent section that led us through the various steps of the planning process to develop a result-oriented program helped us meaningfully integrate results-orientation into the practice of public health nutrition program planning. The practical guidance in this section on setting objectives and targets, selecting interventions, planning for program implementation, measurement of results, the cyclical evaluationplanning linkage, and especially the use of a hypothetical nutrition program example, ‘reducing the prevalence of anemia in pregnant women’ to systematically articulate the program theory helped translate the theory of program planning into practice. Finally, planning for an exit strategy for the program during the planning or early in the life of a program, a crucial but often omitted step, highlighted that the program must deliver results within a defined time-frame and must use appropriate strategies to ensure that its impact is maintained and sustained.

Points for further thought and discussion The following points apply specifically in the context of planning of nutrition programs and relate largely to the ‘how to’ aspects of programming. The scope of the chapter did not permit a full discussion of these, but are critical for nutrition program planners to fully consider. Innovation and operational research related to these points within the program context is one specific aspect for consideration. ●

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The multi-sectoral nature of the causes of nutrition problems and the complexity of applying solutions that lie across many sectors, ministries or departments. Arising out of the above referred issue, and of great significance to

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program planning, is the related question of convergence between the actions of programs that lie across various sectors in a manner that the problem of nutrition is addressed in a holistic manner. The role of social power equations, particularly gender and women’s empowerment and comprehensively integrating these issues with technical solutions to address nutrition Strategies and approaches to effectively address the challenging task of behaviour change at scale. The intervention dosage for nutrition education or counseling - aspects such as length and duration of each session, the total number of sessions, especially from the perspective of retaining the interest and engagement of the participants. Conditional cash transfer programs to improve nutrition.

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Logic model development guide, 2004. W. K. Kellogg Foundation website. Available at http://www.wkkf.org/ World Bank, The Logframe Handbook: A Logical Framework Approach to Project Cycle Management. Available at http://www.wds.worldbank.org/external/default/ WDSContentServer/WDSP/IB/2005/06/07/000160016_20050607122225/ Rendered/PDF/31240b0LFhandbook.pdf (Accessed on December 19, 2009). Department for International Development UK, Tools for development: a handbook for those engaged in development, 2003. DFID website. Available at http://www.dfid.gov.uk/Documents/publications/toolsfordevelopment.pdf (Accessed on December 12, 2009). Canadian International Development Agency, RBM Handbook on Developing Results chain. Available at http://www.acdi-cida.gc.ca/acdi-cida/ACDICIDA.nsf/eng/ANN-923135230-NYD. (Accessed on December 19, 2009). USAID Center for Development Information and Evaluation, TIPS 2000, Number 13: Building a Results Framework. Available at http://pdf.usaid.gov/ pdf_docs/PNACA947.pdf (Accessed on December 13, 2009). World Bank, Resources for Staff – Results Framework. Available at the World Bank’s intranet network. Accessed January 6, 2010. Managing for Development Results, Emerging Good Practice in MfDR, Source Book, 3rd Edition, 2008. Available at http://www.mfdr.org/Sourcebook/ 3rdEdition/SourceBook3FINAL.pdf (Accessed on December 19, 2009). Department for International Development UK, The neglected crisis of undernutrition: evidence for action, Available at http://www.dfid.gov.uk/Documents/ publications/nutrition-evidence-paper.pdf. Accessed 28 December 2009 SHETTY P , (ed). Nutrition through the life cycle, Surrey, UK: Leatherhead Publishing and Cambridge, UK: Royal Society of Chemistry, 2002. NNAKWE NR . Community nutrition: planning health promotion and disease prevention, Sudbury, Massachusetts, USA: Jones and Bartlett Publishers, 2009 PEOPLES - SHEPS MD , BYARS E , ROGERS MM , FINERTY EJ , FAREL A . Setting Objectives, School of Public Health, University of North Carolina at Chapel Hill, revised 2001.http://www.shepscenter.unc.edu/data/peoples/setting.pdf (Accessed on December 12, 2009). Public Health Foundation. Setting Target Levels for Objectives. Available at http://www.phf.org/pmqi/HPtools/state/DE_setting_targets_for_objectives.pdf (Accessed on January 5, 2010). PEOPLES-SHEPS M. Development and Selection of Interventions D. School of Public Health, University of North Carolina at Chapel Hill, revised 2001. Available at http://www.shepscenter.unc.edu/data/peoples/development.pdf. (Accessed on December 12, 2009). World Bank, Repositioning Nutrition as Central to Development: A Strategy for Large Scale Action. Washington DC, USA, The World Bank, 2006. OLANDER C . Nutrition education and the role of dosage, Food and nutrition service, USDA website. Available at http://www.fns.usda.gov/ORA/menu/ Published/NutritionEducation/Files/LitReview_Dosage.pdf (Accessed on January 9, 2010). PEOPLES -SHEPS M, FOSHEE V , BENDER D . Programming and Implementation, School of Public Health, University of North Carolina at Chapel Hill, revised 2001 http://www.shepscenter.unc.edu/data/peoples/programming.pdf (Accessed on December 12, 2009). PEOPLES - SHEPS MD , ROGERS MM , FINERTY EJ . Evaluation: Monitoring Progress

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Towards Achievement of Objectives, School of Public Health, University of North Carolina at Chapel Hill, revised 2001 http://www.shepscenter.unc.edu/ data/peoples/evaluation.pdf (Accessed on December 12, 2009). 29. ROGERS BL , MACIAS K , JICK TD (1979). Mixing qualitative and quantitative methods: Triangulation in action. Administrative Science Quarterly 24 (4): 602–661. 30. GREENE JC, CARACELLI VJ, and GRAHAM WF (1989). Towards a conceptual framework for mixed-method evaluation design. Educational Evaluation and Policy Analysis 11 (3): 225–274. 31. ROGERS BL, MACIAS KE. Program graduation and strategies: a focus on Title II food aid development programs, Washington DC, USA, Food and Nutrition Technical Assistance project, Academy for Educational Development, 2004.

37 Monitoring and evaluation of public health nutrition programmes Jerard M Selvam and Sheila C. Vir

Jerard M Selvam, MD, is Professor and Head of the Department of Epidemiology at the Tamil Nadu Dr. MGR Medical University, Chennai. The author is postgraduate in Community Medicine from Madras Medical College in 1998. He has also completed a Fellowship programme on ‘Public Health Field Leadership’ offered by the Public Health Management Institute, Hyderabad in collaboration with CDC, USA. Selvam has served as Deputy Director in the World Bank supported Tamil Nadu Health Systems Project. Sheila C Vir, MSc, PhD, is a senior nutrition consultant and Director of Public Health Nutrition and Development Centre, New Delhi. Following MSc (Food and Nutrition) from University of Delhi, Dr Vir was awarded PhD by the Queen's University of Belfast, United Kingdom. Dr. Vir, a past secretary of the Nutrition Society of India, is a recipient of the fellowship of the Department of Health and Social Services, UK, and Commonwealth Van den Bergh Nutrition Award. Dr Vir worked briefly with the Aga Khan Foundation (India) and later with UNICEF. As a Nutrition Programme Officer with UNICEF for twenty years, Dr. Vir provided strategic and technical leadership for policy formulation and implementation of nutrition programmes in India.

37.1

Introduction to Monitoring and Evaluation (M & E)

Monitoring and Evaluation (M&E) of development activities, such as public health nutrition, provides development managers, civil society and government officials with information for improving service delivery, learning from past experiences, formulating future strategy and plan as well as in providing information for allocating resources and in demonstrating result with reference to accountability to key stakeholders [1]. Monitoring and evaluation are two distinct sets of organizational activities, related but not identical [2]. M & E is an essential management tool to assist the project or the implementers of the programme to assess

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the progress that is being made against the defined objectives as well as to analyse the constraints and positive attributes for helping in making adjustments for ensuring efficient smooth progress and desirable impact. M & E therefore assist us to know when plans are working and when circumstances have changed. Plans are essential but they are not set in concrete or in a totally fixed mode. If they are not working, or if the circumstances change, then plans need to change too. It is aptly said that “Getting something wrong is not a crime. Failing to learn from past mistakes because you are not monitoring and evaluating is …”. Both monitoring and evaluation are geared towards learning from what one is doing and how one is doing it. Both focus on efficiency, effectiveness and impact (Box 37.1). Box 37.1 Efficiency : assesses whether the input (in terms of money, time, staff, equipment etc) is appropriate in terms of the output. This is an important element of project prior to considering replicability and going to scale. Effectiveness : measures the extent to which the development program or project achieves the set specific objectives. Impact : assesses whether or not the project/program made a difference to the problem situation that was being addressed.

The cycle of monitoring and evaluation is presented in Figure 37.1. It is evident that monitoring and evaluation is best done when there has been proper planning against which to assess progress and achievements. Monitoring and Evaluation system (M & E) should be part of a planning process and an integral component in the implementation plan. Inclusion of monitoring and evaluation in the programme plan is often diluted at various levels due to reasons such as lack of appreciation of its significance, fear of being found at fault, lack of transparency and accountability by programme implementers, lack of knowledge and skills, resistance to change by entire programme team, fear of piracy by external evaluators etc [1]. It is therefore imperative that the stakeholders at different levels in the implementation of any public health or public health nutrition programme understand the significance and principles of M & E and ensure inclusion of M & E component in the stage of programme designing. This chapter focuses essentially on the significance, purpose, principles and design of M & E system for public health nutrition programs.

37.2

Monitoring

Monitoring is the process of continuous and periodic surveillance of the physical implementation of a programme. It pertains to a systematic collection and analysis of information as a project progresses and involves.

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37.1 Cycle of Monitoring and Evaluation [2].

It is essentially an organized and continuous process of following and keeping track of project/program to ensure that it is proceeding as per the plan and to modify it by making corrective actions when deviations occur. Monitoring is an internal function of any project or organization. Monitoring therefore envisages comparison of what is being achieved with what is intended to be achieved [3]. Monitoring is an invaluable tool for effective management and is closely related with programme implementation design (Figure 37.2). Monitoring involves establishing indicators of efficiency, effectiveness and impact, setting up systems to collect information relating to these indicators, collecting and recording the information including documentation of the project activities, analyzing the information and using the information to notify day-to-day management [2]. Monitoring is vital for the following reasons [2]: ● ●

● ● ● ●

Ascertains that implementation is proceeding as planned; Facilitates one to reflect on where one is going and how one is moving towards the objectives/goals; Helps to identify problems and their causes; Suggests possible solutions to problems; Raises questions about assumptions and strategy; Provides with information and insight and encourages to act.

Monitoring is not an exclusive function of the programme implementers. Beneficiaries such as community plays a critical role in monitoring their own health services (Box 37.2).

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37.2 Monitoring and Evaluation – integral component of a program.

Box 37.2 Community-based monitoring A new approach introduced in recent years is ‘community-based monitoring’ of health services. This is one of the key strategies adopted by the National Rural Health Mission (NRHM) in India to ensure that the services reach those for whom they are meant, especially for those residing in rural areas, the poor, women and children. Community monitoring, an important aspect of promoting community led action in the field of health, is executed through the creation of ‘Monitoring and Planning Committees’ at Primary Health Centre (PHC), Block, District and State levels. The adoption of a comprehensive framework for community-based monitoring and planning at various levels places people at the centre of the process of regularly assessing whether the health needs and rights of the community are being fulfilled. Community monitoring reviews the progress to ensure that the work is moving towards the decided purpose, and the purpose has not shifted, nor has the work got derailed in any way. It helps to identify obstacles in the work so that appropriate timely changes can be made to cross the obstacles [5].

The ultimate purpose of monitoring is to see if the programme is heading in the right direction within the defined time frame and to assess the factors that are contributing to the progress or hindering implementation process as well as the expected outputs. Monitoring information is used primarily for management decisions. However, information needs to be verified firsthand by raising suitable questions such as the following: ●

●

Whether the problem has been identified correctly and whether there has been a change in the problem? Are the interventions strategies appropriate for the defined target population and set objectives?

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Whether the indicators chosen are suitable? How efficiently the resources have been utilized? What are the strengths and weaknesses of the programmes? What updates need to be provided to the stakeholders? What can be further improved in the programme?

Monitoring therefore helps in identifying and documenting critical milestones, identifying new issues and/or unforeseen circumstances that may be obstacles and identifying necessary corrective measures such as strategy modifications and re-enforcement of positive aspects of the programme. The exercise entails identifying differences between knowledge and practice in order to take corrective actions. It is also equally important to verify whether resources are being used effectively (including cost effectiveness) to meet the set objectives [3]. Effective monitoring also contributes significantly in strengthening relationships amongst collaborators (donors, implementers and beneficiaries) and serves as a motivation to implementers and beneficiaries [1].

37.2.1 Designing monitoring system – logical framework approach Monitoring system design should answer a range of questions such as are the program inputs and activities transferred into outputs that generate desired results. For designing a monitoring system for a public health program, it is important to take a formative viewpoint and establish a system that will provide useful information on an ongoing basis so as to improve what is being done and the process of how it is being done. The stakeholders involved in the process of programme designing therefore need to be guided to undertake the following tasks which are based on using the logical framework approach. ●

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Draw a logical framework (logframe) – Logframe helps to strengthen project design, implementation and evaluation. Generate a list of indicators for each of the following three aspects – efficiency, effectiveness and impact. Set up systems to collect information relating to these indicators and mode of collection of information. Examine information already collected/available to the project team or the organization. Decide on method of creating database computerized or manual. Storage & analysis of data and reporting (including format to be used). Timely feedback on information to facilitate day to day management.

Developing a logical framework is of paramount importance in conceptualizing a programme and facilitating in designing a comprehensive monitoring system. The ‘Logical Framework’ (logframe) is a tool to help

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in clarifying objectives of any project, program or policy as well as project activities, including implementation, monitoring and evaluation activities. Logical Framework Approach (LFA) helps to clearly state (a) what is being aimed to achieve and how it will be achieved; (b) how will you assess whether you are achieving the set objectives and the monitoring mechanism envisaged; (c) proactively analyse and present assumption and condition that are critical for success but are outside the direct control of the project/ program. Such an analysis includes assessment of risks for the project if the assumption fails or change. Logframe helps to identify most relevant indicators for measuring attainment of project outputs and objectives. Logframe is also an analytic tool that has the power to communicate a complex project clearly and understandably on a single sheet of paper. The logframe is entirely “objective-driven” since any action under a project should be aimed at achieving its objectives. It links project goals and objectives with project components and their respective inputs, processes, activities, outputs, outcomes and impact. The framework leads to identification of the performance indicators at each stage in this chain. In addition, theory-based approach is also used which has similarities to logframe approach but allows a much more in-depth understanding of a programme or activity. This approach does not assume a simple linear cause and effect relationship [6]. The approach maps out determining or casual factors that are viewed as important for the success of the program/ project as well as how these factors interact. Using this approach, design of complex activities is mapped. This approach allows identification of critical success factors and assists in addressing unintended effects of the programme. Early feedback facilitates in prioritizing which issues to investigate in greater depth and what monitoring and evaluation techniques needs to be focused on. The disadvantage is that the approach can easily become rather complex if the scale of activities is large. Logframe is developed by defining the goal and determining the purposes, outputs and the activities needed. It is a participatory planning tool whose effectiveness depends on how well it incorporates the full range of views of intended beneficiaries and others who have a stake in the project design [6]. The terms used in a logical framework are presented in Table 37.1. (a) The advantages and disadvantages of using logical framework are presented below [6]: Advantages: ●

Helps to clarify objectives of any project, program, or policy and aids in the identifications of the expected causal links or the program logic in the programme chain viz. inputs, processes, outputs (including coverage or reach’ across beneficiary groups), outcomes and impact.

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Summarizes design of complex activities. Leads to identification of performance indicators at each stage in this chain as well as risks which might impede the attainment of the stated objectives. Improves quality of project and program designs by clearly stating the objective as well as the performance indicators and assessing the possible risks.

Table 37.1 Terms used in logical framework [7] Goal

Goal is the broader objectives or aims to which project will contribute. Objectives are statement of intentions. Objectives are derived from goals and should be SMART (Specific, Measurable, Attainable, Relevant, Time-bound)

Outcome

Describes the desired impact of the project changes in behaviour/ practices which is a result of programme activities. Right quality and quantity of outputs will result in producing desirable outcome.

Output

These are the project deliverables for meeting the purpose, i.e. all the goods and services delivered to the target population by the programme. The quantity and quality of output is important. Programme inputs have to be transformed into outputs.

Activities

For producing each output, a cluster of 5–10 activities may be required. The activities together form the set of actions planned for the project. Gantt chart is helpful tool for this.

Performance indicators

Describes how well the programme is achieving its objectives and it defines the quality standards of projects along with details.

Assumptions/risks

External conditions, situations, factors which play a role in influencing success of project/program. The achievement of aims depends on whether or not assumptions hold true and the risks do not materialize. The assumptions and risks are thus external conditions or the external logic that are outside the control of the programme.

● ●

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Engages partners in clearly stating the objectives and designing activities. Serves as a useful tool to review the progress during implementation and take corrective action. Assists the preparation of detailed operational plans. Provides objective basis for activity review, monitoring and evaluation. Ensures that decision makers raise fundamental questions and proactively identify and analyse the assumptions and risks. Engages stakeholders in the planning and monitoring process.

It serves as an effective management tool, when used dynamically, to guide in the implementation, monitoring and evaluation tasks. Disadvantages of logical framework (logframe): ● Restrains creativity and innovation, if rigidly managed. ● Risk of using the framework as a static tool that does not reflect changing conditions.

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(b) Development of Logframe Matrix Logframe Matrix is a participatory planning, monitoring and evaluation tool. The effectiveness and potential of the tool depends on the degree to which it incorporates the full range of views of intended beneficiaries and others who have a stake in the programme design [7, 8]. Developing a logframe aims at defining the means and ends as well as clearly stating the linkages between each level of aims. The better the means and end linkages between each level of aims, the better the programme design [8]. A logframe therefore presents purpose, activities and output of the project or the programme (Table 37.2). The following steps are involved in development of logframe. ● Identifying outputs and activities. ● Verifying the vertical logic. ● Identifying the risks and assumptions. ● Verifying the logic of the risks and assumptions. ● Determining the indicators of achievement and means of verification. Table 37.2 Logical Framework — a matrix of 4 columns and 16 boxes [7] Project summary (Objective hierarchy)

Performance indicators

Monitoring mechanism (Means of verification)

Assumptions/risks

Goal (Overall objectives, development objectives)

Indicators to goal achievement mechanism

Source of data for goal level performance

Risk regarding strategic impact

Purpose (project development objectives)

Impact indicators

Source of data for purpose level performance

Risk purpose to goal

Outputs (results) The products, services or results that must be delivered by the project for attaining objectives and purpose

Project output indicators

Source of data for output level performance

Risk output to purpose design effectiveness

Activities Actions taken by the project that are required for delivering of inputs

Input/resource budget by activities; monetary, physical, human resources for activities

Source of data for activity level performance indicators

Risk activities to output risk regarding implementation and effectiveness

This matrix cross-references seven key areas of the project to ensure that the key questions are asked. ●

Goal – what results are expected?

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Purpose – why is the programme being undertaken? ● Outputs – what are the deliverables? ● Activities – what will be done for delivering the outputs? ● Indicators of achievement – how will it be assessed whether the project has been successful? ● Means of verification – how will the reported results be checked? ● Risks and assumptions – what assumptions underlie the structure of the project and what is the risk that will prevail? For example, a framework for monitoring a vitamin A fortification program and a framework for an adolescent anemia control program are presented in Tables 37.3 and 37.4. The logical framework tables cover activity in terms of provision of service, utilization, coverage and impact. It also raises the questions related to each activity, identifies the key indicators, outcomes to be measured and means of verification/data collection methods. ●

Table 37.3 A framework for monitoring a vitamin A fortification program [9] Activity

Questions

Examples of key indicators

Data collection methods

Provision

Is the fortified food available in sufficient quantity? Are the distribution/ sale outlets accessible to the population? Is the quality of the food adequate?

Amount of fortified food produced (Crude and per Capita) Number and location of sales / distribution outlets Vitamin A content of fortified food

Food industry statistics Production records and quality control reports Commercial census Government statistics Food analysis using quantitative or qualitative assay methods

Utilisation Is the fortified food being distributed? Purchased?

Sales and distribution of fortified food (crude and per capita)

Food industry statistics Market survey

Coverage What proportion of the target population is eating fortified foods?

Proportion of all children under 5 or post partum women regularly consuming sufficient amounts of fortified food

Household surveys

Impact

Time trends in serum retinol levels Time trends In deaths and hospital admissions

Household surveys Routine reporting data (if available) or special surveys

Did health and nutrition Improve?

The logical framework for Adolescent Anemia Control Programme presented below in two parts of Table 37.4. First section specifies goal, strategic results, including indicators and means of verification as well outcomes. In the second section of the table, for a selected outcome, details of outputs, inputs, indicators and means of verification are presented. (Table 37.4)

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Table 37.4a Logical framework for Adolescent Anemia Control Programme in district A Goal Strategic results

The nutrition and health status of adolescent girls (10–19 years old) is improved through preventive and promotive interventions for the control of anemia in district A. The prevalence of anemia noted in 2010 is reduced by at least 30% in district A by 2012. Specifically: ● The coverage of the adolescent anemia control programme – comprising IFA supplementation (weekly), deworming (bi-annual), and IEC/BCC (through the project period) – is expanded to one million adolescent girls using school- and community-based interventions as delivery channels. ● The prevalence of anemia among school-going adolescent girls is reduced by at least 40% by 2012 through the delivery of IFA supplementation weekly through school system), deworming (bi-annual), and IEC/BCC (regular). ● The prevalence of anemia among out-of-school adolescent girls is reduced by at least 20% by 2012 through the delivery of IFA supplementation (weekly), deworming (bi-annual) and IEC/BCC (regular) using community-based interventions as the delivery channel. Indicators

Means of verification

•

Middle and secondary school data

• •

•

Percent adolescent girls covered by the school-based component of the adolescent anemia control program. Percent adolescent girls covered by the community-based component of the adolescent anemia control program. Prevalence of anemia among adolescent girls benefiting from the school-based component of the adolescent anemia control programme Prevalence of anemia among adolescent girls benefiting from the community-based component of the adolescent anemia control program.

Secondary census data and survey report-the ongoing nutrition programme Baseline and final survey

Baseline and final survey

Expected outcomes (i) Implementation of district-level advocacy, programme implementation, undertaken in school and community and knowledge management framework established. (ii) The capacity of school-based programmes to provide services or the control of anemia among school-going adolescent girls is strengthened (iii) The capacity of community-based programmes to provide services for the control of anemia among out-of-school adolescent girls is strengthened. For each of these outcomes, following details need to be worked out – outputs, inputs, indicators and means of verification and important assumption and risks. The details of outcome (i) are presented below as an example (Table 37.4b).

(i) Establishing a consultation process to facilitate development of a Plan of Action (POA).

Output 3 (ii) Designing of monitoring A knowledge management framework and framework of the state undertake process government to monitor and /impact assessments. evaluate the implementation Timely dissemination of and effectiveness of the findings for timely action. adolescent anemia control programme.

Output 2 A program strategy of the district authority for control of anemia in adolescent girls through school- and community-based interventions.

Output 1 Sensitizing key An advocacy strategy for the stakeholders’ on control of anemia in importance of anemia adolescent girls through control program using school and communityexisting evidence. based interventions. Key stakeholders: ● Policy-decision makers, program planners, mangers of sectoral depts. (Education, /Social Welfare, Health/Rural Development (community-based organization), Tribal). ● Professional and academic bodies

Outputs under outcome (i) Inputs/Activities

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Number of blocks which have completed assessments. Prevalence of Anemia (block-wise). % of girls who have consumed at least 40 tablets in a year (blockwise).

Number of blocks (smallest administrative units) with POA developed. Number of blocks which have launched the programme

Number of key stakeholders sensitized on the importance of anemia control program using existing evidence. Issue of guidelines by the government authority for initiating/ accelerating implementation.

Indicators

District level coordinating committee reviews

Reports (baseline/monitoring/impact assessments) Field visits.

District and block POA in place Field visit/joint reviews/minutes of meetings/ monthly monitoring reports.

Minutes of meetings, reports / documents / guidelines

Means of verification Election scheduled in three months time could result in education department and teachers being occupied with election duties

Assumptions / Risks

Table 37.4b Outcome (i) – Implementation of district-level advocacy, programme implementation, and knowledge management frameworks

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(c) Identification and selection of appropriate monitoring/evaluation indicators – using the logical framework tool In monitoring and evaluation, indicators are measurable or tangible signs to show what has been done or achieved. Indicators need to be appropriately selected in order to measure programme inputs, outcomes, process and impact. The logical framework tool helps to focus on appropriate indicators and through such selected indicators, the response to following questions can be obtained [2]: ● ● ● ●

Who? How many? How often? How much?

Identification of appropriate indicators for monitoring is critical as it has the advantage of assisting in identifying, developing and taking timely corrections at the lowest to the highest level of implementation so that the goals of the intervention programmes are achieved. The critical indicators have to be examined at the peripheral level so that timely corrective decisions are taken and implemented without any delay or waiting for assessment by top level or external agencies. Monitoring indicators should therefore help in making quick decisions in a de-centralized manner at the lowest implementation level. Selection of indicators for evaluation follows the same principles. Identifying and selecting appropriate indicators for evaluation are expected to serve as “trigger points” for action as they will provide information that will be useful for mid-course corrections [1]. (i) Characteristics of indicators Characteristics required of monitoring/evaluation indicators are presented in Table 37.5. (ii) Types of indicators Primarily there are two types of indicators: (a) Process, and (b) Impact indicators. (a) Process indicators – these indicators monitor the implementation of actions and activities of the programme to see whether or not the intervention is functioning effectively. Examples for process indicators are presented below in Table 37.6. (b) Impact indicators – these measure outcomes and impacts of a programme or a project. One of the major constraint often encountered is regarding lags between project implementation and impact or, in other words between the time of impact and the time it is feasible to collect data

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Table 37.5 Characteristics required of a Monitoring and Evaluation indicators [1] Required characteristic

Description

Simple

Selecting a simple indicator is not always an easy task. Each term of an indicator should be clearly and precisely defined. It may require finding a balance between the ideal (which may be complex and/or impossible to collect) and the practical Both quantitative and qualitative indicators should be measurable. Some indicators are directly measurable, e.g., height and weight, while other indicators need to be defined. A valid indicator accurately reflects the situation it is intended to measure. A valid indicator in one area may be less so in another, therefore it may be inappropriate to transfer indicators from region to region or programme to programme. A reliable indicator will produce the same results every time it is measured, regardless of who collects the data. Indicators to be useful, must show variation between subjects and over time. Indicator should reflect changes for the specific situation concerned. Scope of obtaining the required data is feasible/practical. Indicator should contribute to the understanding of the phenomenon of interest. Indicators must be sensitive to changes in the situation concerned over a period of time. Indicator selected should have acceptability and it must be recognised that acceptability may vary among different populations. Some measures such as dietary intake are more widely accepted as compared to drawing venous blood. Costs associate with the use of certain indicator.

Measurable Valid

Reliable Variable Specific Feasible Relevant Sensitive Acceptability

Costs

relating to impact. Examples of impact indicators recommended for Iodine Deficiency Disorders (IDD) control programme is presented in Table 37.7. (iii) Clustering and selection of core indicators Clustering of indicators is essential to arrive at adequate and practical set of indicators by adhering to the following steps: ●

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Identify a limited number of indicators that adequately measure the outputs. Identify the data sources available and the type of data collection needed for each indicator. Construct a matrix listing the indicators, identifying their importance for programme monitoring and evaluation (high/low), the ease of obtaining data on the indicator (easy/feasible but requires effort/ difficult), and the cost of data collection. Prioritize indicators by importance, ease of obtaining data and cost. Based on the above, select a set of indicators.

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Table 37.6 Examples for process indicators in a vitamin A deficiency control programme [10] Supplement distribution programme ●

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Percent coverage of at risk population by programme (e.g. capsules supplement) received and delivered per year per target population. Percent of the health centres/institutions etc. with sufficient supplement for coverage of the target population(s) for a 4–6 month distribution cycle.

Fortification programme ● Number of vitamin A fortified foods available in selected markets. ● Percentage of fortified foods available in market that meet specified levels of vitamin A. ● Percentage of households containing a specific vitamin A fortified food selected as suitable for consumption by target groups. ● Percentage of target group consuming a specific fortified food. Nutrition education/social marketing programs ● Number of contacts for message delivery per week. ● Knowledge, attitude and practice (KAP) indicators of messages delivered and understood at the household level. ● Percentage awareness of consequences of vitamin A deficiency (VAD) and local vitamin A containing foods. ● Percentage of under 24-month-old infants consuming the recommended dietary intake (RDI) of vitamin A from foods or supplements. ● Feeding patterns for vitamin A rich foods, e.g., percentage of children under 3 years of age eating vitamin A rich foods 3 times a week. Horticulture programme ● Percentage of homes in a district with a garden having pro-vitamin A containing foods. ● Percentage of schools in a district with gardens having pro-vitamin A containing foods. Table 37.7 Examples of impact indicators in an Iodine Deficiency Disorders (IDD) control programme [11] ●

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Median urinary iodine concentration (µg/l) among school-age children and pregnant women. Goitre rate assessed by palpation (%) among school-age children. Goitre rate assessed by ultrasound (%) among school-age children. TSH (mIU/l) levels among newborns Tg (µg/l) levels among school-age children. ●

●

Group the selected indicators by source of data to determine the set of sources which can provide data on clusters of indicators. Make a final selection of a cluster of indicators and decide on a data collection plan in light of available logistical, human and financial resources and time.

A practical example is shown in Table 37.8. The core and optional indicators chosen by a working group on “Infant and Young Child Feeding” are presented in Table 37.8. The indicators that were finally agreed upon and selected were for only two critical age groups (infants, 6–23 months).

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The selection of indicators was based on evidence of their positive association with child survival and/or nutrient intakes as well as feasibility of measurements. Details of these indicators are presented in Tables 37.9 and 37.10 [12]. Table 37.8 Core and optional indicators for infant and young child feeding practices [12] Core indicator ● ●

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Early initiation of breastfeeding Exclusive breastfeeding under 6 months Continued breastfeeding at one year Introduction of solid, semi-solid or soft foods Minimum dietary diversity Minimum meal frequency Minimum acceptable diet Consumption of iron-rich or ironfortified foods

Optional indicator ● ● ● ●

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Children ever breastfed Continued breastfeeding at 2 years Age-appropriate breastfeeding Predominant breastfeeding under 6 months Duration of breastfeeding Bottle feeding Milk feeding frequency for nonbreastfed children

Table 37.9 Indicators to assess breastfeeding practices in infants [12] Core indicator selected ●

Exclusive breast feeding under 6 months

Measurement Infants 0–5 months of age who received only breast milk during the previous day Total Infants 0–5 months age

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Early initiation of breast feeding

Children born in the last 24 months who were put to the breast within one hour of birth Total Children born in the last 24 months

37.3

Evaluation of programmes

Programme evaluation is a process of data collection designed to assess the effectiveness of the programme in attaining its originally stated objectives. Additionally evaluation also assesses and determines the extent to which the observed changes are due to the programme activities themselves and not from inputs and influences outside. Evaluation is the comparison of actual project impacts against the strategic plans that has been agreed to [2]. ‘Evaluation is a systematic investigation of the worth or merit of an object’ [13]. As per WHO, it measures the degree to which objectives and targets are fulfilled and the quality of the results obtained [13, 14]. Evaluation therefore looks at what one has set out to do, what has been accomplished and how it has been accomplished.

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Table 37.10 Indicators to assess feeding practices in children 6–23 months of age [13] Core indicator selected ●

Minimum acceptable diet

Measurement Breastfed children 6–23 months of age who had at least the minimum dietary diversity and the minimum meal frequency during the previous day Total Breastfed children 6–23 months age and Non-breastfed children 6–23 months of age who received at least 2 milk feedings and had at least the minimum dietary diversity not including milk feeds and the minimum meal frequency during the previous day Total Non-breastfed children 6–23 months of age

●

Consumption of ironrich or iron-fortified foods

Children 6–23 months of age who received an iron-rich food or a food that was specially designed for infants and young children and was fortified with iron, or a food that was fortified in the home with a product that included iron during the previous day Children 6–23 months age

Evaluation is a systematic process to assess efficiency, effectiveness and impact of the programme achievements based on the set objectives. There is clear distinction between effectiveness and efficiency of any intervention in public health programmes. Whilst effectiveness refers to the results obtained under real-world circumstances, efficiency refers to the results obtained relative to the resources expended [15]. In an overview of the effectiveness and efficiency of HIV prevention programs by D R Holtgrave et al, ‘effectiveness’ was considered in terms of averting or reducing HIV-related risk behaviours or favourably modifying their determinants and ‘efficiency’ of the intervention was viewed as implementing the intervention using a strategy at a minimal, cost-effective or cost-beneficial level of resource investment [16]. Evaluation should be developed during the design phase of the programme. The purpose of evaluation is to assess the achievement of the stated objectives of a programme, its adequacy, its efficiency and its acceptance by all parties involved [1]. The major purpose of an evaluation will depend on the type of approach and the typical focus questions arising out of it. This is highlighted in Table 37.11. An evaluation helps to answer the following questions: ● ● ● ● ● ●

Is the intervention correct or appropriate? Are additional interventions necessary to achieve the objectives? Is the intervention being implemented as planned? Is the strategy appropriate? Is the programme addressing the right problems? Are the outcomes and objectives being met?

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Table 37.11 Purpose and approaches to evaluation [17] Approach

Major purpose

Typical focus questions

Likely methodology

Goal-based

Assessing achievement of goals and objectives.

Were the goals achieved? Efficiently? Were they the right goals? Is the project effective? Should it continue?

Comparing baseline and progress data; finding ways to measure indicators

Decision-making Providing information

How might it be modified? Goal-free

Assessing the full range of project effects, intended and unintended

Expert judgment Use of expertise

● ●

What are all the outcomes? What value do they have?

How does an outside professional rate this project?

Assessing range of options related to the project context, inputs, process, and product. Establishing some kind of decision-making consensus. Independent determination of needs and standards to judge project’s worth. Qualitative and quantitative techniques to uncover any possible results. Critical review based on experience, informal surveying, and subjective insights.

Is the system in place? What are the lessons learned?

The evaluation process is important since it helps in assessing the work of the programme and also provides information that helps in redesigning the programme and increasing effectiveness of the programme management. Additionally, evaluation measures the productivity of available resources in achieving a set of clearly defined objectives and also the output or cost effectiveness. It checks whether the programme was implemented according to the detailed plan/design and verifies the problem thereby providing an opportunity for problem solving such as strategy modification. Evaluation is significant for other reasons such as maximizing the utilization of resources including re-allocation of priorities and resources on the basis of changing needs, identification of the strengths and weaknesses of the programme, providing information for planning and re-planning, providing learning opportunities and the right feedback to the various stakeholders. Thus it forms a basis for maintaining and/or improving the existing strategy and measures the effectiveness of the programme [1].

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37.3.1 Phases of conducting evaluation The following are the five phases of conducting evaluation [1]: (i) Planning the evaluation ● ●

● ●

●

Determine the purpose and type of the evaluation Review existing information in programme documents including monitoring information Describe the programme Develop/refine conceptual framework, assess strengths and limitations of the programme Put together an evaluation team including stakeholders

(ii) Selecting appropriate evaluation methods ● ● ● ● ●

Identify evaluation goals and objectives Formulate evaluation questions and sub-questions Decide on the appropriate evaluation design Develop an evaluation schedule Develop a budget for the evaluation.

(iii) Collecting and analyzing information ● ● ● ● ●

Develop data collection instruments. Pre-test data collection instruments. Undertake data collection activities. Analyze data. Interpret the data.

(iv) Report findings ● ● ●

● ● ●

Write the evaluation report. Decide on the method of sharing the evaluation results. Decide on communication strategies in terms of the method to be adopted for presentation to different stakeholders involved in the programme. Share the draft report with stakeholders and revise as needed. Disseminate evaluation report. Meet with project stakeholders to discuss and follow-up on findings once the findings have been accepted

(v) Implementing evaluation recommendations ●

Develop a new/revised implementation plan in partnership with stakeholders

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Monitor the implementation of evaluation recommendations and report regularly on the implementation progress Plan the next evaluation

37.3.2 Types of evaluation Evaluation of programs is primarily of two types: (i) formative evaluation; and (ii) impact or summative evaluation (a) Formative evaluation Formative evaluation takes place during the life of a project or organization while summative evaluation is drawing lessons from a completed project or an organization that is no longer functioning. Evaluation theorist, Bob Stakes, has interestingly compared these two types of evaluation by the following description [13] – “When the cook tastes the soup, that’s formative; When the guests taste the soup, that’s summative.” The purpose of formative evaluation is to assess initial and ongoing project activities. It has two components namely ● ●

process or implementation evaluation progress evaluation

Process evaluation begins during programme development and continuous throughout the life of the programme. Process evaluation addresses operational and implementation issues. It helps to assess whether the programme and its components are being conducted or implemented or operating as planned. It may occur once or several times during the life of the programme [13]. Process evaluations answer questions about how well a program is meeting administrative and procedural goals [18]. Results of process evaluation are presented in terms of output measures e.g. changes in users of services such as antenatal care, growth monitoring, and coverage of beneficiaries. Process evaluation provides information on inputs and how the inputs were transformed into outputs intended to contribute to the programme outcome. The objective of progress evaluation is to assess progress in meeting the goals of the programme and the project. It involves collecting information to learn whether or not the benchmarks were met. The progress can be conveniently evaluated in the mid term when it is called mid-term evaluation. The mid-term evaluation, an assessment of the effectiveness and efficiency of a programme when it is half way through the planned period, gives an idea of whether the set objectives will be met within the project period [13].

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(b) Impact and summative evaluation The purpose of impact and summative evaluation is to assess a mature project’s success or failure in reaching its stated goals. Impact evaluation gauges the extent to which the intervention has caused change in the desired direction at any given time. Impact evaluation is done at a set time, based on the requirements of programme or plan for review and re-plan. The evaluation reveals the outcomes, both positive and negative, resulting from the intervention and identifies intervention and external factors that are influencing the change. Summative evaluation is the final assessment done at the end of a project plan. Summative evaluation combines impact data with other relevant data to present a more complete scenario of operations and accomplishments of a programme. Summative evaluations focus on the goals of the program, both in terms of its impact on individuals and its impact on collaborating systems and the larger community [18]. Summative evaluation collects information about outcomes and related processes, strategies and activities that have led or not led to the defined goals. The results obtained help in identifying the extent of achievement of the programme lessons learned, positive and negative outcomes of the interventions, making decisions about continuation/termination of a programme and also to determine reformulation of strategy [13]. In addition, other evaluations methods used some times are spot checks and desk evaluation. ‘Spot check evaluation’ is a brief ad hoc evaluation undertaken when there is an urgent need during programme implementation. It enables specific decisions to be made regarding the programme, provides a quick realistic picture of programme status as part of the accountability process and enables quick implementation of corrective measures. ‘Desk evaluation’ which may be internal or external do not involve field visits but depend largely on secondary sources for information. Programme personnel or implementers using largely secondary sources of information do ‘Self-evaluations’ or ‘Internal evaluations’. They are often subjective and mainly undertaken in small programmes [1].

37.4

Designing the evaluation

Designing the evaluation is the total process of stating the objectives, identifying questions, specifying a plan for collecting and analyzing data, reporting results, and getting the results used. It is to be noted that there is no perfect design. Each design has its own strengths and weaknesses. There are always trade-offs – time, costs, practicality; and it is important to acknowledge the trade-offs and potential weaknesses. In general, the evaluation design consists of the following: evaluation

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questions and sub-questions, indicators and measures, data sources, defining sample size, data collection methods and instruments, methodology for data analysis and procedure for control of data quality. Specification of the evaluation design requires a following thorough process since any design flow would limit the ability of evaluators to make solid conclusions about the intervention. Inappropriate design could render the entire evaluation exercise useless. Therefore, drawing a proper evaluation design matrix and paying attention to the specifics of questions, sub-questions, type of question, design, measures or indicators, criteria for normative questions is very crucial [19]. Table 37.12 presents an evaluation design matrix. Table 37.12 Evaluation Design Matrix [19] Questions

Subquestions

Types of questions

Design

Measures of indicators

Data sources

Sample

Data collection instrument

Data analysis

Comments

Criteria for normative questions

As indicated in Table 37.13, common designs are based on the following three important types of questions: (a) Descriptive (b) Normative (c) Cause–effect questions Table 37.13 Linkages between evaluation questions and design [19] Type of evaluation question

Evaluation design

Descriptive questions

Non-experimental; quasi-experimental or qualitative approaches

Normative questions

Non-experimental; quasi-experimental, or qualitative approaches Plus goals/standards/needs assessment

Cause–effect questions

Experimental, quasi-experimental, or non-experimental with in-depth causal tracing

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(a) Designs for descriptive questions Descriptive questions generally use non-experimental designs. Nonexperimental designs do not involve a comparison group that did not receive the intervention. They focus only on those who received the intervention. The common evaluation designs are as follows: (i) One shot – A one-shot design is a look at the group receiving an intervention at one point in time following the treatment or intervention. This can be used to answer questions such as “How many women were treated?” or “How satisfied are the women with the services they received?” (ii) Cross-sectional – Cross-sectional design shows a snapshot at one point in time but looks into sub-group responses. The sub-groups may be based on age, gender, income, education, ethnicity, or amount of intervention received. This design is often used with a survey method. (iii) Baseline and endline (Before-and-after) – Before-and-after design looks at group characteristics before and after the intervention (also called the pre- and post-intervention characteristics). It is an assessment made at both baseline and endline. There is no comparison group. For example, participants to a food-for-school program can be asked whether the program improved school attendance. The design of this sort, however are subject to variety of biases or threats to validity. Before-and-after designs can be improved by gathering multiple data points before and after the program is introduced and by careful examination of other actors. Baseline data is the information on which problem analysis is based. It is very difficult to measure the impact of the implementing programme if the baseline data on relevant indicators for measuring the impact is not available. The baseline data needs to focus on collecting general information about the situation. At times such data is available in official statistics. If the required information is not available from secondary sources then the information needs to be systematically obtained through a baseline survey keeping the focus on the relevant indicators for measuring impact. It is very difficult to get baseline information after the work has begun and the situation has changed. There are ways of doing damage control; e.g. by gathering anecdotal information from those who were involved at the beginning or know what the situation was at the beginning of the project or through the records/written sources such as minutes, reports and so on. (iv) Time series – Time series design looks for changes over time (either after or before and after the intervention) in order to discern trends. They can be simple time series designs or cross-sectional designs. For example, child mortality rates might be examined before and after an intervention, providing maternal nutrition supplements, to identify the trends in birth weights.

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(v) Longitudinal – Longitudinal study is one in which repeated measures of the same variable are taken from the same people (or from a sample of groups in the same population). A panel design is a special type of longitudinal design in which a smaller group of people is tracked at multiple points in time and their experiences are recorded in considerable detail [19]. (vii) Case studies – The descriptive case study collects in-depth information over time to describe what implementation of the intervention looked like on the ground and why things happened the way they did. Rather than using large samples and following a rigid protocol to examine a limited number of variables, case study methods involve an in-depth, longitudinal examination of a single instance or event. It is a systematic way of looking at what is happening, collecting data, analyzing information, and reporting the results. It is a method of learning about a complex instance through extensive description and contextual analysis. The product is an articulation of why the instance occurred as it did, and what may be important to explore in similar situations. The product is a sharpened understanding of why the instance happened as it did, and what might be important to look at more extensively in future research. Thus, case studies are especially well suited toward generating, rather than testing, hypotheses. Case studies can generate a great deal of data that may not be easy to analyze [19, 20]. (b) Designs for normative questions The logic for normative questions is similar to descriptive questions, except that normative questions are always assessed against a criterion. The only difference between answering a normative and descriptive questions is that in normative questions goal, target or standard to be reached are specified and the actual findings are compared to that standard. Generally, the same designs work for normative questions as well as descriptive questions. (c) Designs for cause–effect questions When answering cause–effect questions, evaluation design needs to address the question “What would the situation have been if the intervention had not taken place?” In order to evaluate impact, one or more types of the following designs may be considered (i) experimental design, (ii) quasiexperimental design, (iii) correlation design, (iv) case study design, and (v) non-experimental designs. (i) Experimental design – The experimental design is the classic design or true experiment design. It is considered the strongest design for cause– effect questions. Experimental designs usually contain before-and-after measures for the comparison groups [19]. Random assignment is an

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essential component of experimental design. It is essential that comparison groups are comparable. One group is randomly assigned to receive the intervention and another randomly assigned group serves as the control group and does not receive the intervention. As long as there is equipoise regarding the benefits and harms of the intervention, potential for participants to benefit, and a means of informed consent, randomization is ethically acceptable. Experimental designs are the preferred method for outcome evaluations. The principal advantage is that a relatively high degree of confidence can be placed in findings of differences in outcomes between the two groups. It is not always feasible, however, to use an experimental design. Firstly, experimental designs that minimize possible “contamination” of the experiment can be expensive. Secondly, the design may not be ethical or legal. For example, there can be an argument that it is unfair or a denial of equal protection of law to arbitrarily withhold beneficial program services from eligible participants who have a demonstrated need for treatment. One strategy that has been used to allay concerns related to defendants’ need for, or rights to, treatment is to assign defendants to one of several different “categories” of treatment. For example, participants might be randomly assigned to a more intensive group (daily outpatient groups, assessment test and health education), or to a less intensive group (only assessment test and health education). This strategy ensures that all participants identified as needing treatment receive some services by falling into one of the groups. Experimental designs are generally more tenable only when participants provide a full and informed consent regarding their involvement in randomization procedures and other program evaluation activities. Evaluation procedures, including legal and ethical issues, should be carefully reviewed before an experimental evaluation design is implemented [20]. (ii) Quasi-experimental design – The quasi-experimental design is similar to true experiment except that the comparison groups have not been formed by random assignment. It is used to carry out evaluation when it is not possible to construct treatment and control groups using random assignments. Sometimes, a comparison group is created by matching key characteristics [19]. In public health, however, random assignment commonly either is not feasible or simply is not done. In such instances, Quasi-experimental-designs can be used for a scientifically rigorous examination of outcomes. Although these designs can improve inferential clarity, they cannot be relied on to yield unbiased estimates of the effects of interventions because the subjects are not assigned randomly. One type of quasi-experimental evaluation is a pre-post design, in which outcomes obtained following discharge from an intervention programme are compared to those obtained prior to program participation. A drawback

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to pre-post designs is that they do not take into account other factors that influence the outcome measured. Another type of quasi-experimental evaluation studies one or more comparison groups, rather than a randomly assigned control group. Using this design, results from the experimental and comparison groups are contrasted. Comparison groups consist of participants who do not participate in (or who do not complete) the intervention program. These groups are otherwise similar to program participants in key areas such as age, gender, ethnicity, employment, income, nutritional problem under study and other areas used as eligibility criteria in the program. It is often useful to “match” subjects in experimental and comparison groups to control for the problem of confounding variables introduced through nonrandom assignment. Using this approach, both groups’ subjects are selected based on factors expected to affect outcomes [20]. (iii) Correlation design – Correlation design is often used when answering questions about relationships. Correlation designs can be used with data already available, or with new data. For example, to find out if having a higher education among women is related to lower maternal mortality, a correlation design could be used. However, correlation evidence alone cannot establish causality [19]. (iv) Case study design – A case study design is used when the intention is to gain an in-depth understanding of a process, event or situation. Case study method involves extensive description and contextual analysis to learn about a complex instance. It is especially useful when the intervention is relatively innovative or experimental or not well understood. The case study finding, present detail of why the instance occurred as it did as well as articulates what may be important to explore in similar situations. Evaluators considering the case study as a design for evaluation must first decide what type of evaluation question they have and then examine the ability of each type of case study to answer it. The crucial next step is in determining whether the methodological requirements of the chosen case study method can be met in the situation at hand. There are six types of case studies as detailed below. Illustrative case studies are descriptive; they utilize one or two instances to show what a situation is like. The most serious limitation is with the selection of instances. The case(s) must adequately represent the situation or program. Where significant diversity exists, it may not be possible to select a typical site. Exploratory case studies are condensed case studies, undertaken before implementing a large-scale investigation. Where considerable uncertainty exists about program operations, goals, and results, exploratory case studies serve to safeguard investment in larger studies. The greatest pitfall in the exploratory study is prematurity: the findings may seem convincing enough

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to be released inappropriately as conclusions. Other pitfalls include the tendency to extend the exploratory phase, and inadequate representation of diversity. Critical instance case studies – This method is particularly suited for answering cause-and-effect questions about the instance of concern. The most serious pitfall in this application is inadequate specification of the evaluation question. Program implementation case studies help discern whether implementation is in compliance with its intent. These case studies are also useful when concern exists about implementation problems. Extensive, longitudinal reports of what has happened over time can set a context for interpreting a finding of implementation variability. A requirement for good program implementation case studies is investment of sufficient time to obtain longitudinal data and breadth of information. Training and supervision is essential quality control for data collection and management. Program effects case studies can determine the impact of programs and provide inference about reasons for success or failure Cumulative case studies aggregate information from several sites collected at different times. The cumulative case study can be retrospective, collecting information across studies done in the past, or prospective, structuring a series of investigations for different times in the future. Retrospective cumulation allows generalization without cost and time of conducting numerous new case studies; prospective cumulation also allows generalization without unmanageably large numbers of cases in process at any one time. The techniques for ensuring sufficient comparability and quality and for aggregating the information are what constitute the “cumulative” part of the methodology. Opinions vary as to the credibility of cumulative case studies for answering program implementation and effects questions [20]. One authority notes that publication biases may favour programs that seem to work, which could lead to a misleading positive view [21]. Others are concerned about problems in verifying the quality of the original data and analysis [22]. (v) Non-experimental design – Non-experimental designs do not involve a comparison group that did not receive the intervention. The lowest level of evidence occurs with non experimental designs, which consist of case series and anecdotal reports. Although such studies can contain a wealth of useful information, they cannot support inference because they cannot control for factors such as maturation, self-selection, historical influences unrelated to the intervention, and changes in instrumentation [19]. Once the particular evaluation design based on the focus question is implemented, the next logical step is to undertake the programme efficiency analysis. The procedures employed in efficiency evaluation are often highly technical and the analysis is based on numerous assumptions [23, 24].

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37.5

Programme efficiency analysis

For decision makers the reference programme is often the one that produces the most impact on the most targets for a given level of expenditure. This simple principle is the foundation for cost-benefit and cost-effectiveness analyses. These are tools for assessing whether or not costs of an activity can be justified by the outcomes and impacts [6]. The analysis estimates the efficiency of programme and projects. The economic assumptions are made explicit. It is useful for informing decisions about the most efficient allocation of resources. The information from such an analysis is useful for convincing policy makers and funders that the benefits justify the activity.

37.5.1 Cost-benefit analysis Cost-benefit analysis measures both inputs and outputs in monetary terms [6]. The cost-benefit analysis is a management technique that has attracted the widest attention for application in the health field. The economic benefits of any programme are compared with the cost of that programme. The benefits are expressed in monetary terms to determine whether a given programme is economically sound, and to select the best out of several alternate programmes. The main draw back with this technique is that the benefits in the health field, as a result of a particular programme, cannot always be expressed in monetary terms. The benefits are generally expressed in terms of birth or deaths prevented or illness avoided or overcome [15]. Cost-benefit analysis is controversial because only a portion of programme inputs and outcomes may reasonably be assigned a monetary value. One must ultimately place a value on human life in order to fully monetize the programme benefits [23, 24]. As an example, the cost-benefit analyses of the outcomes of a nutrition education programmes would express in monetary terms as follows: i.e. focus on the difference between money expended on the nutrition education programme and the money savings from reduced expenditure for treating dietary-related diseases such as anemia, goitre, vitamin A related blindness, etc [25].

37.5.2 Cost-effective analysis Cost effectiveness analysis estimates inputs in monetary terms and outcomes in non-monetary quantitative terms [6]. Cost-effectiveness analysis is seen as a more appropriate technique than cost-benefit analysis [23]. Cost-effectiveness analysis requires monetizing only the programme’s cost, and the benefits are expressed in outcome units. For example, in a

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cost-effectiveness analyses of the outcome of a nutrition education programmes, the outcome would be expressed against the set goal in substantive terms [25]: ‘A cost-effectiveness analysis of a nutrition education programme would focus on the estimation of money expended in relation to the improvement in the consumption of vitamin A rich foods by target groups’. These analyses provide systematic approaches to resource allocation. From a conceptual point of view, perhaps the most significant value of efficiency analysis is that it forces evaluators and programme personnel to think in a disciplined fashion about both costs and benefits. Three major types of efficiency analysis can be undertaken – ex-ante, ex-past or sensitivity. Efficiency analysis done either in the planning or design phases of a programme is called ex-ante analysis. Ex-ante analyses are not based on empirical information, and therefore run the risk of either under or over estimating the benefits of effectiveness. Most commonly, efficiency analyses of programmes take place after their completion, often as part of their impact evaluation. This is called ex-post analysis where the purpose is to assess whether the costs of the intervention can be justified by the magnitude of net outcomes. An important strategy in efficiency analysis is to undertake several different analyses of the same programme, varying the assumptions made which are open for review and checking. This is called sensitivity analysis. Efficiency analysis may be impractical and unwise for several reasons [23]: ●

●

●

●

●

The required technical procedures may be beyond the resources of the evaluation programme. Political or moral controversies may result from placing economic values on particular input and outcome measures. This may obscure the relevance and minimize the potential utility of an evaluation. Efficiency assessment may require taking different costs and outcomes into account, depending on the perspectives and values of sponsors, stakeholders, targets and evaluators themselves. This may be difficult for atleast some of the stakeholders to understand, and may obscure the relevance and utility of evaluations. It is a complex process to look at the stakeholders who are individuals or organizations directly or indirectly affected by the implementation and results of interventions programmes. In some cases, the data needed for undertaking cost-benefit calculations are not fully available. The analytic and conceptual models may be inadequate, and often untested underlying assumptions may lead to faulty, questionable and unreliable results.

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37.6

Quantitative and qualitative techniques used in evaluation

Both quantitative and qualitative methodologies are used in evaluation depending on the type of evaluation. While impact or outcome evaluation is often quantitative, process monitoring and evaluation often use qualitative information. The relative advantages and disadvantages have been debated extensively in the evaluation literature. However qualitative procedures are difficult and expensive to use if the evaluation depends entirely on this alone. For example, it would be very difficult and expensive to build on qualitative observation in large-scale surveys [23]. The situations where quantitative and qualitative techniques could be used in evaluation are presented in Table 37.14. Table 37.14 Applications of quantitative and qualitative techniques [15] Quantitative techniques ● ● ● ● ●

Cost-benefit analysis Cost-effective analysis Input, process and output analysis System analysis Network analysis

Qualitative techniques ● ● ● ● ●

Organization of the programme Personnel management Communication Management Information System (MIS) Management by objectives

The use of both qualitative and quantitative and multiple methods can strengthen the validity of findings if results produced by different methods are congruent and/or complement each other. In summary, it is useful to remember the following points [25]: ● ●

● ●

Both type of methodologies are important and have their own place. Qualitative methodologies are useful in monitoring and for undertaking process evaluation. Outcome/impact evaluation is often quantitative. Use of both type of methodologies strengthen validity of findings.

As stated above, the monitoring and evaluation process requires a combination of quantitative and qualitative information in order to be comprehensive. Some people find quantitative information comforting – it seems solid and reliable and “objective”. They find qualitative information unconvincing and “subjective”. It is a mistake to say, “Quantitative information speaks for itself”. It requires just as much interpretation in order to make it meaningful as does qualitative information [2]. Quantitative measurements tell “how much or how many”. This is the process of presenting and interpreting numerical data, which includes both descriptive statistics and inferential statistics. Quantitative measurement can be expressed in absolute numbers or as a percentage. It can also be expressed as a ratio [2].

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Qualitative measurements tell how people feel about a situation or about how things are done or how people behave [2]. Qualitative research is an inquiry process of understanding a social or human problem based on distinct methodological traditions of inquiry. The researcher builds a complex, holistic picture, analyzes words, report detailed views of informants, and conducts the study in a natural setting. Qualitative data may be collected through open-ended questions in self-administered questionnaires, individual interviews, focus group discussions, or through observations during fieldwork [26].

37.6.1 Methods of data collection – quantitative and qualitative There are various methods that could be followed for data collection when monitoring and evaluating public health nutrition programmes. These are primarily quantitative and qualitative methods. Quantitative methods include project records and reviews, population based surveys while qualitative methods include focus group discussions, observations, ethnographic surveys, social mapping, case studies etc. A few of the commonly used method such as records, surveys, observation, interviews and focus group discussions (FGDs) are presented below. (i) Records These are information routinely collected in nutrition projects, and the core of an ongoing monitoring system. It should be noted that information from records may be reviewed periodically. Another type of record is secondary data. For example, records from national or regional surveys regarding nutritional status, dietary intake, prevalence of micronutrient deficiencies, household income and expenditure can be obtained. Use of records can be a fast, inexpensive, and convenient way to obtain information. However, it requires a careful inspection of the original collection process, keeping in mind that the validity and reliability of the emerging findings will rest upon the quality of data collection skills [1]. (ii) Surveys Surveys can cover an entire project population or a representative sample. They can include open or closed-ended questions. Open-ended questions allow respondents to answer in their own words while closed-ended questions require specific answers or selection from a set of possible answers. Survey data that is derived from open-ended questions, can give both quantitative and qualitative data. Surveys are a very popular method of collecting data

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and the reliability of such data depends on the sampling frame, quality of questions and care taken in administering the questionnaire. The surveys done at appropriate point of time in a project cycle can bring out useful data for inference and action. It can be done at baseline, midline and end line to keep a close track of the developments in the project [1, 27]. (iii) Observation Observations are one method used to assess time-use patterns and behaviours related to desired outcomes. Observation can also offer valuable insights into the social and physical context of the problem being addressed and the use of project inputs [1]. For example, in the field of nutrition, 24 hours feeding behaviour may be observed to learn valuable information. This can be done by one of the following methods: ● ●

A single 24-hour recall Multiple 24-hour recalls or multiple diet records

Single 24-hour recall is the method of choice if the purpose of the study is simply to describe the average intake of a group. That is, it provides a mathematically accurate group mean. However, it does not provide a good estimate of an individual’s usual intake for any individual member of the group. In multiple 24-hour recall or multiple days of diet records method, a number of days of dietary intake are collected; the data begin to approximate an individual’s usual intake. Thus, if enough days are collected on each individual, this could be an appropriate measure to use for research in which the individual’s usual intake is the unit of interest. Generally, at least three days of diet data are required for the most stable nutrient, percent of calories from fat. Other macronutrients require more, and micronutrients such as vitamin C and vitamin A require many more days [28]. (iv) Key informant interviews A key informant interview involves a face-to-face meeting between a trained interviewer and a person who can provide an overview/big picture of knowledge, attitudes or practices of the group being monitored or evaluated. Key informants provide a broad view of the situation and this overview is critical in data collection. Similarly a focus group discussion involves group dynamics that allow participants to respond to one another’s perceptions, generating new ideas and highlighting conflicting attitudes that might otherwise be inaccessible to an outsider [26, 29]. As mentioned above, an interview is a data collection method that involves oral questioning of respondents, either individually or as a group. It is suitable for use with illiterate people. It also permits clarification of questions through

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probing. Interviews are probably the most commonly used evaluation method. The tips to be an effective interviewer include [27, 28]: ● ● ● ●

Be familiar with research material Be familiar with the interview guide Practice interviewing through role-playing exercises or pilot interviews Practice using the recoding equipment

The interviewer skills have an important influence on the comprehensiveness and complexity of the information that participants provide. ●

●

The interviewer must be able to lend a sympathetic ear without taking on a counselling role; encourage participants to elaborate on their answers without expressing approval, disapproval, judgment or bias; keep track of the questions yet let the conversation develop naturally; and manage the interview while still respecting the principle of participant-as-expert. The core skills required establishing positive interviewer/ participant dynamics are rapport-building, emphasizing the participant’s perspective and accommodating different personalities and emotional states.

(v) Focus group discussions Focus group discussions (FGDs) are a qualitative method designed to use group dynamics and the flow of discussion to probe deeply into the images, beliefs, and concepts that people have about a particular subject. Ideally, people become involved in the discussion and react to one another’s comments. It is not a group interview but a group discussion focused on a topic. These guided discussions are held with small groups of people who have similar characteristics. The discussions are led by a trained moderator who uses a question guide to introduce the topics of interest and probe for deeper discussion. In the area of public health nutrition programmes, FGDs can be used for facilitating the following tasks [26–30]: (a) Focus the evaluation and develop relevant evaluation questions by exploring in greater depth the problem to be investigated and its possible causes. It helps to focus on the topic of research and develop relevant research hypotheses by exploring in greater depth the problem to be investigated and its possible causes. For example, a district health officer had noticed that there were an unusually large number of cases of severe undernutrition in under-5-year children in a specific area in the district. The officer wanted to understand the reasons contributing to such situations. Three focus group discussions (one with leaders, one with mothers from the area and one with health

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staff from the area) were organised. The investigator hoped to identify potential causes of the problem through the FGDs and then develop a more intensive study, if necessary. (b) Formulate appropriate questions for more structured larger-scale surveys. FGDs help in formulating appropriate questions. For example in planning a study of the incidence of childhood diarrhea and feeding practices, a focus group discussion showed that in the community under study, children below the age of 1 year were not perceived as having ‘bouts of diarrhea’ but merely ‘having loose stools’ that were associated with milestones such as sitting up, crawling, and teething. In the questionnaire that was developed after the FGD, the concept ‘diarrhea’ was therefore carefully described, using the community’s notions and terms. (c) Supplement information on community knowledge, beliefs, attitudes and behaviour already available but incomplete or unclear. FGDs help to understand and solve unexpected problems in interventions. In district X, a recent national (polio) immunization day (NID) showed widely different coverage for immunization per village (50– 90%) and in a number of villages a marked decrease in the immunization coverage was observed compared to the previous year. Eight FGD were held with mothers, two in town, three in rural villages with decrease trend in NID coverage and three FGDs in villages with a high immunization coverage throughout. The FGD revealed that the overall concept of NID had raised confusion. Most people believed that the mass NID campaign strengthened the children’s immunity against any (childhood) disease, including malaria and Respiratory Tract Infections. In the villages with a low NID coverage, there had been a high incidence of malaria in children immediately after the previous NID campaign and several children died. Mothers therefore, believed that the NID campaign was useless. (d) Facilitate in developing appropriate messages such as for nutrition health education programmmes and also in exploring controversial topics and issues. Qualitative data is in the form of description of events in words or transcripts of interview. In case of qualitative data, technique of handling of qualitative data emerging from focused group discussion is critical. For example to get the best results in case of focus groups discussions, one needs to ensure the following [30]: ● ●

Ensure information provided adds meaning or value. Focus the analysis by concentrating on questions that meet the objectives of evaluation.

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Categorize information – identifying themes or patterns such as ideas, concepts, behaviour, interactions, incidents, terminology, phrases used. Organise information into coherent categories that summarizes and brings meaning to text. Identify patterns and connections within and between categories. Interpret the data – key points and important findings – attaching meaning and significance.

37.6.2 Process of data analysis In the process of M & E, there is normally a large amount of information and data. Skills are required to effectively analyse the data. Figure 37.3 presents the process of data analysis which turns the detailed information into an understanding of patterns, trends, and interpretations leading to drawing and presenting conclusion. SWOT (Strengths, Weaknesses, Opportunities and Threats) analysis technique could be used for interpreting the data and drawing conclusions. Analysis is in fact the intuitive understanding of the key themes that come out of the information gathering process. Once the key themes are identified, it becomes possible to work through the information, structuring and organizing it. Then next step is to write up the analysis of the findings as a basis for reaching conclusions, and making recommendations. The process involved in analysis is depicted in Fig. 37.3.

37.3 Process of data analysis [2]

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37.7

Monitoring and evaluation – decision making and moving forward

Monitoring and evaluation is of value when the implementers of a programme act on the information that emerges from the analysis of data collected. It is therefore critical to have a strategy and method for collecting, storing, reviewing, analyzing data as well as a timely information feedback system to facilitate management decision making. This cyclic tool is referred to management information system (MIS) and should be part of monitoring and evaluation. Once the findings, conclusions and recommendations from monitoring and evaluation process are in place, it is critical to follow the next set of steps for benefiting from the analytical findings [2]. ● ●

●

●

●

Share the findings with stakeholders. Review and reflect on the lessons learned. Draw out a list of options for actions. Identify programme elements that need to be addressed for improving efficiency, effectiveness and impact. Identify issues that are resistance for effective implementation and develop strategy to deal with resistance. Make effective decisions about how to move forward.

References 1. The applied nutrition programme, “Monitoring and evaluation of nutrition and nutrition-related programmes – a training manual for programme managers and implementers”. 1999. University of Nairobi and School of Nutrition Science & Policy, Tufts University. 2. SHAPIRO J (1996). Evaluation, Judgment Day or Management Tool? Olive. 3. BOSE AB (1986). Monitoring survival and Development of the young child. 4. Monitoring & evaluation – some tools, methods & approaches – The World Bank, 2004: www.nrhmcommunityaction.org. 5. Logical Framework Approach to project cycle management – LogFrame Handbook, 1997. 6. http://www.mindtools.com 7. PSI Logframe Handbook (2000). The logical framework approach to social marketing project design and management. 8. Monitoring vitamin A programs (1998). IDRC, Micronutrient Initiative, Ottawa, ON, CA. 9. Performance Monitoring Indicators – A handbook for task managers (1996). Published by Operations Policy Department, World Bank, Washington DC. 10. WHO (1996). Indicators for assessing vitamin A deficiency and their application in monitoring and evaluating intervention programmes. WHO / NUT/96.10. 11. Assessment of iodine deficiency disorders and monitoring their elimination – A Guide for Programme Managers (2007). Third Edition. WHO publication. 12. Indicators for assessing Infant and Young Child feeding practices (2008). WHO publication.

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13. User-friendly Handbook for Project Evaluation (2002). (NSF 02-057). 14. LEVINSON JF, et al. (1999). Monitoring and Evaluation – A guidebook for Nutrition project Managers in developing countries. Published by Human Development Network, The World Bank. 15. PARK K (2007). Preventive and Social Medicine. 16. HOLTGRAVE DR, QUALLS NL, CURRAN JW, VALDISERRI RO, GUINAN ME, PARRA WC. (1995). An overview of the effectiveness and efficiency of HIV prevention programs. Public Health Rep. 110, pp. 134–146. 17. http://www.civicus.org/new/media/Monitoring%20and%20Evaluation.pdf PACT’s Evaluation Sourcebook, 1984. 18. www.ncbi.nlm.nih.gov/bookshelf/br.fcgi? book=hssamhsatip&part=A44942 19. International program for Development Evaluation Training – Building Skills to evaluate development Interventions (2007). Published by The World Bank Independent Evaluation Group & Carleton University. 20. LYNN D (1991). The application of case study evaluations. Practical Assessment, Research & Evaluation, 2(9). 21. BERGER MA (1983). Studying Enrollment Decline (and Other Timely Issues) via the Case Survey. Educational Evaluation and Policy Analysis, 5(3), pp. 307–317. 22. YIN RK (1989). Case Study Research: Design and Methods. Beverly Hills, CA: Sage. 23. ROSSI PH and FREEMAN HE (1993). Evaluation: A Systematic Approach. Sage Publications. 24. SØNBØ KI , EGGEN AE , THELLE DS (1991). Cost effectiveness of incremental programmes for lowering serum cholesterol concentration: is individual intervention worth while? Br Med J. 302, pp. 1119–1122. 25. www.fao.org/docrep/w3733e/w3733e06.htm 26. www.idrc.ca 27. The teaching Module for Research Methodology and Bio-Statistics (2009). Department of Epidemiology, The Tamil Nadu Dr. M.G.R Medical University, Chennai, India. 28. http://www.nutritionquest.com/research/about_dietary_analysis.htm 29. http://www.bmj.com/cgi/content/full/320/7227/114 30. ELLEN TAYLOR-POWELL MARCUS RENNER (2003). Analyzing qualitative Data.

District and village planning – a decentralised implementation approach in public health in India Shraddha Dwivedi, Madhulekha Bhattacharya and Ashish Mukherjee

Shraddha Dwivedi, MD in Community Medicine, is Professor and Head of the Department of Preventive and Social Medicine at MLN Medical College, Allahabad. Madhulekha Bhattacharya, MD in Community Medicine, is Dean of Studies and Professor & Head, Department of Community Health Administration at the National Institute of Health and Family Welfare. Ashish Mukherjee, postgraduate in journalism and management, is currently Executive Director at the Centre for Development Finance (CDF) at the Institute of Financial Management and Research (IFMR), Chennai.

38.1

Introduction

Planning is an essential management function. It can be defined as a process of setting goals, developing strategies, and outlining tasks and schedules to accomplish the goals. The purpose of planning is to ensure efficient utilization of resources to achieve optimum outcomes. For promotion of effective and efficient delivery of health services to the community, public health planning is of utmost importance. In India, soon after independence, a centralised approach to planning was adopted with a view to achieve rapid economic development. However, the centralised approach led to development of plans that had little relevance to local needs and did not promote community participation or generate a sense of ownership at the level of grass root implementation. Approaches to helping people have moved over the years from welfare based programmes to development based programmes. In the latter, the focus is on encouraging people to participate in activity and develop a sense of ownership at the level of grass root implementers with the failure of earlier vertical

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programmes and centralised approaches, decentralised and participative development of plans assumed importance. Numerous efforts have been made in recent times by the government to promote participative district planning approach. The 73rd and 74th Constitutional Amendment Acts, 1992 have accorded a constitutional status to the Panchayati Raj Institutions (PRIs) local bodies as the third-tier of government (Box 38.1). The amendments have also devolved, both, administrative and financial powers to the local governance, i.e. Panchayati Raj Institutions or PRI. The District Planning Committees have the mandate to compile the action plans prepared by the panchayats and municipalities in the district and consolidate them into the Draft District Plan encompassing all sectors, such as, health, education, sanitation, roads, energy, housing, livelihoods, etc. The role of panchayats is central in the multi-sector development plan at the local level (Figure 38.1).

38.1 Functions delegated to local body – Panchayati Raj Institutions (PRIs).

Box 38.1 74th Constitutional Amendment Act and District Planning The 74th Constitutional Amendment Act mandated the establishment of the District Planning Committee (DPC) for consolidating plans. To facilitate the process the Ministry of Panchayati Raj addressed all the Secretaries of Panchayati Raj of the States on 30th May 2005 requesting them to constitute DPCs in their respective States if these had not been constituted. Their attention was also drawn to the meeting of the Committee of Chief Secretaries and Secretaries of Panchayati Raj Institutions (PRIs) in the states/union territories held on 11th April 2005 wherein the Ministry of Panchayati Raj had communicated that the States that had not constituted DPCs in accordance with Article 243ZD of the Constitution should do so before 31st October 2005 [2]. This led to almost universal constitution of the DPCs.

With reference to the District Health Care System, emerging key responsibilities of PRIs are as follows:

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Ensuring accountability, transparency, responsiveness, resource mobilisation, allocation Undertaking decentralised participatory planning Prioritizing of local needs Undertaking resource mapping Undertaking management, supervision, implementation, monitoring Involving community-opinion makers Conducting health education Providing and maintaining infrastructure and logistics Collecting and disseminating information-vital statistics Undertaking health communication, advocacy in locally relevant and acceptable dialect Ensuring inter-sectoral coordination-convergence of service delivery at village level Ensuring access to referral system and transport for reaching centres of referrals

38.2

National Rural Health Mission (NRHM) and District Health Action Plans

The National Rural Health Mission (NRHM) was launched throughout the country in April 2005, with a view to provide accessible, affordable and quality health care to the rural population. The Mission adopts a synergistic approach by relating health to determinants of good health, viz. segments of nutrition, sanitation, hygiene and safe drinking water. The key features in order to achieve the goals of the Mission include making the public health delivery system fully functional and accountable to the community, human resources management, community involvement, decentralization, rigorous monitoring & evaluation against defined standards, convergence of health and related programmes from village level upwards, innovations and flexible financing and also interventions for improving the health indicators. Under the National Rural Health Mission (NRHM), a district has been recognized as the most important operational level for ensuring provision of primary health care. One of the key strategies of the NRHM policy is the preparation of need-based district health plans through intensive participation and consultation among the key stakeholders, which includes the PRI, civil society and the concerned government departments. Each District Health Action Plan (DHAP) is expected to be tailored to the specific needs of each district. Health planning therefore aims at improving the health status of a given population while safeguarding equity and fairness of access, as well as, ensuring responsiveness of the health system to the perceived needs of a community. A district health action plan sets out the goals and strategies that would enable a district to best

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meet the health needs of its population and is expected to contain a situational analysis of the district, objectives and interventions, work plan, budgets and a monitoring and evaluation plan. District health action plan integrates the various interrelated components of health to ensure quality of care and access to service with specific reference to various interrelated paradigm as mentioned below: ●

●

●

●

●

●

Resources – health manpower, logistics and supplies, community resources and financial resources, voluntary sector health resources Access to services – public and private services as well as informal health care services; levels of integration of services within public health system Utilization of services – continuity of care, factors responsible for possible low utilization of public health system Quality of care – technical competence, interpersonal communication, and client satisfaction, client participation in management, accountability and redress mechanisms Community – needs, perceptions and economic capacities, PRI involvement in health, existing community organizations and nature of involvement in health Socio-epidemiological situation – local morbidity profile, major communicable diseases and transmission patterns, health needs of special social groups (e.g. tribals or Adivasis, migrants, very remote hamlets)

Many of the solutions for addressing problems at district level are likely to emerge from block level and village consultations. The district planning process therefore uses a bottom up approach. As the first level of integration, planning of health actions at village level is compiled in the block level action plans and these block level action plans are then consolidated into the district plan. Figure 38.2 presents an overview of the planning process. For this purpose, formation of planning teams and committees at various levels, that is, village, block and district levels have been envisaged. Thus, the DHAP enables village, block, district and state level functionaries to identify the gaps and constraints to improve services with regard to access, demand and quality of health care. District health plan has been envisaged to be the principal instrument for planning, implementation and monitoring, through a participatory and bottom to up planning process. NRHM-DHAP is the cornerstone of all strategies and activities in the district. District Missions and District Health Society have been set up in each district in all states for implementation of the programme, and District Missions have been entrusted with the task of development of the annual and prospective plans for the district.

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38.2 Health and nutrition planning process – district health action plan (DHAP). [V – Village, GP – Gram Panchayat, DPMU – District Programme Mangers of Health Unit, NGOs – Non-Government Organisations, BPM – Block Program Mangers of Health Unit, CBOs – Community-based Organisations, PHC – Primary Health Centre, MO – Medical Officer]

Some of the features of NRHM for increasing community ownership and accountability are as presented below –

Village health planning ●

●

● ● ●

● ● ●

Frontline community health worker known as ASHA (Accredited Social Health Activist) chosen through local consultative processes. ASHA accountable to Village Health Committee (VHC) or Village Health and Sanitation Committee (VHSC). VHSC to oversee implementation and monitoring of village health plan. Involvement of Block PRI in Block plan. Involvement of District PRI in District Health Mission and District Health planning process. Provision for Citizen’s charter. Provision of Community Monitoring and Social Audit. Patient Welfare Committees (Rogi Kalyan Samitis) for community management of public hospitals.

Health sub-centres are expected to report on the performance to the lowest governance body of community (Panchayats), hospitals to the Patient Welfare society (Rogi Kalyan Samitis) and District Health Mission to the District Council (Zila Parishad). For the preparation of a district plan, a planning workflow, as presented in Fig. 38.2, is advised to be followed. At the village level, the Village Health & Sanitation Committee (VHSC), a standing committee on health constituted in each village is responsible for the development of the village health plan. A VHSC ideally consists of about 6–8 members drawn from different strata,

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such as, the panchayat representative, ICDS worker (Anganwadi Worker), school teacher, respected elders of the village and the ASHA, a representative of non-government organisation (NGOs)/Community-based Organisation (CBOs)/Self-help groups (SHGs). The VHSC is entrusted with the task of collecting the basic village data in terms of population status, available resources from standpoint of health and information on burden of diseases, identification of foci of higher morbidities in the village and treatment seeking pattern of different segments of society. Rapid assessment and analysis of the situation is used as the basis for developing health interventions in meeting the health needs of the village population and reducing morbidities and mortalities, mostly owing to childhood diseases or maternal complications. The provision of safe drinking water, sanitation and nutrition of vulnerable groups, such as infants and children, adolescents, pregnant women and the aged, is also considered as an essential part of the plan. These village plans are then collated at the Gram Panchayat level (a cluster of villages and hamlets under the local governance or panchayat. Depending on the size of the villages, one gram (village) panchayat (GP) may comprise a single village or a group of few villages). At this level, the GP chief (referred as Gram Pradhan) and selected members of the VHSC constitute the planning committee which is responsible for integrating the various village plans. The heath workers such as the ANM (auxillary nurse mid-wife) and MPW (male multi-purpose worker) are responsible for providing support to the village planning committee in conducting household survey and development of the village health plan. The next level of consolidation is the cluster level or Primary Health Centre (PHC) level (one PHC normally covers a population of 30,000). The PHC level committee, comprising the PHC Medical Officer, representatives of the VHSCs and representatives of local civil society organizations, is responsible for over viewing the activities of the gram panchayat planning teams and consolidation of their plans to form the PHC plan. Ideally, at this stage the PHC medical officer is expected to identify resource requirements based on the assessment of the workload in the PHC area and include these in the PHC plan. The PHC plans are consolidated into a Block Health Plan. Generally, there are about 2–4 PHC plans developed in a block. The Block level monitoring and planning committee comprising the Block Pramukh – (referred as Adhyaksh of the Block Panchayat Samiti), the Block Medical Officer, the Block Development Officer, NGO/CBO representatives, Block Program Managers of Health Unit (BPMU), wherever available, is responsible for finalizing the block health plans. As per the NRHM guidelines, additional human resources may also be contracted. In order to make the planning more intensive, organisation of public discussions and camps for interaction with key stakeholders are organised.

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Finally, the block health plans are assimilated and consolidated to form the district health plan. A District Planning Team (DPT) is recommended to be constituted at the district level by the District Health Mission. DPT is responsible for monitoring the process of plan preparation at the various levels and formulation of the District Health Action Plan. The core members of the DPT team include the District Chief Medical Officer (CMO), Nodal Officers of the Health Department, District Programme Managers of NRHM (DPMU), and representatives of stakeholder departments, development partners and NGO/civil society organisations. The draft plan developed by the team is required to be presented before the District Health Society for approval and onward submission to the State National Rural Health Mission. For operationalising the concept of participative decentralised planning, strengthening of the district planning process assumes great significance. The advantages of district health action plans lie in the fact that: ● ● ● ● ●

● ●

Planning is based on local evidence and needs Planners are in proximity and close contact of the target audience Area specific strategies are formulated to achieve health goals Higher interest and ownership of plans by health functionaries Mechanisms to partner with community suited to local social fabric is built in Cost-effective and practical solutions are expected There plans are outcome oriented and not budget-based plans

38.3

District Planning Development Cycle

The planning cycle is a sequence of steps which must be followed in deciding what is to be included in the plan [1]. Preparation of the plans at each level constitutes the stages of the planning cycle. The cycle seeks to answer the following questions: Where are we now? The first step in the planning process is to assess the current status of health and health-related needs and problems in the district. This requires carrying out a situational analysis with regard to health issues. Where do we want to go? Based on the situation analysis, the selection of priorities and identification of objectives and targets to be met in order to improve the health situation and/or service delivery in a district can be done. Objectives should be SMART (Specific, Measurable, Achievable, Realistic & Time bound).

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How will we get there? Details and organization of tasks or interventions to be carried out, by whom, during what period, at what costs and using what resources in order to achieve set objectives and targets. How will we know when we get there? As we progress with the project/program, we shall have to make an assessment whether we are moving in the right direction to achieve the desired objectives. This requires the development of Objectively Verifiable Indicators (OVIs) for monitoring progress and evaluating results. In heath programmes, indicators are generally depicted as rate, ratio or proportion. The above questions form a planning cycle as represented in Figure 38.3.

38.3 The Planning Cycle [1].

As already described, a district plan includes situational analysis which identifies the existing health and health-related needs and problems, as well as an analysis of health service delivery problems. Recognising the fact that all issues cannot be addressed at one time, prioritization of identified problems is essential. This requires identification of objectives and targets to be met in order to improve the health situation and/or service delivery in a district. Accordingly, actions are prioritised and operation plans are prepared to address the identified issues which include assessment of resource requirements, planning implementation details and budget estimates. For effective implementation of the plan and for monitoring progress and outcome, monitoring and evaluation plans are developed in the beginning and included in the district plan.

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Under the NRHM a district plan is encouraged to consider the following ten thematic areas so that important health related parameters are not over looked or missed out. These are expected to be incorporated in each of the plans starting from the village to the block level. Box 38.2 presents the format recommended to be used for the documentation of the NRHM district plans. (i) (ii) (iii) (iv) (v) (vi)

(vii)

(viii) (ix) (x)

Provision of quality service and achieving IPHS (Indian Public Health Standards) norms. Support systems in terms of transport, human management, logistics, drug supplies, equipment gaps and infrastructure gaps. Community participation initiatives like training and capacity building of front line workers. Behaviour change communication and other community initiatives. Management, Administration and Governance like human resource availability, sector reforms etc. Reproductive Child Health (RCH I now RCH II) program such as Maternal and Child Health and Mortality, other women issues and immunisation, also Pulse Polio Immunisation (PPI). Disease control programs concerned with the local population as well as the National disease Control Programs like TB, Leprosy, Blindness, HIV and AIDS and other diseases in Integrated Disease Surveillance Program. Nutrition and food supplies, water, sanitation and school health programs. Special programs for urban areas, tribal populations and other vulnerable groups. Cross-cutting issues and a separate section such as gender and equity issues, private sector interventions which may need to be addressed with every issue in the above thematic areas.

Box 38.2 The NRHM District Plan Presentation Framework ●

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Profile of district ■ Brief history, geographical area, terrain, demographic data, types of habitations, social structure, etc. ■ Status of health indicators ■ Health infrastructure status ■ Human resource position Situational analysis Implementation/activity plan (should provide the need (justification) for the activity, operational modalities and expected output) Training needs/training plan Procurement plan Implementation arrangements Budget estimate

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38.4

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Development of a district plan – capacity building and situation analysis

Preparatory activities for the development of a district plan include constitution of district planning teams at various levels and orientation and capacity building of these teams. The team is responsible for disseminating government instructions pertaining to planning and work out a road map for action. The planning teams are therefore oriented on the objective of the exercise and the processes to be followed. Such orientations are undertaken by organising meetings at various levels – district, block and village levels. It may be noted that a key factor in the successful implementation of decentralised planning is capacity-building at the grassroots level. Therefore, in practical terms a substantial initial investment is required to train local people for conducting situational analysis at the lowest level of operation, i.e., village and based on these developing village plans. Some of the issues to be considered for successful village health planning are ● ● ● ● ● ●

Community orientation to the role of VHCs and representation in it Village ownership of plan and participation in development Support to the village health plan by the civil society Monitoring of the plan by the VHSC Integration of the plan with the government system A gender sensitive leadership

Moreover, it is important that the following barriers to successful decentralised planning and implementation by the Village Heath and Sanitation Committee are recognised and taken into account right from the launch of the planning process: ●

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Lack of capacity to develop a need based heath and nutrition plan for the village. A long and formal process which needs simplification and hand holding of the VHSC members. Participation and ownership by villagers take time due to lack of understanding of the usefulness of the system. Lack of representation from all social classes especially marginalized/ vulnerable groups. Viewed as a government owned programme and hence lacking in credibility, resulting in lack of ownership. Lack of initiative of NGOs, and Self Help Groups to facilitate the planning process.

Besides capacity building, the planning teams are also required to be equipped with data and information for effective planning exercise. The NRHM guidelines in this respect provide a number of templates to facilitate

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in data collection. A number of sources of data are recommended to be – out of range from community and village level as well data sources from district level is also used to orient about indicators at the State and National level (Box 38.3). However, the Village Health & Sanitation Committee (VHSC) is the key unit which is responsible for the development of the village health plan and carries out household survey for collection of the basic village data. Discussions and application of Participatory Rural Appraisal (PRA) techniques, described below, is recommended for ascertaining the gaps in health service delivery and identification of village health needs. Box 38.3 shows the sources for gathering data and the planning process. Box 38.3 The data sources for decentralised planning ● ● ● ● ● ● ● ●

Household surveys at village level. Facility surveys Eligible couple register village wise. Integrated Disease Surveillance Programme (IDSP) Routine reports from sub-centre to district level. District data available with the CMO and the District Magistrate. Reports under ICDS. State Annual Reports.

Data sources from district to orient about indicators at the state and national level ● ● ● ● ●

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●

National Family Health Surveys I, II, III. District Level Household Surveys I, II, III. Sample Registration System for vital statistics. Reports of National Sample Survey Organization (NSSO) on health. UNICEF/CARE/UNFPA/YBDO/World Bank/European commission/GTZ/NIPI/ USAID etc. for health related studies done at local level. Special surveys by medical colleges/other organizations etc in the area on nutritional status, disease pattern and utilization of services. Multi-indicator coverage surveys.

Desk review by the planning teams for (a) Assessment of functioning of the government system ●

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Compare district RCH/disease/utilization of services status with state average and NRHM objectives, at block level and village level data may be used for comparison. Map health care facilities/services available- staffing, infrastructure, proximity to habitation, population served etc. Map patient load and utilization rates of PHCs and CHCs. Review performance of National Programmes in the last year. Map the performance of the ANMs/MPWs Mapping of ASHA, TBA, AWW-ANM-LHV linkages – geographically subcentre wise. Listing of NGOs – geographic outreach and focus of work. Community level groups existing in the district- block and activity wise. Last year’s budget and expenditure analysis.

(b) Community assessment ●

Resource mapping-service providers, communication facilities, drinking water sources, sanitation, nutritional status, levels of poverty.

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Understanding main health problems of women and children, providers used, perception of public health services and providers by focus group discussion. Main illnesses in the community, health care related expenditure, problems faced in referral and transport, perceptions about family planning and gender, Role of PRI in health related areas (water, sanitation). Understanding process of pregnancy, labour and post natal care, beliefs and practices –based on response to key informant interviews with elderly, TBAs.

(c) Understanding community participation and ownership ● ●

● ●

Meeting with the village health and sanitation committee. Meeting at block level with PRI members to understand their perception of health Needs and role of PRI in addressing these needs. Meeting at district level with PRI members to understand their perception of health needs and role of PRI in addressing these needs.

(d) Additional information ●

38.5

Have there been any special health related studies in the district by any other agency – government, international, NGO?

Village planning – understanding the community/ village situation – a shift from central to decentralised planning

This involves assessing the needs of the community from the following two perspectives: 1. Community’s needs as perceived by members of community. 2. Community’s needs as perceived by the service providers. The only way to identify what the community feels its needs is to solicit their views and listen to them. One of the effective ways to ensure that the community accepts and acts on identified needs is by involving them in planning and decision making at all stages of service delivery. The community members should feel that the program is owned by them rather than the health worker or the government. For effective assessment, it is essential to interact with a large number of people representing all socio economic groups in the village such that, in a short time, all the relevant information is collected. Thus, any method which encourages people’s participation in expressing and analysing their views will be an effective method for assessing community’s needs. This is known as Participatory Learning for Action (PLA). The PLA consists of a process of communication which enables active community participation in analysis of the situation and based on the analysis, plan, implement and monitor services relevant to their needs. The complete process involves.

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1. Assessment of needs. 2. Analysis of problems. 3. Actions to be taken for correction. It is referred to as the Triple A approach.

Methods of PLA [5] The following PLA methods are more commonly used and recommended: 1. 2. 3. 4. 5.

The chapatti diagram Village transect walk Participatory mapping The seasonality diagram Relative ranking

(1) The venn (chapatti) diagram. These diagrams show relationships of various institutions, organizations, programs or individuals with each other and with the village as perceived by the villagers. The purpose of venn diagram is to examine the community’s access to different services, that is to say how easily available are the services to them such as health centres, schools, balwadis, block development office, agriculture office, electricity office, irrigation etc. This exercise can be conducted by following steps: ● ●

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At the meeting place, a circle is drawn to represent the village. Participants cut papers in circles to represent services according to their availability in rendering the service e.g., a hospital may be represented by a large circle. They can arrange circles of different sizes as per their utility to them in descending order so that the sizes reveal their accessibility. The services close to the village are placed closer to the circle representing the village, and the services which are more difficult to reach in distance are placed farther away (Figure 38.4). Similar exercise, using the venn diagram is also undertaken for a specific service, e.g. care and services of pregnant women (Figure 38.5).

(2) Village transect walk. This is an observatory walk through the village living area, observing and making notes of the layout of the village, housing, drainage, backyards, infrastructure such as schools, shops, wells, health facility etc. This is a pre-requisite for mapping. This walk also helps to locate areas in the village which are in need of greater attention/ development. The village transect also gives a greater insight into the aspects of village life that are of a social nature such as caste, religion, customs, culture, health and interactions between various groups. Through

District and village planning – a decentralised implementation...

38.4 Venn diagram – services available at a village level.

38.5 Venn diagram – care and services to the pregnant women in a village.

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this exercise, it is attempted to determine the ownership, type, productivity and present status of different resources from an area’s geographical conditions by conducting the following activities. ●

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First, select persons from the community with good knowledge of the area’s resources. Divide them into two groups, e.g. A and B. There should be a facilitator in each group who is responsible for conducting these exercises. In each group, start with a boundary of the area and set a distance e.g., 20 m, 30 m or 50 m (decided by the community). Collect information about all resources within that distance, including ownership, types, productivity, and uses. For example, Group A could begin on one side of the selected area and continue until they reach the other boundary, while group B could start at a different location as shown in the picture below. Usually, two groups take two opposite routes, one going vertically across the village and the other horizontally. Collect information about different resources on the basis of aforementioned parameters. For example, for water we would note canals, hand pumps, tube wells, public taps, ponds, irrigation tanks, etc. In this way, both groups will continue to gather information as they continue from one side of the area to the other.

38.6 Village transect walk.

(3) Participatory mapping. In this method villagers’ groups undertake social and resource mapping of the village using chalks, coloured rangoli powder or other locally available materials. (i) Social mapping – social mapping is an exercise to study social structures of an area, including elements such as households, castes, community centres (gathering places, temples, well, panchayat ghar, ration shop for PDS, veterinary centre, cooperative bank, health

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sub centre, shops, post office, bus stop etc), ratio of male / female and literacy status. The steps followed in social mapping are: ■ This exercise is done in an open area. ■ Facilitators must ensure participation by people from different castes and ages. Both men and women must participate. ■ With the use of local materials such as coal, sandstone, and colored powder, participants are encouraged to map their local area. ■ The map presents location of commonly used places, such as health centres, veterinary centres, ICDS Centres, schools, mahila mandal gathering places, panchayat etc. ■ On the basis of participants’ knowledge about the area, participants will create such a map. ■ The facilitator must systematically collect and record information gained. ■ It will aid in studying the socioeconomic status of the village. The habitation of different castes separately and together will emerge. The exercise helps eventually in identifying names of the head of the family, the castes pattern and their habitations, number of men/women/ children and distribution of different age groups, their literacy status, main as well as other occupations, the livestock and grains and vegetables grown by the family in the land etc. (ii) Resource mapping – resource mapping is a study and analysis of resources like water, forest, land etc. The existing situation is mapped and the resources available are analysed. Following method is followed for conducting resource mapping: ■ In a community meeting, participants draw a map of their village using local materials. ■ In this map, different resources are represented by using specific signs and materials. ■ By using specific signs and materials, participants are encouraged to distinguish and classify specific types of resources. For example, different types of water resources include river, ponds, canals, tube wells, irrigation tanks, hand pumps, etc. ■ By this method information on most aspects of rural life, resources within the community, location of various social and economic groups and houses of beneficiaries like pregnant mothers and children with diseases is put together in a visual map (Figure 38.7). (4) The Seasonality diagram. This exercise helps to understand the seasonal problems related to disease prevalence, cropping pattern,

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employment etc. Additional information on events such as needing a loan, grains for sustenance, festivals, sickness and weddings are collected. The activity is conducted as follows: Represent each event with a different, locally available material, for example, a scarcity of food could be represented with a small quantity of such grains. Another example could be that during the rainy months of June and July, people have greater need for money due to lack of livelihood and may need loans. This could be represented by coins. Loan needed January February March April May June *** July *** August September October November December

Grains Festival Illness Seasonal Drought Migration Wedding rainfall

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Another seasonal exercise useful in health programmes is to analyse the months in which children suffer from diarrhoea or respiratory diseases. By this exercise, we can work with community to increase their understanding of courses and effort to be made to prevent and manage diarrhoea and acute respiratory infection. (5) Relative ranking. This method indicates the priorities and the preferences of the people. It is a very useful method if the list of felt needs is long and prioritization as per their needs has to be done.

38.6

Village plan to district level plan

The understanding gained from this community needs assessment and the use of the triple A approach results in development of a plan for the village which can effectively use the resources of the community for the best result and ensure their participation to achieve the desired targets and goals related to health. Figure 38.8 shows the village level process and the collation of data up to the district level.

38.7

Conclusion

In conclusion it can be stated that the district health planning is now being followed under NRHM. All states use district planning as the base from which to formulate the Project Implementation Plan (PIP). Over the years,

District and village planning – a decentralised implementation...

38.7 Resource mapping at village level.

38.8 Village level process and collation up to district level [3].

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based on lessons learned, the district planning activity is continuously being refined and effort is being made to make the data base projections realistic. District plan of action also forms the basis for measuring achievements and for documenting the constraints faced in achieving the stated targets.

References 1. District health management team training module: planning and implementation of health services, WHO Regional Office for Asia. 2. The State of Panchayats: 2007-08, An independent assessment. Volume I, Thematic report. Chapter 3a, pp. 117–134. Govt. of India, April 2008. 3. Broad Framework for Preparation of District Health Action Plans (2006). Ministry of Health & Family Welfare, Govt. of India. 4. Training of Auxiliary Nurse Midwives for “Building Effective Community Partnerships for implementing the Reproductive and Child Health programme” Facilitator’s Guide. Ministry of Health & Family Welfare, Govt. of India. 5. CORD. CORD training manual, Book 1. CORD’s Resource and Lead Centre, Sidhbari, Himachal Pradesh.

39 Nutrition–Health education and communication for improving women and child nutrition Shubhada Kanani

Shubhada Kanani, PhD, has been a faculty member in the Department of Food and Nutrition, the M.S. University of Baroda, Vadodara, India, for the last twenty two years. Her areas of expertise include nutrition anthropology, nutrition program management and evaluation, health systems research, gender sensitive nutrition research, and nutrition–health education communication. In particular, Dr. Kanani has been a trainer to build capacity in qualitative-participatory research, and behavior change communication interventions including methodologies such as Trials for Improved Practices (TIPS).

39.1

Introduction

One has heard these familiar lines: Give a man a fish, and you feed him for a day; teach him how to fish, and you feed him for life. This underscores the crucial importance of self-empowerment; and one of the most effective and long lasting empowering tools is knowledge. This chapter traces the beginnings of nutrition-health education, its critical importance in the prevailing nutrition scenario of the country and the emergence of the behavior change focus in program settings. This is followed by an overview of experiences and lessons learnt from major international and national projects. Key elements in the design of a successful behavior change intervention are described with the hope that readers can apply this knowledge in their own settings.

39.2

An operational definition of nutrition–health education

Although nutrition is a discipline distinct from health (including public health), in practice, nutrition services are most often linked to health services

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and commonly monitored in terms of both nutrition and health outcomes. Secondly, operationally speaking, education and communication programs for improving nutritional status are implemented under the umbrella of national health and development programs. Thirdly, nutritional improvements depend as much on addressing health disorders (for example, diarrhea) as they do on ameliorating nutrient deficiencies. Hence, integrating nutrition and health issues in education and communication efforts makes sense from both, the biological and programmatic perspectives. With this view, the term Nutrition–Health Education (NHE) refers to a systematic process, focusing on behavior change; that educates and facilitates people to understand the significance of optimal nutrition-health practices and to make the best use of available food–health and care resources with the ultimate goal of improving nutritional and health status. This definition encompasses the importance of both knowledge and behavior change and keeps in focus the eventual goal, which is improving the state of nutrition and health. Thus, effective NHE is one that ●

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enhances knowledge regarding desirable nutrition-healthcare practices; positively influences attitudes and traditional beliefs; motivates vulnerable families to act on that knowledge for their own health and nutritional well being.

An important feature of good NHE is that it is culture and gender sensitive; for example, in a country like India, NHE should acknowledge girl child discrimination and women’s constraints.

39.3

Why is nutrition–health education important?

Undernutrition, especially among women and young children from low socioeconomic strata has a multi-factorial etiology which includes the triad of food insecurity, infections coupled with poor access to health services and inadequate caregiving attention towards both, the woman and the child. NHE has the potential to address all these factors in an integrated manner. Secondly, NHE helps create demand for the available nutrition and healthcare services which often remain under-utilized simply because beneficiaries are not aware of them or their benefits. For example, educating women about the benefits of iron-folate tablets and how to manage side effects (if any) through effective NHE helps create a demand for these tablets and improves compliance. Thirdly, contrary to what is widely believed, NHE does show a positive and significant impact among vulnerable groups even in poverty situations – if designed, planned, implemented and evaluated properly by committed personnel.

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How can NHE favorably influence nutrition–health-care practices in households [1]? Following are few examples with reference to nutrition: ●

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In poor communities, NHE can play an important role in educating families regarding best use of available resources. Even if calorie adequacy is ensured to some extent through increased income, effective NHE is often needed to bring about qualitative improvements in diets such as enhancing levels of several important micronutrients like vitamin A, iron and iodine. Due to strong traditional beliefs (rather than inadequacy of resources) foods are often withheld or given in inadequate amounts to infants or women. Feeding is discontinued during diarrhea. NHE has a strong potential to counter harmful beliefs and to change dietary practices. Urbanization, misinformation by health/medical practitioners and influence of mass media erode healthy traditional practices, like breastfeeding and encourage development of unhealthy lifestyles and food habits. NHE can help reverse such unfavorable trends and reestablish favorable practices. There is often an inability by parents or caregivers to recognize malnutrition (poor weight gain) in preschool children, especially 6– 24 months of age. When moderately malnourished children (about 40% in India) escape notice, and are deprived of prompt attention in the early stages of growth faltering; many slip into severe malnutrition. NHE can help families and communities identify and recognize the ‘invisible’ problems of malnutrition so that timely remedial measures can be taken. NHE creates demands for services such as iron folic acid supplements, vitamin A supplements and other services.

Further, effective NHE which improves both awareness and practices can accelerate our progress towards achieving several of the Millennium Development Goals (MDGs) pertaining to not only child and maternal health but educational goals as well.

39.4

Shift in focus from nutrition education to behavior change communication

The beginning of modern nutrition education may be traced to the early attempts at prevention of protein energy malnutrition (PEM) in infants and children, primarily due to faulty complementary feeding. The need for nutrition education in developing countries gained international recognition in 1950 with the first report of the Joint Food and Agriculture Organization / World Health Organization (FAO/WHO Expert Committee on Nutrition, which emphasized the importance of

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nutrition education in the health sector. By 1958 the same committee reported, “Education in Nutrition is a necessary part of practical programs to improve human nutrition...” and recommended as channels for nutrition education, schools, maternal child health (MCH) and public health centers, community development and related programs as well as agricultural extension and home economics extension services. The 1960s saw an emphasis on audio-visual aids and the creation of programs such as the Applied Nutrition Programs (ANP), in which nutrition education was placed at a level of priority equal to that of other project activities, rather than being considered a casual adjunct to curative health [2].

39.4.1 From awareness to behavior change Since the 1960s, and in particular, in the last twenty years, health programs, and along with them nutrition programs as well, evolved in many ways. One noteworthy change has been in the paradigm shift from viewing NHE activities as ‘transfer of information to the intended beneficiary’ to NHE which ‘promotes and sustains behavior change based on the information imparted and knowledge given to the beneficiary’. For many years now, organizations have used the term “information, education and communication” (IEC) to refer to strategies to improve people’s awareness and practices. However, in implementation of IEC activities, the attention has remained limited towards increasing awareness without enough focus on whether practices have indeed improved. Since the 1980s, as experience accumulated and better understanding of communication and behavior change theories developed, the term ‘behavior change communication’ (BCC) has been the preferred terminology instead of IEC. BCC builds on IEC, and emphasizes that communication should be strategic and guided by systematic processes and behavioral theories with the objective of influencing practice. Strategic BCC programs use a systematic process to understand people’s situations and influences on behavior. They develop messages that respond to people’s concerns. They draw on behavioral theory, define clearly the specific objectives they want to achieve, integrate these objectives into their program plans, and use them as a basis for measuring success. Another important dimension of BCC programs is priority given to community involvement. Community participation can range from assisting with needs assessment, planning, implementing or evaluating activities to direct involvement in decisions about all aspects of program management, resource allocation, and assessing impact [3].

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39.4.2 Social marketing – a major contributor to the behavior change focus The term “social marketing” was first introduced in 1971 and described the use of marketing principles and techniques to advance a social cause, idea or behaviour [4]. With the emergence and application of the Social Marketing (SM) concept in the 80s and 90s, the significance and the means for behavior change promotion have been realized. SM is a systematic approach to solving problems, which is related to service utilization, product development and acceptance, and behavior adoption. Social marketing may involve both the selling of a commodity and the selling of an idea or practice; this also implies the promotion of a related attitude or belief which influences the nutrition or health practice. Social marketing is distinguished by its emphasis on “non-tangible” products such as ideas, attitudes and lifestyle changes. The central tenet is that effective strategies are based on the needs and interests of the target consumer. Empirical consumer research is used to identify possible consumer segments, to understand their needs in the context of their lives, and for developing appropriate programs and communication strategies to meet their needs [5, 6]. Since the fundamentals of SM approach come from marketing principles, program management is often structured to reflect a marketing operation (e.g. health workers are trained to become better sales agents for the program, not just deliverers of services); and a result orientation of marketing implies that progress is measured in terms of outcomes, not mere coverage. Planners need to have a conceptual overview of how a social marketing intervention works (Table 39.1) [7]. Table 39.1 Conceptual overview of a social marketing intervention [7] Stage (1) Planning research (2) Development of campaign strategy (3) Prerequisite training and networking activities (4) Project implementation activities (5) Summative evaluation

Outcome Behaviour change objectives and other project goals defined Messages, materials designed, products and services established Infrastructure prepared Social marketing campaign carried out Project outcomes assessed

Four features of social marketing (SM) highlight the unique aspects of SM and distinguish it from other forms of NHE – two are related to objectives and two are related to techniques of SM [5].

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Two major objectives of SM are aiming for change in behavior (not just imparting information) and creation of demand (concentrating on that half of the marketing equation that is often ignored – the people). The behavior change emphasis encourages social marketers to beam their efforts on strategies that result in adoption of a desirable practice – whether it is at the household level (example, adding green leafy vegetables to complementary food of a toddler) or use of an available service (taking the regular supply of IFA from the health centre and consuming the tablets). Unless information is relevant to changing behavior, it usually does not find a place in SM approaches. Behavioural change can be marketed to the individual directly (through direct action) or it can be facilitated by the provision of a new product or service (Table 39.2) Table 39.2 Marketing strategies for behaviour change objectives [7] Health outcome Family planning

Marketing/promotion focus

Manufactured goods, e.g. condoms Personal hygiene reduces Direct action incidence of diarrheal diseases Immunisation to children Service, e.g. administration of vaccine as per the schedule

Type of behaviour change objectives Purchase and use Skill and adherence Access and compliance

In the case of family planning, the products to be marketed are the means, e.g. condoms or other contraceptives by which contraception behaviour can be altered. An ideal family planning social marketing campaign should have the dual task of promoting (through more effective distribution, pricing and promotional mechanisms) a family planning product as well as providing consumers with the knowledge and motivation to appropriately use contraceptives. Some behavioural change objectives do not require the marketing of a supportive good or service. For example, marketing personal hygiene is a question of individual knowledge, skills and motivations. In this case, the products to be marketed are knowledge and practices that will facilitate in taking direct actions to solve their problems [7]. Projects such as Brazilian breastfeeding campaign, contraceptive marketing efforts in Thailand and Bangladesh, social marketing of vitamin A rich foods in Thailand and social marketing of iron folic acid tablets to women in reproductive age group in Cambodia, Philippines are examples of well designed social marketing interventions [7–10]. Box 39.1 presents details of a social marketing intervention.

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Box 39.1 Social marketing – vitamin A rich foods [10] The three year social marketing of vitamin A rich foods project was implemented in a district of north east Thailand between October 1988 and September 1991. The project used nutrition communication as its main approach for reaching 134 villages with a population of 122,000. The preliminary research (quantitative and qualitative) sought answers to four key questions:

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What is the vitamin A status and fat/oil consumption of people living in the target area? Who are the vulnerable groups for vitamin A deficiency?

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What potential strategies are available?

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Which strategies are feasible given existing cultural, economic and environmental conditions?

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The findings revealed that dietary diversification, as a long term strategy, would need to focus on local production and consumption of vitamin A rich vegetables. With proper knowledge and motivation, community members, through social gardens could produce enough vegetables for the entire year which were drought resistant. The research also segmented the intended audience into primary, secondary and tertiary groups. The social marketing strategy was used for a nutrition communication programme. The project design focused on gaining the support and confidence of national / local government administrators. New communication techniques were used to motivate the behaviour change process and there was influence from fields of marketing and advertising. It was recognised that while knowledge is important for change, there are a host of personal and environmental factors which play a role in the communication and behavior change process. Formative research was used to design the communication programme (i.e., identify factors that could influence adoption of practices, define audience and their needs, selection of food items), select and pretest media, materials and channels as well as monitor educational program progress and evaluate the projects success. All factors contributing to behaviours – personal, community or environmental – were taken into consideration. The campaign was implemented in three stages – first stage focused on creating and monitoring a nutrition information society. This was followed by ivy gourd as an image representing other vitamin A rich vegetables. The third stage entailed combining nutritional messages with concrete action programmes which was designed and carried out by community and local government collaborations. In the first stage, the focus was not only on ‘why’ a dietary or related practice needed changing, but on how this could be made feasible and acceptable. The second stage involved boosting the ivy gourd image. A social advertising approach was used. The communication strategy focused on fulfilling two specific behavioural objectives – raising community member’s awareness about ivy gourd and getting them interested in it as a food item. In addition of mass media communication (radio, pamphlets/posters, newsletters, public address system, cassettes, direct manual, direct mail), community action programmes, schooland community-based activities were also organised. Significant change in KAP (knowledge, attitude and practice) regarding consuming vitamin A rich foods was achieved. Ivy gourd was believed to be a food item of high nutritive value and was observed to be family and their children’s favourite vegetable. Over 50% families actively grew ivy gourd. Results revealed that the project most successfully changed the usage of green leafy vegetables by lactating women, mothers of preschool children and school children. Positive impact was also observed among government officials and the community.

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Demand creation is important because until we understand consumer needs; their view of ‘good quality’ in nutrition service or health care; and also cater to these needs, merely attending to the supply side will not help. When the importance of a service or a household practice is understood by the beneficiary and it is clearly perceived as meeting a felt need, then programs become more cost effective and behavior change is more rapid and visible. Two techniques which are integral to SM include ●

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using a feed forward approach as popularized by Dick Manoff: an approach that minimizes “feed back shocks”, that is, we first go to potential users of the messages or products being promoted to find out what they want, through formative research. focusing on creativity in message design and implementation strategy. Creativity is not just for message design where persuasive, captivating and memorable messages are the goal, but also developing program strategies through creative interpretation of research findings. Box 39.2 presents four principles of SM in practice.

Box 39.2 The marketing mix – the four P(s) of social marketing SM conceives of the consumer as the centre of a process involving four variables: product, price, place, and promotion [5]. ●

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A proposed Product (whether a commodity, idea, or health practices) is defined in terms of the users’ beliefs, practices, and values. If the community perceives diarrhea in 1–2 year olds as a ‘normal part of development’ or looks for medicines to stop diarrhea rather than prevent dehydration, these concerns need to be addressed while encouraging the use of ORS packets when a child has diarrhea. A product can be positioned using several different strategies including pricing attributes (e.g., regular consumption of iron–folic acid tablets by mothers for health of foetus), benefits (e.g., contraceptives that prevent unwanted pregnancies), or attributes (e.g., low price). Positioning strategy also can be applied to health related behaviour change objectives and are best positioned in relation to target audience “resistance points”. For example, for years breastfeeding was glamorized as the “ideal thing” to do whereas women viewed it as hard work. The successful media campaign in Brazil therefore positioned the media campaign with emphasis “breastfeeding is hardwork but is well worth that effort.” An element of empathy was introduced in the message and was reinforced by health professionals and community-based mother support groups. Price can refer to a monetary expenditure, an opportunity cost, a status loss, or consumers’ time. Even if a rural woman pays no money getting an ORS packet from the health centre, it does not mean that it costs her nothing. The day of travel to the centre to get her child examined by a doctor or nurse, the inconvenience to family, time taken to make the ORS at home, or the lack of conviction regarding usefulness of ORS may all seem too costly relative to perceived benefits. The price of a particular product is never fixed; it varies according to the target audience segment, and often according to the individual.

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The concept of Place refers to the channels through which products flow to users and the points at which they are offered. Product availability and distribution may involve not only retail and wholesale supply system, but also the efforts of health providers, volunteer workers, friends and neighbours. “Place” may be a store, a health centre, or even a person such as a traditional birth attendant who carries a supply of ORS. In any SM activity, Promotion requires more than simple advertising. It requires extensive consumer education to assure appropriate use of products. Motivational strategies are also essential in encouraging adoption of new ideas and social products. Correct ORS packet utilization or even educating households on how to make home-made ORS requires culturally sensitive and relevant promotional activities.

39.4.3 Focus on education for “optimal food intake” rather than “nutrient requirements” Many countries have dietary guidelines expressed in scientific terms, with quantitative recommendations of nutrients and food components (Recommended Dietary Allowances – RDAs, Reference Nutrient Intakes – RNIs, or Recommended Dietary Intakes – RDI). However, such recommendations are commonly misunderstood and often applied inappropriately by both nutritionists and the public. Realizing the limitations of ‘nutrient-based guidelines’ for public education, the ‘ICN Plan of Action’, adopted in the 1992 International Conference on Nutrition (ICN) of FAO–WHO, included a significant section, ‘Promoting appropriate diets and healthy lifestyles’. It stated, ‘Governments are called upon ...to provide advice to the public by disseminating qualitative and/or quantitative dietary guidelines relevant for different age groups and lifestyles and appropriate for the country’s population’. The ICN Plan of Action is notable for the absence of numerical targets for food and nutrient intakes. This indicates broader thinking among nutritionists, away from policies dictated by nutrient recommendations toward ones defined by prevailing public health issues and consumer needs. Subsequently to the ICN Plan of Action, Food-based Dietary Guidelines (FBDG) were developed by FAO–WHO after an international consultation in 1995 [11]. FBDGs are intended for use by the general public; and provide nutrition education and dietary guidance in terms that are understandable to most consumers. FBDGs are a practical way to assist people to reach appropriate nutritional goals, as they take into account customary dietary patterns and indicate modifications needed to address particular concerns; they are based on diets (foods) and not nutrients. These guidelines consider the total diet; they recognize the varied social, economic, agricultural and environmental conditions that affect eating patterns and acknowledge that various dietary patterns can be consistent with good health. They strive to ensure that they are easily understood by the people at various levels of literacy, refer

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to foods wherever possible, rather than nutrients and recommend use of educational approaches that avoid radical changes in current dietary practices, but rather build on existing practices. According to FAO [12], the National Institute of Nutrition, India, initiated the process of developing FBDGs in 1997 and published and disseminated these guidelines in 1998. Some examples from these guidelines are as follows: ●

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Nutritionally adequate diet should be consumed through a variety of foods. Green leafy vegetables, other vegetables and fruits should be used in plenty. Cooking oils and animal foods should be used in moderation, and vanaspati/ghee/butter should be used only sparingly. Overeating should be avoided to prevent overweight and obesity.

39.4.4 NHE – holistic approach for addressing undernutrition Over time, it was clearly evident by practitioners of NHE programs that NHE needs to be holistic; given the fact that malnutrition and disease have a multifactorial etiology. The UNICEF conceptual model for childhood malnutrition (Figure 39.1) has accorded higher focus to NHE and has included all the three primary dimensions – food, health and care – for addressing undernutrition. This model set the stage for further development of NHE as an integrated intervention and not merely limited to influencing food or nutrient intake. As the UNICEF framework reveals, the immediate causes of malnutrition and death are inadequate dietary intake and/or disease which in turn are caused by conditions that affect (1) household food security; (2) health services and healthy environment; and (3) care for women and children, especially care of the girl child. The framework further reveals that the basic causes of undernutrition relate to poverty (poor availability of resources), social status (women’s inferior status) and the government policies and priorities. Thus, while NHE needs to have a clear focus on selected behaviors, it also needs to take into account the underlying and contextual factors influencing the behaviors and the problem being addressed.

39.5

Design and implementation of a nutrition health education program with a communications perspective

The acid test of successful NHE is that practices improve significantly in a majority of the vulnerable households in a sustained manner, and eventually become a ‘norm’ in the community. In the area of nutrition and

Nutrition–Health education and communication for improving ... M alnu tritio n in C h ildre n & W o m e n

In ad eq u ate d ieta ry in take

In ad eq u ate a ccess to fo od

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In ad eq u ate E d uca tio n R e so urce s & C o ntrol H u m a n, E con o m ic & O rg an isatio na l

B a sic cau se s

P o litical & Ide o lo gica l facto rs E con o m ic Structu re

P o te ntial R e so urce s

39.1 The UNICEF conceptual model for childhood malnutrition [13].

health communication, many communication models and theories have been put forward. In this section is presented an adapted version of a simple and comprehensive model by Hubley (1993) [14] which gives four components of a communication process—these could be applied to any communication strategy. This framework has been found to be useful for imparting training on communication skills to grassroots functionaries and supervisors.

39.5.1 The receiver (audience) It is absolutely critical to first become familiar with the belief systems, current practices, family and community environment of the intended audience. A method that will be effective with one audience may not succeed with another. Different individuals respond differently to the same message, one reason being differences in the characteristics of the receivers themselves. For example, a rural woman or adolescent will respond very

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39.2 Components of nutrition–health education communication [14].

differently to the same message compared to the urban counterpart. Similarly, less educated groups will receive a message differently compared to better educated groups. There are myriad differences among different ethnic groups from different regions; even in the same region or cultural group, among families at different socio-economic levels and so on. Secondly, it needs to be realized that the recipients do not form a homogeneous group; and that audience segmentation is required. Communications should be directed not only at the key beneficiary but also at the persons who influence the primary recipients of message in the family and community [14, 15]. Segmenting recipient groups or the target audience is important and it is critical to identify ●

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The primary target audience: those who will actually perform the new or modified nutrition–health practices. The secondary audiences: those who can be motivated to teach, support, and reinforce the practices and beliefs of the primary audience (e.g., health care providers, family and friends).

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The tertiary audience: decision-makers, financial supporters, and other influential people who can make the program a success.

Design a different communication strategy and different educational materials for each. Given limited time and resources, designate the audience segment most critical to program success. Using formative research, ensure that the following questions are answered: ●

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What are the behaviours of our audience groups and how can we describe them? What influences their behaviours? What are the underlying beliefs, gender issues? What is the role of culture, their family, and economic factors in determining behaviours? Which behaviour change messages will meet program needs as well as audience needs?

Formative research helps to understand the cultural, social, economic and political factors that influence beliefs and behaviors of the target groups. The results of formative research aid in establishing measurable objectives and realistic strategies for the communication program. Some commonly used methods for formative research include the following ●

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Focus group discussions (FGDs) – They bring together eight to ten respondents typical of the intended target audience. A trained interviewer uses a prepared list of probing questions to collect information on vocabulary, attitudes and concepts related to the selected nutrition problem. Here the group atmosphere may stimulate more in-depth discussion than individual interviews do. Also insights into commonly held beliefs can be obtained relatively quickly. Individual in-depth interviews – They build on information gathered during other research efforts, to probe deeper into individual attitudes and concerns. They are useful when sensitive topics are addressed, when issues must be probed deeply, when individual rather than group responses are needed, or when it will prove difficult to gather respondents for a group meeting. Participant observation – The researcher participates in the daily life of the community he or she is studying- observing what is happening, listening to what people talk about, asking questions in various ways over a period of time. Direct observation – The researcher observes, but does not participate in an event. She usually has a checklist of behaviors to be observed and a recording format for the observations which may be unstructured or structured.

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Informal conversations – The researcher takes advantage of any opportunity to converse informally either individually or in small groups with the members of the community being studied. Ethnographic studies – They combine anthropological open-ended techniques to analyze how specific nutrition practices relate to the larger cultural context. An ethnographic study may employ several qualitative methods in a complementary manner to get a holistic picture of the nutritional problem.

Analysis of formative research and setting objectives Analysis of the formative research results helps to identify the gap between the desired and the current behavior which is sought to be addressed through the NHE program. Define the expected behavior in as much detail as possible; specifying not only what the behavior should be but who is to carry it out and when. This in turn helps to set and refine the objectives. The objectives of NHE program could be related to improving understanding of a practice (cognitive) or improving the practice itself (behavioral). They must preferably be quantifiable and should cover the different dimensions of the communication effort such as exposure, knowledge, behaviour adoption and outcome. For example, As compared to baseline, after ‘y’ months of implementation of NHE, ●

●

●

●

X% more in the target audience will have heard a radio programme, or possess a growth chart, or have attended anganwadi sessions (Exposure). X% more in the target audience will state that children need to start on complementary foods at 6 months, or x% more will know where to obtain ORS packets (Knowledge). X% more of the target audience will report introducing their child to complementary foods at 6 months or will state treating child’s episode of diarrhea with ORS (Behavior Adoption). Nutritional status due to the targeted nutritional problem will be reduced by X% in the target audience (Outcome).

39.5.2 The communicator (source) A sender or communicator is the source of the message. S/he is the most important component of the communication program and may be the primary factor underlying the failure or success of the program. A poor message in the hands of a good communicator is better than an excellent message in the hands of a poor communicator. The reason why the same individual responds differently to different communications is often because of the characteristics or attributes of the communicator. People are exposed to communications from many different

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sources and more likely to believe a communication from a source they trust, has high source- credibility. For example, a pregnant woman is more likely to believe and follow a village dai’s (trained birth attendant) or Auxiliary Nurse Midwife (ANM) advice regarding her diet compared to a nutrition educator or health worker coming from another community or background. If nutrition and health care program functionaries are not adequately equipped with the skills of how to communicate the messages, there is likely to be very limited impact on actual behavior change. In fact, managers, trainers, supervisors and functionaries need to reflect equally on their own behaviors and attitudes and change these first before reaching out to the community and make a difference. With training, practice and above all, an understanding and empathetic attitude, most of us can become reasonably successful communicators, provided the required effort is made.

39.5.3 The message The message consists of what is actually communicated including the actual appeals, words, and pictures and sounds that the communicators use to get the ideas across. A message is a methodically designed communication for information and/or motivation. A nutrition communication message must be based on a thorough understanding of the behaviors underlying the nutritional or health problem. If the various audience groups are well understood; including the reasons underlying their behaviour, it is more likely that effective and focused messages, which are relevant to the audience, will be imparted. Secondly, a well designed message addresses itself clearly to the problem to be dealt with. Messages should be practice oriented and do-able. More time, patience and perseverance will be required for changing the more complex behaviours (e.g. complementary feeding) than relatively simpler behaviours (e.g. initiating breastfeeding within an hour of birth). Thirdly, a good message takes into account the resistance points to the desired action and has a motivational element. For example one reason why pregnant women may not increase their diet in pregnancy is because messages often do not take into account the resistance factors (why women believe it’s harmful to increase food intake) or are unrealistic for the women to follow. Formative research as well as the process of pretesting of messages, including using a method called ‘Trials for Improved Practices’ or TIPS (see below) are useful to identify resistance points in the audience for each message as well as ways of overcoming them. Pretesting messages Pretesting is essential for ensuring that the content and the accompanying visuals are understood and culturally acceptable to the recipient groups.

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Thus, once messages are drafted and a series of visuals are prepared, interviews are conducted with representatives of the intended audience in order to test the message and visuals. Pretesting helps project staff know whether the draft materials are understandable to the target audience. Through pretesting, it is possible to find out how well the message is communicated and the visual is understood by the recipient groups in terms of their understanding the symbols and pictures correctly; the content of the message and its relevance to their own lives and needs; whether there are unnecessary details. Pretesting should be done before the materials are finalized so that they can be revised based on the audience’s reactions and suggestions. Most materials must be pretested and revised several times. Each new or revised version is tested again until the material is well understood by, and acceptable to, the target audience. Pretest sites must be similar to those of intended audience for communication so that there are greater chances of the pretest predicting the responses of the audience. Developing strategies to change behaviour require knowledge of not only how materials are acceptable to audiences (pretests) but also information about improved practices that are acceptable and feasible for families. All practices should be tested, ideally in people’s homes, before they are recommended. This is done through Trials for Improved Practices (TIPS), which may be done simultaneously or before material pretest [16]. TIPS is a frequently used method for pretesting messages and recommended practices among mothers and caregivers; who are given a choice of recommendations for action, questioned about their reasons for that choice and then followed up (usually after 2–3 weeks) to see what actually happened after the trial period. In this way the proposed recommendations are tested in a real environment and information is gathered on their acceptability. This information helps program planners to set priorities among the many seemingly important nutrition practices and messages. TIPS usually follows formative research in which the behaviors to be targeted for change have been decided; and counseling material has been prepared for each behaviour. Table 39.3 below gives an example of a counseling guide that was prepared for TIPS prior to initiating an intervention to improve household dietary practices among pregnant and lactating women in Angarah block in Ranchi, Bihar [16]. The TIPS experience proved to be invaluable to design communication materials and strategies in this project.

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Table 39.3 A section of the counseling guide prepared to the TIPS process related to improving diets of pregnant women in Angarah, Ranchi Behaviour change recommended

Benefits

Expected resistance

Response

Improve quality of food eaten at home: (a) Eat at least one katori of Saag (50 g) four or more days of the week (b) Eat an egg at least twice a

●

●

●

week

Raataundhi (Night blindness) can be prevented Woman gets strength, does not breathless

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●

(d) Eat ripe papaya 1–2 times a week or more

●

●

feel weak, tired,

(c) Eat ripe (not raw) pumpkin 2–3 times a week or

Woman’s blood improves

●

Recovery from delivery is faster

Saag (green leafy vegetables

Saag (GLV), when plucked from veg-

–GLV) quantity not enough for family

etable gardens or the farms, should be plucked in more

Eggs are expensive, not cooked

quantity to last for 2–3 days a week

frequently ●

●

●

1–2 Kadchul

Ripe papaya,

(tablespoon) should

pumpkin are not available in

be left aside for the woman at mealtime

Lactate better

market, are

Child’s development– improves physical and mental

expensive

●

Women should buy egg during the market visit and eat it there

●

These foods not only benefit the woman but also the fetus; explain the benefits especially of Saag, ripe papaya, ripe pumpkin, egg

39.5.4 The channel This is also referred to as the communication method; the medium, the delivery system or a vehicle for communicating a message. There are basically three types of channels or vehicles to carry the messages [14]: (a) Face-to-face (‘interpersonal’) (b) Mass media (c) Traditional/folk media (a) Face-to-face or interpersonal methods include all those forms of communication involving direct interaction between the source and receiver: One-to-one counseling; small group counseling (less than 12 persons); intermediate group/lecture (between 12 and 30) and large group lecture/ public meeting (more than 30). The advantage of face-to-face method is that it is possible to contact specific groups, make the advice relevant to their social needs, develop problem-solving skills and community participation. It creates

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opportunities for questions, discussion, participation and feedback. However, face-to-face methods are slower for spreading information in a population because of the need to mobilize field workers and travel to different communities to hold meetings. A communicator may be ineffective if s/he is “ill-informed, uses an unsuitable approach, or holds a status in the community felt to be inconsistent with his/her role”. Further, as the size of the group increases, it is more difficult to have feedback and discussion. Many persons feel shy speaking out. Person-to-person education carried out by paid workers is often difficult to justify in terms of cost-effectiveness. (b) Mass media include broadcast media and print media – It provides a rapid way to reach a very large (even non-literate) audience; makes good use of scarce manpower and can be inexpensive, at least in terms of cost per person reached. However, as mass media are broadcast to the whole population, it is not possible to make the message appropriate to the special situation of local communities, whose problems and needs may be different from the rest of the region. Mass communication cannot possibly have the required cultural, linguistic, and social sensitivity nor receive individual feedback that will help assure that messages are relevant, appropriate, and understood by the audience. (c) Traditional media – This includes traditional forms of communication such as storytelling, drama, song, dance, proverb telling and puppetry. Community gatherings, religious meetings and ceremonies can also provide opportunities for NHE. A well-planned NHE program will involve a carefully chosen mix of the following media. Visual aids are a common tool used for communicating messages and the following are the key features of a good visual aid. ●

●

●

●

Only one key action message is depicted on each visual; not more. Other related messages/explanatory notes may be behind the visual (e.g. back of a flash card) or in a separate guidebook. The visual has many pictures; is culturally appropriate and easily identifiable by the audience. If words and numerals be used, they are as few as possible and the size of the words is large enough for all in a group to be able to see clearly. Colours can be liberally used as they can increase the effectiveness of a picture and emphasize key points; provided they are appropriately used. However, if budgets are limited, even black and white or just two color visuals are effective if they are well made and used properly. More important than the visual itself is the proper use of the visual aid or other channels – for example, using it effectively to hold the group’s interest, arouse curiosity; encourage questions and experience

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sharing. The aid is held such that all can see it and adequate time is given to point out and explain the message given on the visual or multi-media/print channel.

39.6

Evaluation of NHE programs

Evaluation is defined as a systematic and scientific process determining the extent to which an action or set of actions were successful in the achievement of pre-determined objectives [14]. Evaluation involves assessing whether NHE resulted in making the difference that was planned and that the amount of effort required to produce the change was worthwhile. Evaluation should be built into all phases of program planning, implementation, and management. Evaluation plans should be integrated into program planning phase for process evaluation and impact. Evaluation of NHE implies the objectives are defined precisely with details of specific outcomes expected under defined conditions. Many evaluations show that program planners consistently underestimate time and effort needed to adopt a new practice. Thus, a well-planned NHE program may fail at the implementation level, hence continuous monitoring is essential. It is much better to change a program during implementation than await a retrospective analysis to find out where it went wrong and who was responsible for the failure – when it is too late. NHE programs have a lot in common in the evaluation process of other nutrition–health programs. However, additionally, NHE process evaluation needs to consider whether in keeping with the behavioral objectives, the communicators (functionaries) are reaching the primary-secondary audience groups with communication strategies decided and at appropriate frequency; and the audience is attending the various program activities in sufficient numbers (coverage); understanding and implementing the messages in the desired manner. Since an important function of process evaluation is to provide information about the match between program design and implementation as well as deficiencies needing attention, the results should be fed back to project managers and staff on a continual basis and prompt corrective action taken. To conclude, both process and impact evaluation together provide a comprehensive picture of whether the NHE is being implemented in accordance with the objectives and whether impact is being achieved; what are the modifications required in the next phases to enable goals to be reached.

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39.7

NHE in action – successful program experiences

When NHE programs are well designed, implemented with a strong BCC emphasis, they have shown results. An overview of some such programs is presented below.

39.7.1 The Nutrition Communication Project (NCP) of The Academy for Educational Development An international project was implemented by USAID supported Academy for Educational Development (AED), with many international and country level partners including those in Government and NGOs [17]. Essential Principles for success in improving nutritional practices as analysed from the evaluation results of six country projects of NCP are as follows. Select specific action-based behaviors. Experience shows that focusing on a limited set of very specific behaviors is key to improving nutrition. These behaviors must be practical for the target audience to implement – in terms of cost, time and compatibility with existing practices and beliefs. Give attention to coverage and maximize exposure. Interpersonal, community and mass media channels must be maximally used to reach sufficient numbers of each different target audience to achieve impact. A combination of channels is usually most effective. Frequency of contact, and repetition of messages, is important. Create social support. Nutritional habits are deeply imbedded in family tradition and local customs. Behavior change can be facilitated by identifying each of the groups of people that influence the target audience or can facilitate the behavior by contributing financial, emotional, or other essential support. Different messages and strategies are required for each. Aim for simplicity. Most important is to begin getting the message out. Strategies should be simple to start with. New audiences and additional channels can be brought in gradually. Pursue a long-term effort. Messages must be conveyed with enough saliency and for a long enough time that the practices being promoted become routine behavior, fully supported by social norms. Structuring interventions. Nutrition social marketing offers a unique opportunity to integrate disparate health, population, and agriculture interventions. Capacity building. Beginning with a short pilot phase (12 months or less) and limited goals can be a highly effective way to strengthen the capacity of implementing agencies and individuals and to build confidence.

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Monitoring. Adequate monitoring (usually neglected) is an essential tool for understanding operational dynamics and for detecting what does and does not work in nutrition education interventions. Documentation of program inputs and implementation experience is essential to understanding program success and failures. Evaluation. Projects do not always learn as much as they can about what works and what doesn’t and under what circumstances. Systematic evaluation is critical to learn valuable lessons, to disseminate the success stories, to advocate for more resources and a higher priority to behaviour change interventions. In addition, support and involvement of policy makers, government officials, program managers and other decision makers for strengthening nutrition communication programs by focusing on following actions is critical. ●

●

●

●

●

Give nutrition communication higher priority and adequate resources, including staffing with well-trained program managers and health educators. Link nutrition interventions to other health and socio-economic development programs. Provide an adequate time frame and longterm commitment of personnel. Enlist help from universities and other groups with essential expertise that government and development organizations rarely keep in-house. Focus on the minimal per-recipient recurrent costs, rather than the cost-intensive start up, when making budget decisions. Remember that communication will be only part of the solution and that intersectoral collaboration and commitment of resources for development are also necessary.

39.7.2 NHE for behavior change based on the positive deviance concept The term ‘positive deviance’ has been used to describe the performance (regarding health, growth and development) of certain children vis-à-vis the performance of other children in the community and families. It has been seen as a form of social, behavioral and physiological adaptability to nutritional status [18]. The application of the positive deviance concept implies that household level factors related to feeding, health and care-giving of children are identified in those families where children are growing well (at rates equal to or higher than the relevant growth standard for that region) – the positive deviants. This knowledge of determinants of positive growth in positive deviant children who live in the same impoverished environment as other malnourished children (for example, feeding and hygiene care practices)

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should be used to develop and implement education and communication strategies to rehabilitate other malnourished children. Successful BCC interventions to improve child feeding practices and nutritional status based on the PD concept have been implemented in many countries, a few of which are illustrated here. One of the well known PD models is PD-Hearth model [19, 20]. In the intervened communities, small groups of mothers (4–5 or more) having malnourished children (below 2 or 3 years) met daily for 2–3 hours at the house of a volunteer mother (having a positive deviant or PD child) where they received nutritionhealth messages and their child receives a well balanced meal. Nutrition Health messages and meal components were determined using information gathered from interviews with the mothers of PD children in the community who were well nourished despite their family’s limited economic resources. These Hearth participants were then followed for a specified period (for example, six months) in their own home by the program village functionaries (known as “monitrices” in Haiti) who were women hired from each village and intensively trained to supervise the Hearth program. They also periodically weighed the children to evaluate their progress, and liaise between health centers/hospitals and the community. The PD informed Hearth approach has been adopted to suit regional needs and conditions and also has been systematically monitored and evaluated; for example, in Haiti and Vietnam. In Haiti [18], where the program was known as Ti Foyer (Hearth) Community Based Nutrition Model, monitoring data indicated that a majority of children (above 50%) in intervened villages continued to gain weight as fast or faster than the international standard median, six months after participating in a Hearth program. Similarly, technical deliberations held by CORE-PD-Hearth Expert group in 2002 [20], distilled the lessons learnt from several PD-Hearth interventions and the findings pointed out to the effectiveness of this model for improving child feeding – health care as well as growth velocity; though there were considerable variations between country experiences, as expected. The highlights from the “VISION Project” (Vietnam Study to Improve Outcomes In Nutrition), were presented; this was a partnership between Save the Children, Emory, AED, and the Research and Training Centre for Community Development in Hanoi, with support from USAID and the Linkages project. Research-based evidence pertaining to many of the important quality aspects of a successful PD/Hearth model in Vietnam revealed the following impact on children and women: (i) Growth – Though overall, the intervention children did not show better growth than comparison children, children who were younger (less than 15 months old) and more malnourished (less than –2WAZ) at baseline had significantly better growth than similarly young, malnourished

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comparison children. Intervention children consumed more food and energy and had fewer respiratory illnesses than comparison children. More significant impact seen among younger children was believed to be due to 3 factors: high velocity of growth rate (weight gain/month) in infancy, high prevalence of growth faltering and hence greater impact, and the fact that it is easier to prevent growth faltering than reverse it. (ii) Empowerment of women – Participant mothers reported increased knowledge and confidence in child feeding and care practices and increased sharing of advice with others (such as mothers-in-law, neighbours) as compared to comparison mothers. The Vietnam project demonstrated that a message given through lecturing had no effect but a message based on dialogue and problem solving did produce a change. Peer reinforcement through dialogue was helpful. Many of the messages provided by trained health workers were not effective, since they wanted to “tell” what to do, rather than help people understand that the recipes and knowledge came from the community. Thus, it is important to involve the volunteer health workers in nutrition health education activities. Some findings from the evaluations that negatively impacted on the program’s success in Vietnam were long distance travel by care givers and children to the Hearth sessions (in some sites), workload of women restricting participation, less impact seen in scattered and dispersed communities as compared to more densely populated rural or urban areas, at times women not wanting to share their household food with others, meal prepared in the Hearth session replacing the home meal, the social stigma of being defined as a “negative” family. To take care of some of the limitations, several adaptations were made, with mixed success. Overall, the PD-Hearth model has contributed to our understanding of what makes NHE and BCC work. Another successful PD programme is reported from India – an initiative called Kano Parbo Na, meaning “Why can’t we do it?” This programme was launched in West Bengal, India [21]. The project identified the feeding practices of mothers in the community with healthy children below 3 years of age (positive deviants) and transmitted messages related to these practices to other mothers through a community based approach using locally available resources. Nutrition Counselling and Childcare Sessions (NCCS) were conducted in ICDS or Anganwadi centres, where caregivers of malnourished children obtained hands-on training (learning by doing) over 12 days relating to the best local childcare practices from mothers of PD children. Attention was also paid to related health issues such as immunization, vitamin A supplementation, hand washing practices, diarrhea management, prevention of low birth weight, early registration of pregnancy, antenatal care. The behaviour change messages were then practiced for the next 18 days by

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recipient mothers. The cycle continued for 6–9 months. The PD strategy also mobilized the community around the positive deviance approach through participatory processes; for example setting up village committees, ensuring convergence and partnership between the service providers, administration and NGOs involved in implementation and building capacity of childcare functionaries and the community using the “triple A” approach (assessment, analysis, action). The Impact was evident from the case study of the district of Dakhin Dinajpur. This district was one of the first ones that had adopted the PD strategy, and it recorded a reduction in moderate and severe malnutrition from 25 per cent to 5 per cent in two years in 168 ICDS centres. Some factors explaining the impact include: extensive use of resource maps and community growth charts; mothers regularly contributing food for NCCS sessions; preponderance of girl children at the entry stage; ‘ripple effect’ resulting in improvement of nutrition status of siblings.

39.7.3 ICDS-III (World Bank Assisted) Project: 1999–2006 In the ICDS-III project, which operated in over 10 states of India, Information, Education and Communication (IEC) was one of the major interventions in the project and it had a major BCC focus for ensuring appropriate child caring practices in the households. It sought to primarily address the needs of under-3s through family based interventions instead of centre-based interventions [22]. A family-based approach involved extensive outreach and one-to-one contact through home visits as opposed to centre based approach wherein beneficiaries were expected to come to the health centre or anganwadi to avail the services. Significant improvements in household behaviors regarding IYCF practices were seen when the Baseline Survey (BLS) results were compared to the Endline survey (ELS): ●

●

●

Proportion of children under 3 years who were breastfed within 2 hours of birth (37% in BLS to 51% in ELS) Proportion of children age 6–9 months receiving complementary feeding (38% in BLS to 64% in ELS) Proportion of children age 6–36 months consuming vitamin A rich food (53% in BLS to 71% in ELS)

The states adopted various strategies for implementing the IEC with a BCC focus: ●

Interpersonal communication through home visits and NHE sessions;

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Social mobilization through door-to-door contacts, rallies, mobile video van, gramin mela (rural fair), exhibitions, special campaign days; Print/electronic/audio–visual media such as brochures, ICDS newsletter, booklets and guidelines, flip-books, leaflets, pamphlets, calendars, hoardings & boards, audio jingles, TV spots, wall paintings and documentary films. Many states did not limit the IEC interventions to the ICDS blocks under the project, but covered the entire state.

A key factor also contributing to this impact was a marked improvement in quality of implementation of services by AWWs such as regular growth monitoring of under-3 children and weighing newborn at birth. Awareness of infant breastfeeding practices among the AWWs also improved. Experiences such as these contributed insights which helped formulate recommendations for strengthening the BCC component of the ICDS programme (Box 39.3). Box 39.3 Nutrition and health education and ICDS Health and nutrition education is one of the six important components of the Integrated Child Development Services (ICDS) Programme. However, it remains a very weak component. A per NFHS-3 [23], only 10.9 percent pregnant mothers and 8.3 percent lactating mothers, even under the ICDS project, received health and nutrition education. Recognising the significance of this component, Government of India, in the XI Five Year Plan (2007–2012) made several recommendations, for “Strengthening Nutrition and Health Education”. The Working Group (sub group – ICDS and nutrition) report for the XIth Plan [24] points out that the fundamental objective of Education in Nutrition is to help individuals to establish food habits and practices that are consistent with nutritional needs of the body and adapted to the cultural pattern and food resources of the area in which they live. While recommending that States develop specific IEC strategies for their own regions, it emphasizes that Behavior Change Communication (BCC) needs to go beyond the traditional printed materials and should involve identification of local communications’ needs, use of multiple channels including folk media and mass media in addition to inter-personal communication (IPC) through AWWs and community level volunteers. Considering the fact that home visits are important for effective inter-personal communication (IPC), a welcome recommendation in the Plan is the suggestion that a Home Visit planner be introduced to help AWW to prioritize and plan home visits to households at critical periods of life cycle. To strengthen the NHE function of ICDS, the Plan also recommends the redesigning of mahila mandals to enable these to become a more comprehensive parenting support initiative involving both mothers and fathers and not mothers alone. In addition to continuous NHE in ICDS, the Plan suggests inclusion of a fixed day in a month (‘Mother & Child Day’ or MCD) – in place of Nutrition & Health Day (NHD) – wherein AWWs, ANMs and supervisors would monitor sessions on health and nutrition issues both for the mothers and children; encourage participation of parents, local PRI members, NGOs and mahila mandals and particularly carry out one to one counseling for behavior change on infant feeding practices and improved care.

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39.7.4 Community-based Maternal and Child Health Nutrition (MCHN) Project Uttar Pradesh – Interpersonal Counseling and BCC The MCHN project implemented in four districts of UP was a multi-sectoral project and involved the Health–Family Welfare Department, ICDS, Panchayati Raj Institutions (PRI) and Department of Social and Preventive Medicine (PSM) of the medical colleges [25, 26]. In order to reduce child malnutrition and micronutrient deficiencies of iron, iodine and vitamin A, among the key strategies adopted were: ●

●

Influence behavioural care practices (maternal–child health, nutrition, sanitation and hygiene) at family level with the help of the Bal Parivar Mitra (community based trained mobilizers). Establish a community based intervention and monitoring system for improving maternal and child health and nutrition.

The MCHN Project resulted in a significant decline of 43% among severely malnourished children; with this decline being slightly higher in case of female children in comparison to their male counterparts. Overall, the positive shift in nutritional status could be primarily attributed to adoption of practices pertaining to infant feeding (early initiation of breastfeeding and colostrum feeding), use of safe drinking water and other hygiene practices; as well as special attention given to children presenting with clinical signs of protein energy malnutrition. From a communications perspective, some of the features leading to success of this project were: ●

●

●

●

●

Sound planning of MCHN project which was a positive attribute that helped methodical execution of all the envisaged activities. Mobilizing community volunteers that is, BPMs (Bal Parivar Mitra) meaning ‘friends of families’ (mostly women) who made regular contacts with the target groups, helped increase correct knowledge and practices among households. Developing a pictorial monitoring format for the use of non-literate BPMs; this also served the purpose of IEC material as it carried uniform messages and pictorially illustrated all the activities using ‘life cycle approach’. Defining the target audience, as ‘risk-families’ proved to be a timeefficient approach which enabled early identification of the population segments that were to be reached and counseled urgently. In other words, reaching the right message to the right recipient at the right time. Employing ‘Inter-Personal Counseling (IPC)’ as a major approach to communicate with largely non-literate community on MCHN issues.

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39.7.5 Improving infant feeding project in Haryana An infant feeding project in Haryana [27] aimed to assess the impact on prevalence of diarrhea and physical growth, of a community based intervention to promote exclusive breastfeeding until age 6 months and complementary feeding thereafter. The project focused on development of communication skills as well as clarity of messages. The study was a cluster randomized controlled trial in communities which implemented an intervention primarily based on nutrition–education–communication and built on existing health and nutrition services, with involvement of local NGOs. In four intervention and four control pair-matched communities, newborns (552 in intervention and 473 in control) were followed up every 3 months to the age of 18 months. For the communication component: health and nutrition workers were trained in the intervention communities to counsel mothers for exclusive breastfeeding –complementary feeding at multiple opportunities. The training was based on the Integrated Management of Childhood Illness (IMNCI) approach which places major emphasis on communication skills. Among the factors which influenced feeding practices, an important one was increase in frequency of contact with households at multiple opportunities – immunization sessions, home visits, weighing sessions – which in particular facilitated contact with the target group soon after birth and thereafter. Enhanced clarity of messages and communication skills also contributed to the success of the intervention. For example, replacing ‘4–6 months’ in the message with ‘6 months’ of exclusive breast feeding was important, resulting in a large proportion of the infants in the intervention group starting complementary feeding at appropriate age. Results showed that as compared to control communities, exclusive breastfeeding rates at 3 months were significantly higher in the intervention communities (79% versus 48%) – and the 7-day diarrhea prevalence was significantly lower – at 3 months and 6 months. The intervention promoted recognition of malnutrition as a problem, complementary feeding initiation at 6 month of age, optimal meal frequency, portion size and food density, and active feeding practices. Hygiene practices also improved – mothers reported washing their own and their child’s hands before feeding the child. Further, energy intakes from complementary foods overall were significantly higher in the intervention group children at 9 months and 18 months. However, the improvement in physical growth was less than that expected from the substantial increases in energy intakes perhaps because several inter-related factors (including maternal malnutrition) influence child growth, including birth weight and child morbidity. It was concluded that in this pragmatic and educational intervention, the promotion of exclusive breastfeeding until age 6 months through existing

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primary health-care services was feasible, effective and potentially sustainable; it reduced the risk of diarrhea, and did not lead to growth faltering; particularly in low-birth weight infants. An important recommendation (emerging from the subtle gender discrimination seen in this project) was that interventions aiming for behavior modification toward improving child feeding practices must pay greater attention to gender bias in communication. It is evident from these examples that NHE with a BCC focus had a significant measurable impact within a limited time frame and within the existing social and economic constraints of the environment; provided NHE is accorded a high priority and is effectively implemented.

References 1.

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3. 4. 5. 6. 7.

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10.

11. 12.

(2002). Effective Nutrition Education and Communication: Issues and Challenges in Government Health Systems. Medico Friend Circle Bulletin. pp. 292–293, 6–9, ZEITLIN MF (1988). The potential impact of nutrition education In: Effective Communications for Nutrition in Primary Health Care. Andersen JE and Valyasevi A, (eds). Report of the Asian Regional Workshop, Bangkok, Thailand, 3–7, 1983. The United Nations University. Population Reports (2008). Communication for Better Health. Info Project: Centre for Communication Programs. John Hopkins Bloomberg School of Public Health. KOTLER P and ZALTMAN G (1971). Social marketing: an approach to planned change. Journal of marketing, 35, pp. 3–12. RASMUSON MR , SEIDEL RE, SMITH WA , BOOTH EM (1988). Communication for Child Survival. Academy for Educational Development. HEALTHCOM Project. AED. Health Canada. Broader Nutrition Education and Health Behavior Change Research: www.hc-sc.gc.ca/fn-an/label-etiquet/nutrition/educat/ ISRAEL RC, FOOTE D , TOGNETTI J (1987). Operational guidelines for social marketing project in public health and nutrition. Nutrition education series issue 14 UNESCO, ED – 87 / WS / 52. KANAL K , HALLEN JB, SFORZA TC, CRAPE B , SMITASIRI S (2005). Cambodian weekly iron folic acid program team. Weekly iron folic acid supplements to prevent anaemia among Cambodian women in three settings: process and outcomes of social marketing and community mobilisation. Nutrition Reviews, 63(12), pp. S126–S133. GARCIA J , BARRETT ED , DIZON M (2005). Industry experience in promoting weekly iron folic acid supplementation in the Philippines. Nutrition Reviews, 63(12), pp. S146–S151. SMITASIRI S, ATTIG GA , VALYASEVI A , DHANAMITTA S , TONTISIRIN K (1993). Social marketing of vitamin rich foods in Thailand – A model nutrition communication for behaviour change process, UNICEF and Institute of Nutrition, Mahidol University, ISBN 974-587-516-3. FAO / WHO (1996). Preparation and use of food-based dietary guidelines. Report of a joint consultation, Nicosia, Cyprus, FAO/WHO, Geneva. Food-Based Dietary Guidelines. Food and Agriculture Organization of the United Nations. www.fao.org/ag/humannutrition/nutritioneducation/fbdg/49850/ en/ind/ KANANI S

Nutrition–Health education and communication for improving ... 13. 14. 15.

16.

17.

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26.

27.

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UNICEF (1992). Care and Nutrition. Theme Paper for International Conference on Nutrition by Engle P. United Nations Children’s Food, New York. HUBLEY J (1993). Communicating Health: An Action guide to Health Education and Health Promotion. The Macmillan Press Ltd., London and Basingstoke. KANANI S , DAXINI M , SHARMA M (2006). Behavior Change Communication Guidelines, Supported by UNICEF (Gujarat). Department of Foods and Nutrition, The Maharaja Sayajirao University of Baroda, Vadodara, India. KANANI S (1998). BEHAVIOUR Change Trials for Better Nutrition Of Pregnant And Lactating Women in Angarah Block, Bihar. A Report for the Linkages Project of Academy of Educational Development. CARE – BIHAR. Department of Foods & Nutrition, the Maharaja Sayajirao University of Baroda, Vadodara, India. ACADEMY FOR EDUCATIONAL DEVELOPMENT (1996). Final Report NCP: Nutrition Communication Project: Nutrition Education and Social Marketing Field Support Project. (Funded by the US Agency for International Development). AED, Washington, D.C. ZEITLIN M, GHASSEMI H , MANSUR M (1990). Positive Deviance in Child Nutrition with Emphasis on Psychosocial and Behavioral Aspects and Implications for Development. Food and Nutrition Bulletin, Supplement No. 14, United Nations University. BOLLES K , SPERAW C, BERGGREN G , GUY LAFONTANT J (2002). Ti Foyer (hearth) community-based nutrition activities informed by the positive deviance approach in Leogane, Haiti: A programmatic description. Food and Nutrition Bulletin, 23(4), pp. 9–15. CORE: Child Survival Collaborations and Resources Group (2002). Positive Deviance/Hearth for Nutrition. Technical Advisory Group Meeting, Washington, DC.. MUSTAPHI P (2005). Addressing Malnutrition through Surveillance and Innovative Community based Strategies. UNICEF: Knowledge Community on Children in India. GOVERNMENT OF INDIA (2006). Implementation Completion Report of World Bank assisted ICDS-III / WCD Project Borrower’s Evaluation Report, GOI. National Family Health Survey (NFHS)-3 (2005–06). International Institute of Population Sciences, Mumbai. GOVERNMENT OF INDIA, PLANNING COMMISSION (2008). Eleventh Five Year Plan (2007–2012). Volume II. Social Sector. Oxford University Press, New Delhi. GOVERNMENT OF UTTAR PRADESH and UNICEF (2006). Community Based Maternal & Child Health Nutrition (MCHN) Project (MCHN) Project. Evaluation Report. Submitted to GoUP (Directorate of FW & Directorate of ICDS) and UNICEF, Lucknow. ORG Centre for Social Research (A Division of ACNielsen ORGMARG Private Limited), Lucknow. VIR S, JAIN A , SINGH R (2006). Mission Poshan – Project to redesigning state programme for addressing malnutrition in under threes in Uttar Pradesh. In: Report of the Nutrition Foundation of India on “late infancy and early childhood (6–24 months)”. BHANDARI N , MAZUMDER , BAHL R , MARTINES J , BLACK RE , BHAN MK (2004). An Educational Intervention to Promote Appropriate Complementary Feeding Practices and Physical Growth in Infants and Young Children in Rural Haryana, India and other members of the Infant Feeding Study Group. J. Nutr., 13(4), pp. 2342–2348.

40 From research to programs: Applying knowledge to improve nutrition outcomes Purnima Menon

Purnima Menon, Phd, is a Research Fellow in IFPRI’s Poverty, Health and Nutrition Division. Among other projects, she leads the monitoring and evaluation of Alive and Thrive, a Bill and Melinda Gates Foundation-supported initiative to improve infant and young child feeding and child nutrition, at scale, in Bangladesh, Vietnam and Ethiopia. Prior to joining IFPRI, Dr. Menon was a Research Associate in the Division of Nutritional Sciences at Cornell University (2006–07), a consultant to IFPRI (2001–06), and a Scientific Officer with the Nutrition Foundation of India (1994–95). Menon is Ph.D. in International Nutrition from Cornell University, a M.Sc. in Nutrition from Lady Irwin College (University of Delhi) and a B.Sc. in Nutrition from the University of Madras.

".1

Introduction

Evidence-based decision-making for programs and policies has emerged as a critical ingredient for effective programs and policies. Evidence-based decision-making has been well integrated now into clinical medical practice overseas, but has entered the realm of public health programming only recently [1]. High quality research should be the basis for generating evidence for program and policy decision-making. However, the question of what types of research are most relevant to program decision-making is still often debated. Traditional public health specialists continue to defer to randomized controlled trials (RCTs) as the definitive evidence-base for decision-making about interventions. This is increasingly, however, being viewed as inadequate for effective decision-making, largely because RCTs often only yield information on “what” interventions are most efficacious, but not on “how” interventions had their impact [2]. Relying only on evidence from RCTs, without consideration of context and impact pathways, then, can be misleading and lead to lowered effectiveness in non-optimal program circumstances. Broadening the scope of the type of research, therefore, is important to consider when developing programs [3].

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This chapter describes the different types of research that are relevant to the process of decision-making about programs. It does so by using a framework that demonstrates the links between different types of research and programmatic decision-making for the reader. First, however, it is useful to explain the concept of “program theory”, which forms the backbone for how research links to programs.

40.2

Program theory

“Program theory” refers to the definition of the processes by which a program is intended to achieve its intended impact [4]. It is by now well accepted in the field of program evaluation that evaluations should be theory-driven to the extent possible as this allows for the best understanding of whether, why and how programs achieve, or do not achieve, their intended impacts [5]. Usually, program theory includes impact theory (which specifies the impact pathways) and two elements of process theory (which specifies the operational and utilization plans). Impact theory is intended to lay out the steps through which a given intervention in a program is expected to have an impact on the desired outcomes of interest. In effect, it specifies the causal pathways through which impacts are to be achieved, and forms the basis for any social program. It is important in specifying such impact theory to also define some of the conditions that need to be in place to achieve the intended impacts and some of the assumptions being made in statements about how the program will achieve the stated impacts. Process theory lays out the steps through which an intervention or program is implemented and includes steps related to the organization plan for delivering interventions as well as a service utilization plan for ensuring use of the program services and interventions. Of particular importance at an early stage in development of a program, or the planning of an evaluation of program, is the development of program theory. An example of a program theory pathway for behavior change communications programs is shown in Fig. 40.1. The program theory developed at an early stage in program planning should be expanded, clarified and refined as various components of program strategies get further developed. This allows program implementers and researchers to articulate pathways of possible impact of program investments, to clarify which barriers are outside the scope of program plans, and to highlight where inputs from other stakeholders, programs, and initiatives will have to be leveraged to achieve desired impacts [6]. Most critically, it helps identify critical points on which research is needed to identify how best to move forward with program design, implementation or program refinement. Program theory also helps define the best approach for estimating program costs by identifying factors in program inputs and operations or program utilization that need to be mapped and the cost estimated.

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.

. . . . .

40.1 Example of program theory of a behavior change communications programme.

40.3

Framing the links between research and programs

The framework (Figure 40.2) shows the types of research studies that have application to programs. As depicted in the framework, the program process itself consists of multiple stages, which are interlinked. They flow from early program decisions about intervention choice and operational designs, to later decisions on program scale-up, sustenance or even program termination. There is a role for program-oriented research to support each of these phases of program and policy-decision making. Figure 40.2 also shows the links between different types of research, and the different program decisions. Building strong and meaningful links between program decision-making and program-oriented research is not straightforward. It requires vision on the part of program planners, policy-makers and donors, who must commission research to answer questions that are most relevant to the problems they are trying to solve. It also requires a creative and skilled set of researchers and research institutions who can either respond to the needs of a program, or who have the vision to invest in program-oriented research as part of their core research areas. More importantly, it requires that

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40.2 Framing the links between research and program stages/decisions.

program managers, bureaucrats and policymakers, including politicians, to often accept programmatic findings that are at odds with their perceptions about the value of certain policy investments or programs. There are few examples of the institutionalization of a program-oriented research focus within governments and national research programs; those countries that have invested in such links, however, have demonstrated improvements in the quality and scale of programs as well as the impacts of programs. An excellent example of this is the link between the nutrition and poverty alleviation program in Mexico (Progresa/Oportunidades) and the types of research studies commissioned by the government of Mexico. These studies spanned the gamut of the types of research shown in the Fig. 40.2 and each piece of research contributed to specific program decisions, from intervention choice (such as the choice of iron fortificant) to program targeting and scale-up [7, 8]. This approach to program-focused research has been largely absent in India. Even though many of the design and implementation bottlenecks in the Integrated Child Development Services (ICDS) – programme of India and other nutrition programs have been well-documented, there has not been a systematic effort to conduct research to identify effective solutions to these bottlenecks (Box 40.5). Major types of program-oriented research, with the primary goal of providing an overview of the different types of research, rather than

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providing an in-depth methodological orientation is presented in the chapter. The reader is referred to the references in each of the sections for further reading.

40.4

Categories of program-oriented research

The major types of program-oriented research and their contributions to program decisions are described below, using the example of various nutrition interventions, including multiple micronutrient powders (MNPs) to reduce anemia among young children, and behavior change communication to improve infant and young child feeding (IYCF) practices.

40.4.1 Efficacy and effectiveness research Clinical or community based efficacy studies use highly controlled research methods to answer very specific questions pertaining to the efficacy of certain treatment regimens or certain preventive interventions on nutritional or functional outcomes. These research studies often provide the basis for choosing efficacious interventions to include in programs to improve nutrition. It should be taken as an essential prerequisite that interventions chosen for inclusion in large scale nutrition programs meet basic standards of proven efficacy. In the case of MNPs for reducing anemia, first, efficacy trials tested the efficacy of using the MNPs against other iron supplements for reducing anemia; studies also tested MNPs in different dosages [9, 10, 11]. Following this set of basic research in controlled community based studies, a set of effectiveness studies that examined the impact of MNPs on anemia under less controlled, and “real life” program settings provided the evidence that this approach to reducing anemia had impact even in programs [12, 13]. Taken together, this set of studies provided the basis for inclusion of this approach in large scale national programs [14], and this innovative approach to reducing anemia is now being embraced in a variety of programs globally.

40.4.2 Formative research Formative research is a basic prerequisite for introducing new programs or new program elements in communities. With origins in social marketing and behavior change communication, formative research is essential to tailoring program choices, key behavior change messages and approaches, and communication strategies to local contexts. It is particularly important where public health outcomes are dependent on behaviors that vary widely from place to place, because of differences in social and cultural context.

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This is particularly true for nutrition-related behaviors such as infant and young child feeding [15, 16]. Formative research can either be used to design new content for behavior change communications programs [17, 18], or to adapt existing global or national technical materials to local requirements, as in adaptations to the counseling materials developed under the Integrated Management of Childhood Illness (IMCI) and Control of Diarrheal Diseases at WHO [19]. In the case of the IMCI counseling materials, the World Health Organization developed a set of basic counseling materials related to infant and young child feeding as part of the overall IMCI package of tools and materials. Along with this, recognizing that infant and young child feeding is strongly influenced by local context, available foods and resources, and cultural beliefs, WHO also developed a formal guidebook for how to adapt the IMCI counseling materials to the local context. Formative research uses primarily qualitative methods such as in-depth interviews, focus group discussions, unstructured observations, case study as well as structured ethnographic methods [20]. The use of qualitative research for formative research, however, should be rigorous, and should follow all principles of strong qualitative research [21]. Sampling for formative research is usually purposive, as the goal should be to capture the range of expected variability in implementation contexts, e.g. in sociocultural, religious, economic, rural versus urban, etc. Box 40.1 Hallmarks of good qualitative research ● ●

● ●

●

●

Clear research protocol is developed. Sampling, even where purposive, is well thought through, and ideally, linked with sampling used in quantitative research (where mixed methods are used). Question guides are well-developed, pre-tested and refined. Data collection methods include detailed interview notes, taped transcripts of interviews and field notes describing context of interviews. Analysis methods include use of qualitative data analysis software to code text data; where software is not used, analysis methods include explicit procedures to code data, ensure reliability of codes (through multiple coders and debriefing techniques). Write-up of qualitative research findings aim to convey majority tendencies as well as minority tendencies, as well as the richness of data.

Quantitative data is also invaluable for formative research, but the use of the term ‘formative research’ largely implies the use of qualitative methods. However, with the increasing availability of large scale survey data such as the National Family Health Surveys (NFHS) in India, and the Demographic and Health Surveys (DHS) for other countries, on the internet, it is now possible to use these data to understand patterns, trends, and determinants of undernutrition before embarking on program strategy development. These data are often representative at the national and state/

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regional level only, however, and therefore provide little information on more localized contexts. They are extremely useful for understanding the broad context, and comparing results from local formative research studies using qualitative methods. Still, quantitative analysis of large scale data sets should not substitute for rigorous qualitative field-based research, which is fundamental to the success of many programs that need adaptation of key health and nutrition messages, counseling approaches, or service delivery mechanisms. The literature on behavior change communication for nutrition, in particular, is unequivocal in stressing that building nutrition communication programs, but also advocacy strategies and health systems strengthening strategies, should be based on a sound base of knowledge about the existing context and the major influences on behaviors. The major contribution of formative research is in developing this base of knowledge, and enabling the crafting of program strategies that are well-grounded in the contexts that the programs must operate in. Box 40.2 Methods for assessing impact and operational pathways Quantitative methods ● Facility assessments, ● Staff and client knowledge assessments ● Skill assessments ● Exit interviews on service use ● Structured observations ● Knowledge-trial-adoption surveys Qualitative methods ● Focus group discussions ● In-depth narrative interviews ● Participant observation ● Event analysis ● Process tracing

40.4.3 Operations research Operations research is a process that culminates with the effective use of applied programmatic research information for action. It is also particularly useful when embedded with impact evaluations, in which case it might also be referred to as a “process evaluation”. However, here, the term “operations research” is used here to encompass both operations research and process evaluation since the difference between the two is most often in what the information from the research process is used for. In both, data is gathered on program implementation and utilization, and the results are used either to provide feedback to program implementers and improve program implementation quality [22], or to document the process of

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program implementation and utilization as part of an impact evaluation [23, 24]. Gathering data on intermediate processes using operations research contributes to impact evaluation since it provides information on potential explanations for differences in program impact between comparison groups [25, 26], and is particularly relevant where an expected impact is not found [27]. In many cases, lack of impact could be because the program, as implemented, was quite different from the program as intended. Problems in implementation, therefore, compromise the ability of impact evaluations to determine the true effectiveness of nutrition and public health programs. Since problems in implementation are usually due to various factors upstream of the actual implementation (e.g., logistical arrangements and resources, supervisory structures, staff technical skills, etc.), it is optimal if these factors are also assessed as part of the operations research conducted during an impact assessment [28]. From the point of view of scaling up a program, detailed information on implementation and factors influencing implementation are needed to plan the scaling up process. Of particular importance is information that can help identify and prioritize key infrastructural and staff level factors that need to be addressed for optimal impact of a specific intervention when implemented at a large scale. Key infrastructural factors include resource needs and the logistical arrangements for delivery of an intervention. Staff level factors include staff skills and capacity, supervisory systems and staff incentive structures, all of which directly impact optimal implementation of a program at the frontline level [29]. A variety of methods can be used when conducting operations research and process evaluations. These are described in Box 40.2. Ideally, operations research should rely on mixed research methods – using both qualitative and quantitative methods of research. It should also be based on program theory (described above), such that the set of research methods used is able to bring together insights from different perspectives and different stakeholders on the processes through which a program or intervention is being delivered and used by its intended beneficiaries. The methods used in operations research come from the fields such as quality assurance in health systems [30], medical anthropology, organizational behavior, and the policy sciences, among others. The primary requirement for conducting high quality operations research, however, is not disciplinary training in any of these disciplines; rather it is the ability to map and identify the critical impact and process pathways for different program components or interventions. Once such pathways are mapped, it is possible to then develop a protocol of research methods for understanding and elucidating these pathways using a variety of operations research methods. Table 40.1 depicts an example of the kinds of steps to be assessed when assessing the

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Table 40.1 Mapping research methods to steps in program theory [24] Steps in program pathway

Types of methods

Sample

Program staff distributes adequate amounts of micronutrient powders

Exit interviews at distribution points

Caregivers/children at distribution points

Program staff possess adequate knowledge to educate mothers about use of micronutrient powders

Knowledge assessments of program staff

Program staff who deliver behavior change comm.unication messages

Program staff are able to incorporate micronutrient powder component activities into their routine activities in the integrated program

Qualitative group or individual interviews with program staff

Program staff who deliver behavior change communication messages and undertake supply-related activities for MNPs.

Mothers possess adequate knowledge about use of micronutrient powders

Knowledge assessments with mothers

Mothers of children targeted by the program

Mothers use micronutrient powders for children as advised

Qualitative group interviews to understand barriers to use Surveys include questions on use patterns and barriers to use

Mothers of children targeted by the program

feasibility of incorporating an MNP distribution into an ongoing maternal, child health and nutrition program and illustrates how specific research methods can inform different elements of a program pathway [24].

40.4.4 Impact evaluations Impact evaluations, including evaluations of pilot projects, should be used for decision-making about scaling-up or replication of public health programs. They are the mechanism for providing evidence (or the lack thereof) of the effectiveness of mechanisms of using public health and nutrition services to improve health and wellbeing [31]. In spite of this understanding, impact evaluations are not invested in as much as they should be by donors and policymakers. However, with many recent international initiatives focusing on impact evaluation, there is increasing emphasis for the development and use of solid impact evaluations for decision making in the global health and development arena. A variety of study designs can be used in impact evaluations, and often are, but it is useful to place these methods in relation to the level of rigor each approach to evaluation offers. The most rigorous designs are called

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Box 40.3 Case study: Use of formative, operations and impact evaluation research on the use of micronutrient powders (MNPs) to improve childhood anemia in Haiti As part of the design of an intervention to improve child nutrition in Haiti, a formative research study, using mostly ethnographic methods [20] was conducted to understand the facilitators and barriers to moving from non-optimal to optimal recommended infant and young child feeding practices. The results of one component of the formative research demonstrated that the particularly salient nutrient gaps for infants and young children in this part of Haiti were gaps in iron and zinc [20]. Based on this, a rigorous cluster-randomized trial was designed to investigate the potential of MNPs for reducing childhood anemia in this population. The design of messages to ensure appropriate use of the MNPs was based on initial pretests of the use of the MNPs, and the communications on the use of the MNPs was integrated into the overall communications strategy of the program. A baseline assessment was conducted as part of the impact evaluation, and demonstrated very high levels of anemia among infants and young children (above 45% anemia), thus strengthening the findings from the formative research on the dietary gaps in iron. Implementation of the MNP intervention through an established integrated MCHN program commenced shortly after the baseline assessment. Operations research methods, including a variety of qualitative and quantitative methods were used to document the process of program implementation and of utilization of the MNPs by mothers of children in the program. The operations research methods used included structured observations at different program delivery points, structured and semi-structured interviews with stakeholders and focus group discussions with program staff. Two impact assessments were conducted; the first assessment was 3 months after the start of implementation, and covered intervention and comparison groups, and demonstrated that anemia was halved in the intervention group. The MNPs were then rolled out into the comparison areas. Following this, about 7 months after the MNPs were first distributed to the intervention group, anemia was re-assessed in the intervention group alone. This second assessment demonstrated that anemia had dropped from 53% at baseline to 14% at the second assessment in the intervention group. The series of research in this case culminated in the demonstrated effectiveness of MNPs for reducing childhood anemia in this part of Haiti [12] as well as the demonstrated feasibility of integrating MNPs and accompanying behavior change communication into an existing maternal and child health and nutrition [24]. Concurrent with these studies, the roll-out of the sales of MNPs through social marketing has led to the sustained sales and scaleup of MNPs to many other parts of the country. The rigorous effectiveness study also contributed to the Lancet Nutrition Series review of MNPs and the recommendation to include MNPs as an effective strategy for reducing anemia among infants and young children.

‘probability’ designs and enable evaluators to assign a probability level to the impact seen and attribute causality to the intervention or program using rigorous study designs such as randomization. Less rigorous designs include ‘plausibility’ designs, which are not set up to assign causality to the intervention. Rather, through use of a combination of statistical methods to control for confounding factors, and detailed data on mediating processes, plausibility evaluation designs aim to make it possible to assess the impact of the program with a high level of confidence but not assign

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causality to the program. The least rigorous of evaluation designs are called ‘adequacy’ designs; these designs usually include only before–after assessments which aim to assess progress against benchmarks, with no comparison group and little data on mediating or confounding factors. The choice of evaluation design must, ideally, be made in consultation with organizations and individuals who will use the results of the evaluation for decision-making. The level of rigor and the extent of data collected on different program steps should be made based on interactions with evaluation funders and program teams on the nature of decisions to be made based on results of the evaluation [32]. Planning for impact evaluations should begin as early as when intervention choice and program design/re-design are being contemplated, rather than as an afterthought to the program design and planning process. This is important because impact evaluation planning requires substantial discussion between evaluation/research teams and program implementation teams about evaluation goals, as well as decisions related to timing of baseline assessments, geographic scope of the evaluation, timing of end line assessments, and choice of impact indicators, among other issues. In this chapter, given recent trends in the field of impact evaluation, the most rigorous of the impact evaluations designs have been described i.e., probability designs with program impact pathway documentation are described, to enable the reader to appreciate the requirements for an impact evaluation that unequivocally attributes impact in certain outcomes to a specific program or intervention. This can only be done with impact evaluation designs that are rigorous enough to rule out all other explanations for impacts seen on target populations. In such a rigorous quantitative assessment of the impact of any program/intervention, the design needs clearly attribute and rule out the impact seen to the interventions/programs. It is necessary for the design to compare outcomes for recipients of the program interventions to what those outcomes would have been had the program not been implemented at all. Two essential ingredients for achieving are (a) the double difference approach and (b) finding an appropriate comparison group that is not exposed to the program. Other features of high quality evaluations are mentioned in Box 40.4; many of these aspects are also covered in other sections of this chapter. Two issues that relate to the rigor of impact evaluations are the use of a double-difference approach and the selection of a comparison group. These are described below. (a) Double difference approach – The difference-in-differences (or double-difference) method is a central component of any rigorous impact evaluation. This method relies on baseline data collected in intervention and comparison areas before interventions are implemented and followup data (an end-line survey) collected as close as possible to the end-date

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Box 40.4 Characteristics of a high quality impact evaluation ●

● ●

●

●

●

●

●

Double difference method is used, i.e. before-after assessments with a comparison group Comparison group is valid and unbiased (ideally selected using randomization) Adequate data are gathered as part of baseline and endline assessments to ensure other explanations for impact are ruled out Data are gathered on intervention mediating factors as well as contextual factors Solid operations research/process evaluation component is included, and appropriate methods are used Mixed methods are used where appropriate, particularly to understand program impact pathways and operational pathways Attention is paid to the kinds of decisions that will be made based on results of the evaluation Stakeholders who must use the information are engaged from the planning stages of the evaluation

of the project to develop a “before/after” comparison. Unfortunately a majority of program evaluations, even today, use simple before–after assessments only in intervention communities, without comparison groups, making it impossible to make inferences about the specific impacts of the intervention activities or the program. For a rigorous double-difference approach to program evaluation, data need to be collected from areas covered by the intervention or program and those that are not covered by the program (the “comparison” group). The difference between the change in the outcomes for intervention and comparison groups in the baseline and end-line surveys will provide the difference-in-differences impact estimates [33, 34]. (b) Identifying an appropriate comparison group – Identifying an appropriate comparison group for individuals exposed to the interventions being evaluated is central to the application of the double-difference method, and of any rigorous impact evaluation. To isolate the impact of the intervention, it is important that intervention and comparison groups be identical in all characteristics, except for being exposed to the intervention/program such that the only plausible explanation for differences in stunting and IYCF practices between groups is the intervention. A major problem with identifying an appropriate comparison group that is not exposed to the selected interventions is selection bias (e.g., areas chosen for coverage with the intervention could be fundamentally different from comparison areas in ways that bias the outcomes and impacts). For some programs, another challenge could be that very rapid scale-up can limit the number of areas in the country that are not covered by the program, thus eliminating many areas from being comparison areas. This is often the case in large scale national programs.

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Options for establishing an appropriate comparison group include randomization of areas or individuals to the interventions. If holding back programming in comparison areas is not feasible for the entire duration of a project, another appropriate way to randomize in the context of largescale programs is the randomized stepped-wedge approach. In this approach the staging of program roll-out is done using a random selection of areas for different phases of roll-out. Another approach is to set up comparison groups where certain program elements are absent or where interventions are delivered with differing intensities, and the choices of where to hold back program elements or to scale back on intensity are made randomly rather than purposefully. Randomization is considered the gold standard for impact evaluation, is simpler to analyze and communicate results, and therefore, should be a first choice for evaluating the impact of new programs or interventions, particularly those that are not being scaled up immediately to large areas. Where randomization is not feasible at all, options for establishing valid comparison groups include quasiexperimental designs, which involve choosing comparison groups based on certain criteria. Other options also include matching using econometric methods such as propensity score matching (PSM) or nearest neighbour matching (NNM) [35]. An important consideration for rigorous impact evaluations is that the surveys that generate the data for the double-difference analyses should gather adequate information on exposure to the interventions as well as on other relevant factors that might influence the impact of the interventions. This is important regardless of whether the evaluation design uses randomized methods or other approaches to identify comparison groups but is particularly important where randomized designs are not possible and where additional data are needed on program performance and on coverage, utilization and confounding factors to enable analyses that can build the case for plausibility. Unfortunately, most impact evaluations do not gather detailed information on implementation and factors influencing implementation that are actually needed to provide the evidence base for scaling up to a full scale program, or for replicating a program in another setting. This is necessary both from the point of view of how evaluation results are used for scaling up pilot programs and from the point of view of interpretation of impact evaluation [2, 27]. The section on operations research above has more details on approaches and methods that can be used to understand program implementation and utilization processes. Last, but not least, it is critical to consider the time it takes to assure that program implementation is of high quality and has achieved the desired scale and coverage in the interventions, before investing in the endline survey. Undertaking endline surveys to assess impact without assessing

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and assuring implementation scale or quality is not useful. The forms of research that can help assess whether programs are well designed and well implemented are described in the sections on formative and operations research.

40.4.5 Cost-effectiveness research For policymakers and donors, assessing whether a program or intervention is cost-effective is a prime concern. Research on cost-effectiveness, therefore, is of critical importance in relation to programs. Most often, cost effectiveness research is embedded in program impact evaluations. Impact evaluations yield data on the effectiveness of an intervention, either in terms of decreased prevalence of undernutrition or improved nutritional status outcomes. Data on program costs are usually derived from a combination of sources, including program accounting systems, operations research, as well as baseline and endline surveys. It is important to consider a variety of costs when compiling data on program costs – the types of costs to consider include program operational costs as well as costs to program users. Different methods have been used to calculate program costs in the past; these include the CHOICE method developed by the World Health Organization [35], which is mainly input-based, as well as a more recently used approach known as “activity-based costing” [37]. Input-based costing is more “top down” in that broad financial inputs into programs are estimated mainly based on program financial accounting systems. These then are combined with information from surveys on the costs to beneficiaries of using program services to yield an overall cost figure. Although this sounds simple, it is quite complex and timeconsuming. It requires a separation of costs by categories that are meaningful for the program inputs (e.g., technical, staffing, supplies, etc.) to be able to estimate the costs of “fixed” inputs versus of “variable” inputs. Fixed costs are costs that are often incurred in program start-up phases, and relate to the costs of capital investments, infrastructure, major equipment, etc. Variable costs, on the other hand, are the costs of operations such as training, supervision and monitoring, IEC and supplies such as medicines, nutrient supplements, etc., that are driven substantially by the level of use of the program by beneficiary populations. Activity-based costing is a method of costing that is considered more “bottom-up” and is based on an approach that breaks a program down into the smallest activities and attempts to assign costs to each activity. It has been used successfully in the past [38, 39]. It is substantially more burdensome to compile program costs based on an activity-based costing approach even though this approach can be more meaningful in terms of identifying the most and least costly operational aspects of a program.

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Regardless of the costing approach chosen, as with operations research and impact evaluations, it is useful to plan activities related to cost studies early in the program design and implementation process. This ensures that cost data are compiled from the start of a program and that total costs related to operations and utilization of a program are well-captured. Once both impact and cost data are available for a program and for non-program areas, it is then possible to calculate the cost-effectiveness of a program or an intervention. High quality impact evaluations that include a comparison group almost always also include cost studies as part of the evaluation design. Box 40.5 India’s nutrition-related programs: some important programmatic research questions It is useful to consider the current status of research in informing the design and evolution of nutrition and other programs in India. India’s flagship nutrition program is the Integrated Child Development Services (ICDS) program. Other programs that can have impact on nutrition through direct and indirect routes, include the Reproductive and Child Health (RCH) program that is part of the National Rural Health Mission (NRHM), water and sanitation programs, the National Rural Employment Guarantee Scheme (NREGS) and a variety of other food-entitlement programs intended to improve either individual or household food security. Most of the programmatic research in India, as it applies to nutrition, has been done on the ICDS program, with many other aspects of research on programs to improve nutrition being largely neglected. Questions remain, therefore, on issues such as the following (among others): ●

●

●

●

●

What is the potential to use the Reproductive Child Health (RCH)/ National Rural Health Mission (NRHM) platforms to improve nutrition outcomes for women and young infants and children? What is the nature of the links between the National Rural Employment Guarantee Act (NREGA) and nutrition? How can the implementation of the NREGA be improved to also address nutrition outcomes? How can water and sanitation programs in India be optimized to be able to deliver critical interventions for nutrition (such as hand-washing and hygiene interventions)? How should agricultural programs be conceived of and implemented so as to ensure that nutrition improvements are achieved? What gender-related aspects constrain the use of interventions for nutrition?

For the ICDS program specifically, some of the key design and implementation bottlenecks in the ICDS and other programs have been well-documented. At the same time, there has not been much investment in conducting research on how changing design features and/or implementation modalities can yield improvements in program performance and program effectiveness. Many studies are continuously being conducted on many aspects of the programs. However, there is no mechanisms known to coordinate program-oriented research in relation to the national and state level programs to address direct and indirect determinants of nutrition (questions such as those posed above) or to align the different pieces of research, and ensure that high quality research that is responsive to the program needs is routinely commissioned, funded, and implemented. More importantly, the process of integration of the existing global and national evidence on nutrition interventions is slow. Attention to these issues is critical if research is to play an important part in yielding program benefits in the Indian context.

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Conclusions This chapter has provided an overview of the links between research and programs, with a focus on introducing the reader to different types of research that are essential to inform different aspects of decision-making about programs. It is not intended to be an exhaustive chapter on the various methods of research but primarily an introduction to the kinds of research that can be, and should be, undertaken to improve programs and lead to better public health outcomes. It is encouraging to note where donors and governments have invested in programmatic research, there is a clear movement towards evidence-based decision-making about program strategies and intervention choices, both of which are important in an environment of limited funding for public health, nutrition and social assistance programs. Additional references provided along with this chapter provide resource materials on study examples that have used such research methods, as well as to textbook and toolkits/manuals for applying these research methods. Acknowledgements Jean-Pierre Habicht and Gretel Pelto at Cornell University and Marie Ruel at IFPRI are deeply acknowledged for their decade-plus of mentoring on program research. The author also acknowledges numerous colleagues at IFPRI for discussions and insights about program evaluation and applied programmatic research.

References 1. 2. 3.

4. 5.

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FIELDING JE and BRISS PA (2006). Promoting evidence-based public health policy: can we have better evidence and more action? Health Affairs, 25(4), pp. 969–978. VICTORA CG, HABICHT JP , BRYCE J (2004). Evidence-Based Public Health: Moving Beyond Randomized Trials. American Journal of Public Health, 94(3), pp. 400–405. HABICHT JP , PELTO GH , LAPP J (2008). Methodologies to Evaluate the Impact of Large Scale Nutrition Programs, Washington DC, World Bank (in press). http:/ /web.worldbank.org/WBSITE/EXTERNAL/TOPICS/EXTPOVERT Y / EXTISPMA0,menuPK:384336~pagePK:149018~piPK:149093~theSitePK:384329,00. html#doingIE ROSSI PH , LIPSEY MW , FREEMAN HE (2004). Evaluation: A Systematic Approach, 7th edn. Thousand Oaks, CA: Sage. WHITE H . “Theory-Based Impact Evaluation”. 3ie Working Paper 3, June 2009 (available at: http://www.3ieimpact.org/temp2.php?path=pdfs_papers/ 48.pdf&name=Theory Based%20Impact%20Evaluation%20by%20Howard% 20White). R O B E R F R O I D D , P E LTO G H , K O L S T E R E N P (2007). Plot and see! Maternal comprehension of growth charts worldwide. Tropical Medicine and International Health, 12(9), pp. 1074–1086.

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Progress against poverty: sustaining Mexico’s Progresa-Oportunidades Program. Brookings Inst Press. Washington, DC. LEROY JL , VERMANDERE H , NEUFELD LM , BERTOZZI S (2008). Improving Enrollment and Utilization of the Oportunidades Program in Mexico Could Increase Its Effectiveness. J. Nutr., 13(8), pp. 638–641. ZLOTKIN S , ARTHUR P, ANTWI KY , YEUNG G (2001). Treatment of anemia with microencapsulated ferrous fumarate plus ascorbic acid supplied as sprinkles to complementary (weaning) foods. American Journal of Clinical Nutrition, 74, pp. 791–795. ZLOTKIN S, ARTHUR P , SCHAUER C , ANTWI KY , YEUNG G , PIEKARZ A (2003). Homefortification with iron and zinc sprinkles or iron sprinkles alone successfully treats anemia in infants and young children. The Journal of Nutrition, 133, pp. 1075–1080. GIOVANNINI M et al (2006). Double-blind, placebo-controlled trial comparing effects of supplementation with two different combinations of micronutrients delivered as sprinkles on growth, anemia, and iron deficiency in Cambodian infants. Journal of Pediatrics Gastroenterology and Nutrition, 42, pp. 306–12. MENON P et al (2007) Micronutrient Sprinkles Reduce Anemia among 9- to 24month old Children When Delivered through an Integrated Health and Nutrition Program in Rural Haiti. The Journal of Nutrition, 137, pp. 1023–1030. HYDER SM , HASEEN F , RAHMAN M, ZLOTKIN S (2004). Delivery of microencapsulated iron Sprinkles in rural poor through female health workers: Lessons learnt at BRAC in Bangladesh. Abstract. Presented at INACG, Peru. WORLD VISION MONGOLIA (2005). Report on the Effectiveness of Home-Based Fortification with Sprinkles in an Integrated Nutrition Program to Address Rickets and Anemia. World Vision Mongolia, Ulaanbaatar. PELTO G , LEVITT E , THAIRU L (2003). Improving feeding practices: current patterns, common constraints, and the design of interventions. WHO Global Consultation on Complementary Feeding. Food and Nutrition Bulletin, 24, pp. 43–82. KANASHIRO HC , FUKOMOTO M , BENTLEY ME , JACOBY E , VERZOSA C , BROWN KH (1991). Use of recipe trials and anthropological techniques for the development of a home-prepared weaning food in the Central Highlands of Peru. Journal of Nutrition Education, 23(1). BENTLEY ME , DICKIN KL , MEBRAHTU S , KAYODE B , ONI GA , VERZOSA CC , BROWN KH , IDOWU JR (1991). Development of a nutritionally adequate and culturally appropriate weaning food in Kwara State, Nigeria: An interdisciplinary approach. Social Science and Medicine 33(10), pp. 1103–1111. DICKIN K , GRIFFITHS M , PIWOZ E (1997). Designing by Dialogue. A program planners’ guide to consultative research for improving young child feeding. Washington, DC: Manoff Group & The Academy for Educational Development. WHO ( WORLD HEALTH ORGANIZATION ) (1994). Focused Ethnographic Study of Diarrhoeal Disease Manual. Division for the Control of Diarrhoeal and Respiratory diseases. World Health Organization, Geneva MENON P, RUEL MT , LOECHL C , PELTO G (2003). From research to program design: use of formative research in Haiti to develop a behavior change communication program to prevent malnutrition. Food Consumption and Nutrition Division Discussion paper #170. Washington, D.C.: International Food Policy Research Institute. BERNARD HR (2006). Research Methods in Anthropology: Qualitative and Quantitative Approaches. Newbury Park, CA: Sage Publications.

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and WORLD HEALTH ORGANIZATION (2003). Making choices in health: WHO guide to cost-effectiveness analysis. Geneva, World Health Organization. 37. FIEDLER JL (2003). A cost analysis of the Honduras Community-Based Integrated Child Care Program. Washington, DC: The World Bank. 38. FIEDLER JL and CHUKO T (2008). The cost of Child Health Days: a case study of Ethiopia’s Enhanced Outreach Strategy (EOS). Health Policy and Planning, 23, pp. 222–233. 39. WATERS H, PENNY ME, CREED- KANASHIRO H, ROBERT R , NARRO N, WILLIS J, CAULFIELD L, BLACK RE (2006). The cost-effectiveness of a child nutrition education programme in Peru. Health Policy and Planning,. doi:10.1093/heapol/czl010.

41 Research methods in public health nutrition: Critical factors Arun K. Nigam and Padam Singh

Arun K. Nigam is currently the Executive President of Institute of Applied Statistics & Development Studies (IASDS). Nigam obtained his MSc degree in Mathematical Statistics in 1962 followed by PhD in 1970. He has taught at postgraduate level for nearly thirty years at Banaras Hindu University, Indian Agricultural Statistics Research Institute (IASRI) and Lucknow University, India. Padam Singh holds a PhD degree in Statistics from Delhi University, India. He has been Member National Statistical Commission Government of India. He has held many important positions such as Director of the National Institute of Medical Statistics, Indian Council of Medical Research (ICMR), Additional Director General of ICMR, Joint Advisor Planning Commission of Government of India and Professor Indian Agricultural Statistics Research Institute (IASRI). He is presently Head, Research & Evaluation EPOS Health India and President, Institute of Applied Statistics and Development Studies (IASDS).

".

Introduction

Research is a serious and determined bid to investigate an issue through a systematic and planned methodology. Systematically planned research involves a sequence of steps as presented in Fig. 41.1. Knowledge generated by good and relevant research generally finds applications. The criteria for a good research are as follows: ●

●

●

●

Reproducibility – The results obtained should be reproducible under similar conditions. Replicability – The results and findings should be replicable in other areas as well. Generalisation – The results and findings should allow for generalization. Standardisation – The research should have been completed following the standard research protocol.

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41.1 Steps in systematically planned research.

Most research studies aim to answer fairly simple questions like ● ●

●

●

● ●

What is the prevalence of anemia among under-3 children? What should be the RDA for Indians according to age, sex occupation categories? What should be the reference standards for Indians categorizing them as undernourished and normal? What is the nutritive value of traditional foods consumed by primitive tribes? What is the dietary intake of adolescents? Assessing the nutritional status of a programme.

A researcher is faced with a number of queries. Some of the frequently asked questions in a research study are as follows: (i) Why this study? ● Generate new information ● Proof for a hypothesis: investigate what, why and how? (ii) Where or in which areas, the study will be carried out? ● Community based ● School based

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Hospital based ● National or regional level How much material or how many cases will be needed? ● Few based on availability of resources ● Adequate and scientifically planned ● Large countrywide What is the basis of the selection? ● Purposive ● Scientific ● Particular target group What techniques of gathering data will be adopted? ● Interview method ● Anthropometric measurements ● Biochemical measurements ● 24 Hour recall method ● Actual weighment method What method of analysis will be used? ● Software ● High level of statistical analysis ● Simple summarization and test of significance ●

(iii)

(iv)

(v)

(vi)

The following sections will address all these issues.

41.2

Designing a research study – critical factors

Rationale of a study is based on undertaking a detailed review and identifying the gap as well as highlighting the dire need for undertaking the study including its relevance to national or regional priorities. The overall objective and the specific objectives need to be clearly defined. Formulation of relevant hypotheses is a pre-requisite to any research study. The two components of research objectives and hypothesis are interlinked and both of these must be clear, unambiguous and specific. An appropriate research design, which is relevant for studying the objectives, is then chosen. The adequacy of sample size is critical and should be determined on a scientific basis taking into account the desired precision, confidence level as well as nature of character to be studied, expected/likely outcomes and extent of variability. An appropriate choice of the sampling design is imperative for obtaining efficient and valid estimates Questionnaires have to be designed to elicit information from the respondents through direct or indirect probing. The data collected through such a survey should be adjusted for non-sampling errors, depending upon their type and magnitude. Relevant estimates are then developed allowing for standard errors. While, the type and coverage of questionnaires is an

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important deciding factor about the quality of the data collected, any illconceived questionnaire may lead to substantive non-response and also to incorrect and evasive responses. At times questionnaires are unduly lengthy or contain many questions which are not relevant to the study, or one too short to provide a satisfactory coverage. A lengthy and clumsy questionnaire not only increases the cost of the survey but also makes management and supervision work, as well as editing and cleaning of data, much more cumbersome. Similarly, a questionnaire with insufficient coverage leads to loss in efficiency, because of the failure to collect some vital information. Each question must be unambiguous and non-overlapping, and the spirit of the question and possible response(s) must be clear to both the interviewer and the respondent. It is for these reasons that pre-testing of the tools (questionnaires) is considered an important step toward finalization of tools. Through effective pre-testing more than half the battle is won and the follow-up checks and corrective measures go a long way in improving not only the quality of data generated but also is critical for making the emerging estimates much more relevant to the objectives of the study. A pre-requisite to good quality data is effective training of the field staff as well as data editors/cleaners, and data analysts on the information sought along with all possible responses. Sufficient time should be given for field practice and the training should be evaluated. During field work there should be effective and quality monitoring. Even at ‘Data Entry Level’ there should be data validation employing range check, valid value check as well as internal consistency checks. Analysis and tabulation plan should be consistent with the objectives and the hypothesis. It is important to mention that the ‘Sample Size’ is determined only for analyzing the data at the aggregate level but invariably there is an attempt to present disaggregated analysis in terms of related socio-economic, demographic, housing or household characteristics. This leads to decomposition of sample size according to these disaggregated groups and to invalid estimates, with unduly large standard errors. For impact assessment studies, comparison of key indicators in the pre and post stage of the project is essential. The pre stage determination of key indicators is often done through a baseline survey carried out in the project area and even some times in a neighboring (control) area having similar features as the project area. One finds that many of the projects are implemented without any valid baseline survey. Further for making valid comparisons between findings of end line and baseline surveys one has to ensure that these are comparable. Usually simple difference in value/ percentage of the two stages is compared, though such comparisons should be relative in the intervention area versus control area after adjustment for baseline differences in two areas. Many evaluation surveys give emphasis

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merely on process indicators, rather than outcome indicator(s) directly related to the main objective.

41.3

Hypothesis testing and P value

Every research has an objective which could be translated into a research hypothesis. Importantly the research hypothesis has to be converted into a “Statistical Null Hypothesis”. A hypothesis is called the Null Hypothesis (HO) if it specifies that the effect of interest is zero; this statistical null hypothesis is often the negation of the research hypothesis. It proposes no difference or no relationship (significant one) in the variable under study for the groups. On the other hand, an “an alternative hypothesis” (H1), implies that the effect of interest is not zero i.e. there exists a significant difference (positive or negative) in the variable between the groups under investigation. Alternate hypothesis is true when null hypothesis is false. Example 41.1 Research hypothesis: Adolescent girls are more anemic than adolescent boys. Null hypothesis: Anemia level is same in adolescent girls and boys, i.e. there is no significant difference between the anemia levels of adolescent girls and boys. P b = P g, where, P b = Proportion of anemic boys (P1) and P g = Proportion of anemic Girls (P2) Generally, the Alternate hypothesis is anemia level is not the same among adolescent girls and boys. Mathematically,

Pb # P g

Anemia level is more among adolescent girls than boys; this could also be an Alternative hypothesis for testing. Mathematically,

P g > Pb

The Alternative hypothesis could also be if anemia level is less among adolescent girls than boys. Mathematically,

P g < Pb

Example 41.2 Another example could be comparing two groups of children receiving

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fortified food under ICDS programme or receiving usual non-fortified food under ICDS. In this case the Null hypothesis is Pf = PU, where Pf = Proportion of severely malnourished children among those receiving fortified food. P U = Proportion of severely malnourished children among those receiving usual non-fortified food. In this case the Alternate hypothesis would be that: Proportion of severely malnourished children is less among those receiving fortified food as compared to those receiving usual non fortified food. Mathematically, Pf < P U In general, Null hypothesis (H0): Any hypothesis under test implying null ness/ negation. H0 : P 1 = P 2 Example: There is no difference in the prevalence of anemia among adolescent boys and girls. Here P1 = Prevalence of anemia among adolescent girls P2 = Prevalence of anemia among adolescent boys Alternate hypothesis (H 1): The competing hypothesis with the null hypothesis. The Alternative Hypothesis could be one of the following Two-tailed H1: P 1 # P2 Example: There is difference in the prevalence of anemia among adolescent girls and boys One Tailed H1: P1 > P2 Example: The prevalence of anemia is higher among adolescent girls than boys One Tailed H1: P1 < P2 Example: The prevalence of anemia is lower among adolescent girls than boys interpretations on hypothesis (H0 or H1) are subject to sample fluctuations and as a result, two types of errors can occur. Below Table 41.1 indicates possible errors in drawing statistical inferences while testing the Null hypothesis.

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Table 41.1 Possible errors in drawing statistical inferences while testing the Null hypothesis In Actual H0 True H0 False

Inference Accept H 0 √ – Confidence level (1 – α) Type 2 error β

Reject H 0 Type-1 error α

√-Power (1 – β)

Wrongly rejecting a H0 is called type-1 error. Example: When in reality there is no difference in the prevalence of anaemia among adolescent girls and boys, (H 0 is true) but on the basis of a sample we draw the inference in rejecting the above. This is type-1 error. Here, level of significance α = Probability of type-1 error Confidence level of the test 1 – α = Probability of accepting Null hypothesis when it is True. The probability of this error is commonly known as P value. The maximum P value allowed in a study/problem is called level of significance or α level. The level of significance is generally fixed at 5%. When we say that a difference is statistically significant at 5% level of significance all that we mean is that the observed difference could have occurred by chance in only 5% of the occasions or less. However, the level of significance could be 10% when only the leads are explored through exploratory study. But in case of introduction of new drugs or an intervention dealing with humans the level of significance has to be fixed as low as 0.1% to ensure safety. Type-2 error is failure to accept H1 when it is true, i.e. interpreting H0 is true when it is not. Example: When in reality there is difference in the prevalence of anemia among adolescent girls and boys, (H0 is false) but on the basis of a Sample we draw the inference in accepting the Null hypothesis. This is type-2 error. Here β = Probability of type-2 error and Power of the test 1 – β = Probability of rejecting Null hypothesis when it is False. The probability of this error is β error. The complementary of type-2 error is power of test i.e. 1 – β. The power of a test is the probability of correctly accepting H1 when it is true, i.e. it is the probability of getting statistically significant result. The power of test is high if it is able to detect small differences in variable under study between groups.

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"."

Cut-off levels for different levels of significance in one-tailed and two-tailed test

While accepting or rejecting a Null hypothesis the decision is based on the value of the Test Statistic falling in the ‘Acceptance Region’ or ‘Rejection Region’. If the value of Test Statistic falls in the ‘Rejection Region’ the Null hypothesis is rejected. Conversely, if the value of the Test Statistic falls in the ‘Acceptance Region’ the Null hypothesis is accepted. The size of the Rejection/Critical region is related to level of significance. That is if the level of significance is 0.05, the Critical region will correspond to the area under the assumed distribution as 5%. All tests of significance assume normality. The cut-off values based on normal deviates (z α) corresponding to desired level of significance for one tailed and two tailed tests are summarized in the table below. α 0.01 0.05 0.10 0.20

Zα one-tailed 2.327 1.645 1.281 0.841

Zα two-tailed 2.575 1.960 1.645 1.281

In a two-tailed test the rejection region is located in both the tails. If we are testing a hypothesis at 5% level of significance, the size of the rejection region is 0.025 on both sides of the tails. If we consult the table of areas under the normal curve we find this corresponds to 1.96 on each side. If the sample mean falls into the area beyond 1.96 S.E., the hypothesis is rejected. For one tailed test at 5% level of significance the Rejection Region would correspond to the value of Standard Normal Deviate beyond 1.645 on one side of the tail.

".5

Research designs

There are different types of research designs which could be used in a given situation depending upon the objectives of the study. Some of the important research designs are as under: ● ● ●

Observational or experimental Prospective or retrospective Longitudinal or cross-sectional

In an observational study the researcher collects information on the attributes or measurements of interest, but does not influence events. Observational studies are often descriptive. An example would be a study of prevalence of anemia among children. Observational studies include

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surveys. By contrast, in an experimental study the researcher deliberately influences events and investigates the effects of the intervention. Experimental studies are usually carried out to make comparisons between groups. Experimental studies include clinical trials. In general stronger inferences can be made from experimental studies than from observational studies. For example, the effect of Iron–folic acid (IFA) supplementation to pregnant women versus anemia level could be studied in an experimental situation or through intervention study. However, many times data collected in the cross sectional surveys are also analyzed for the same objective by analyzing the anemia levels according to consumption of IFA. But the inference drawn from intervention study will be more stronger than observation study. In prospective studies, data is collected forwards in time from the start of the study. Cohort studies are prospective. Experimental studies are also prospective. In retrospective studies, data refer to past events. Case-control studies are retrospective. Cross-sectional studies are those in which individuals are observed only once. Observational studies are mainly crosssectional. Most surveys are also cross-sectional. Longitudinal studies are those which investigate changes over a period of time, in relation to an intervention. Observations are taken on more than one occasion. Clinical trials are longitudinal because we are interested in the effect of treatment commencing at one time point on outcome which is measured at a later time.

41.6

Sampling

A sample is a part of a population, called the ‘universe’, ‘reference’ or ‘parent’ population. Sampling is the process or technique of selecting a sample. Appropriate sample selection is very critical element of design set up for carrying out the research. The reference population may be populations of people who process a particular attribute cases of a certain disease, clients of a clinic, acceptors of a certain programme, residents of a geographical area, workers in a certain occupation, recipients of a specified treatment, or people exposed to a certain intervention. The population is the aggregate of the elements or the sampling units. Listing of the sampling units with identification according to certain specifications is called the ‘sampling frame’. Sampling procedures Random sampling ensures chance of selection to every unit in the population. Simple random sampling guarantees that each member of the population has an equal chance of being included in the sample. The

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common methods of random sampling are lottery and use of random numbers. The lottery method assigns numbers to the population; these number are then thoroughly mixed and a sufficient number drawn at random (without replacement) to provide the desired sample size. Tables of random numbers are used after numbers (e.g. sequential counts) have been assigned to members of the study population. One can start anywhere in the random number table and continue selecting numbers until the desired sample size is reached. Digits of currency notes could also be used as a substitute of random number table. Systematic sampling In systematic sampling, the first unit is chosen at random and then other units for the sample are chosen in a systematic way with an interval for example, every fifth household in the reference population. Stratified sampling In stratified sampling population is divided into homogeneous groups (or strata) according to certain common characteristics; then a random sample is drawn from each stratum. For example, a population might be divided according to social class, race, sex or age. Appropriate estimation procedure has to be used with proper weighting. There is an important issue of allocation of sample to different strata. Cluster sampling Cluster sampling involves choosing groups of units or clusters at random. The information relating to all the units in each cluster are collected. This method is operationally simpler and is less expensive than simple random sampling. Multistage sampling Many times the frame of ultimately observable units is not available. In such a case sample is selected using different stages. For example in a survey for a district on nutritional status of children stages could be: 1st stage : village 2nd stage : household 3rd stage : child

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Probability proportional to size In probability proportional to size (PPS) sampling the probabilities to different units are assigned in proportion to their size. Box 41.1 30 Cluster WHO Methodology for coverage evaluation surveys (CES) In a 30 cluster survey, the sample of 30 villages is selected by PPS method and the sample of mothers of children with index child is selected is as follows: ● ●

●

●

●

● ●

●

Prepare a rough sketch and identify a center. Draw all lanes/sub lanes from the centre as under-presented below:

Select one of the lanes/sub lanes randomly using digits of currency note. Let the lane so selected is 5th. In the selected lane walk across from the center till the end and count the steps say ‘L’. Then select a random number from 1 to L using the digits of currency note and let the number so drawn is ‘r’. Again walk from the center and stop at step ‘r’. The House on your left is the randomly selected house. Enquire whether there is a child in the age group 12 to 23 months. If Yes collect the information about the child on the immunization status else proceed to next house following right hand rule. Continue till 7 children are selected. This is to be followed in all the 30 selected villages.

41.7

Determination of sample size

It is imperative that the sample size be sufficient to be dependable and to allow tests of statistical significance to be applied to the data collected. Unfortunately, there is no thumb rule or magic formula for determining the sample size without some knowledge or assumptions. Such as the prevalence of the condition or characteristic to be studied, the variability between different sampling units, the desired level of statistical significance and the magnitude of sampling errors. The determination of Sample Size to situations that is (a) estimating average/proportion; or (b) in testing significance of two proportions/ averages are presented in the following sections. (a) In estimating average or proportion ●

The parameter (Hb level, prevalence of anemia) to be estimated;

1144 ● ● ●

Public health nutrition in developing countries

The degree of precision required; The desired confidence level; and The estimated degree of variability of observation, i.e. standard deviation.

Sample size: The formula for calculating sample size (n) is as follows: n = (zα2 pq)/d2 p = Likely value of the parameter q = 1 – p; d = permissible margin of error; and zα = value of standard normal deviate corresponding to level of significance. For 95% confidence level, this formula can be simplified as follows: n = 4 pq/d2 The term ‘d’ in above formula is the absolute margin of error. It is desirable to compute sample size with relative margin of error especially in situation where prevalence is low. Expressing, d = Ep, Where E = relative permissible margin in error, the formula simplifies to n = zα2q / pE 2, Thus, n α 1/p; higher will be n for lower value of p [rare diseases]. Further, n α 1/ E2; Higher will be n for lower value of E [Higher Precision], and n α Zα2; Higher will be n for higher confidence level. For estimating prevalence of anemia level among preschool children the computation of sample size is explained as under p = 0.70 (70%), q = 0.30 and E = 0.10 (10% of P) For α = 0.05 the value of zα = 1.96 In this case, n = zα2q / pE2 = ((1.96*1.96)*0.30)/(0.70*0.10*0.10) = 165 Table sample size

p

E

n

0.50

0.10 0.20 0.10 0.20 0.10 0.20 0.10 0.20

400 100 7600 1900 80,000 20,000 8,00,000 2,00,000

0.05 0.005 0.0005

Research methods in public health nutrition: Critical factors

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The Sample sizes for some typical values of p (likely value of parameter) and E (relative permissible margin in the error) are given in the above Table for a = 0.05. This sample size has to be multiplied by Design Effect, which is the ratio of statistical efficiency of the sampling design used to that of simple random sampling. (b) In testing for significance between two averages or proportions: intervention studies, Experimental Group versus Control Group The information required in arriving at the sample size is as follows: ●

● ●

The amount of difference between two means (or proportions) that is to be regarded as practically important; The size of α-error and β-error; and The estimated degree of variability of observation (i.e. standard deviation).

Example: ●

●

● ●

The approximate value of the parameter/proportion for control group (e.g. 70%) Difference in the proportions (between the control and the experimental group) regarded as of practical importance (e.g. 20%). Level of significance required (usually 5% level, in a 2-sided test). How high should the probability of obtaining a significant result (“power”) be (e.g. 90%)?

One may calculate the (reduced) power for detecting the difference of interest (e.g. 20%) or the (larger) difference that can be detected with 90% power. The sample size is calculated using the formula: n = 2[(Zα + Zβ) /K]2 Where K = D/σ; D = p 1 – p 2; σ2 = pq, p = Average of p1 and p2 Sample sizes per group for two-tailed test on proportions are presented in Tables 41.2 and 41.3. The above examples are for proportions. The formulae for computation of sample size for averages are as under: One sample situations (with usual notations) n=

Zα2σ 2 d2

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Table 41.2 Sample sizes per group for two-tailed test on proportions P1 = 0.60 ———————————————————————————————————————— | POWER | —————————————————— P2 ALPHA | 0.99 0.95 0.90 0.80 ———————————————————————————————————————— 0.65 0.01 | 4580 3416 2867 2268 0.65 0.02 | 4133 3033 2518 1960 0.65 0.05 | 3519 2513 2047 1549 0.65 0.10 | 3032 2106 1683 1237 0.65 0.20 | 2516 1682 1309 923 | 0.70 0.01 | 1127 847 714 569 0.70 0.02 | 1019 754 629 494 0.70 0.05 | 870 628 515 395 0.70 0.10 | 752 529 427 319 0.70 0.20 | 627 426 336 243 | 0.75 0.01 | 489 370 314 252 0.75 0.02 | 443 330 278 220 0.75 0.05 | 379 276 229 178 0.75 0.10 | 329 234 191 145 0.75 0.20 | 276 190 152 112 0.80 0.01 | 266 203 173 140 0.80 0.02 | 241 182 154 123 0.80 0.05 | 207 153 127 100 0.80 0.10 | 180 130 107 83 0.80 0.20 | 152 107 86 65 ————————————————————————————————————————

Suppose an estimate is desired of the average retail price of twenty tablets of a commonly used tranquillizer. A random sample of retail pharmacies is to be selected. The estimate is required to be within 10 paisa of the true average price with 95% confidence. Based on a small pilot study, the SD = 85 paisa. How many pharmacies should be randomly selected? n=

4 ( 0.85) ( 0.85) = 277.56 ( 0.10) (0.10)

Two Sample Situations (with usual notations) σ 2 ( Zα + Z β )

2

n=

( μ1 − μ 2 )

2

Example: A survey had indicated that the average weight of men over 55 years of age with newly diagnosed CHD was 90 kg. It is suspected that the average weight of such men is now somewhat lower. How large a sample would be necessary to test, at 5% level of

Research methods in public health nutrition: Critical factors

1147

significance with power of 90%, that the average weight is decreased to 85 kg, with an estimated SD of 20 kg? σ =20; α =0.05; β = 0.90; μ1= 90; μ2 = 85 n=

(20)2 (1.64 + 1.28)2 (90 − 85)2

= 137

Table 41.3 Sample sizes per group for two-tailed test on proportions P1 = 0.70 ——————————————————————————————-————————— | POWER | —————————————————— P2 ALPHA | 0.99 0.95 0.90 0.80 ——————————————————————————————-—————————— | 0.75 0.01 | 3907 2917 2450 1940 0.75 0.02 | 3527 2591 2153 1678 0.75 0.05 | 3005 2149 1753 1330 0.75 0.10 | 2590 1803 1443 1064 0.75 0.20 | 2151 1443 1125 796 | 0.80 0.01 | 935 704 595 476 0.80 0.02 | 846 627 525 414 0.80 0.05 | 723 524 431 332 0.80 0.10 | 626 442 358 269 0.80 0.20 | 523 358 283 206 0.85 0.01 | 393 299 254 205 0.85 0.02 | 356 267 225 180 0.85 0.05 | 306 224 186 146 0.85 0.10 | 266 191 156 120 0.85 0.20 | 223 156 125 94 | 0.90 0.01 | 206 158 136 111 0.90 0.02 | 187 142 121 98 0.90 0.05 | 161 120 101 80 0.90 0.10 | 141 103 85 67 0.90 0.20 | 119 85 69 53 ——————————————————————————————-——————————

41.8

Analysis

General issues of analysis of data revolve round the following: ● ● ●

●

Data entry and management. Data cleaning and validation. Choice of analytical techniques for obtaining valid estimates and inferences. Choice of appropriate software.

It is observed that at times objectives are not clearly spelt out and are simply the statement of intentions. Further the objectives are too ambitious

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to be covered in a single research effort. Also the associated hypotheses are sometimes complex and consequently difficult to be tested. In such situations, one simply ends up with generation of tables without any linking with objective or hypothesis. Further the inferences may be erroneous, misleading having serious policy implications. There are ways for controlling errors, bridging data gaps and improving the quality of data. These are applicable at different stages, viz. handling of data, sample selection and estimation. Every survey encounters the problem of missing data or data with inconsistencies. The problem of missing data occurs when some, or all of the responses, are not collected for a sample element, or when some responses are deleted because they fail to satisfy certain edit checks. Inconsistencies in data may also occur due to a variety of reasons, such as errors in tabulation, data entry or even in copying from a secondary source. In all such cases, it is a norm to treat it as missing data and handle it accordingly. Whereas total non-response, i.e., when all of the responses on a unit are not available, is handled by some form of weighting adjustment techniques, item non-responses are taken care of by imputation. Imputation is a technique to handle non-responses by replacing each missing value with a real value. A number of imputation procedures are now available for assigning values for missing responses. These are deductive imputation, overall and class-mean imputations, random imputation, hot-deck imputation and imputation based upon regression. Among the commonly used analytical tools are t, F and chi-square tests of significance. While t test is carried out to test the difference between two treatments (intervention vs. control), F test is used in analysis of variance for testing more than two treatments. Chi-square test is used to test the association between two or more categorical variables. Examples: t test: Testing the difference of anemia among boys and girls based on small samples . F test: Testing the difference of anemia among scheduled caste, scheduled tribe and others (for more than 2 groups). Chi-Square test: Testing the association of female literacy/education on infant feeding practice. Among other commonly used statistical tools are regression. Of particular interest is the logistic regression for identifying risk factors in any causal factor analysis. For instance, one can determine risk factors along with their loading factors associated with undernutrition.

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Disaggregated analysis Most studies are planned to provide aggregated results but many times disaggregated results are desired for identifying the target groups and areas requiring special focus. The disaggregated/subgroup analysis can sometimes be more revealing. Example 1: The map of UP given below provides pattern of underweight children in UP in 17 districts of UP from a survey based study carried in 1995 for UNICEF. On mapping the district-wise prevalence of underweight incidence (DWCD, UP, 1999) of <50 per cent, 50–69 per cent and ≥70 per cent, a distinct geographical pattern was observed (Figure 41.2). Highest incidence of malnutrition was observed in the waterlogged Tarai area bordering Nepal, followed by Central belt comprising the entire tract of Gangetic plains, and the lowest underweight percentages were observed in the Vindhyachal ranges which also include the dry Bundelkhand region.

41.2 Pattern of underweight children in UP.

This distribution of underweight in the state was not in concurrence with the common belief that the highest incidence of malnutrition in the state was in the poorer socio-economic region of Bundelkhand. Higher incidence of under nutrition was in fact noted in the waterlogged eastern region and in the wet Gangetic belt. This can be attributed to possibly

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higher occurrence of diarrhoea, infection and worm infestation which adversely affect the nutritional status of children. Example 2: Analysis of underweight pattern through age groups of unequal widths 0–6, >6–11, 12–23, 24–35, 36–59 months indicated maximum underweight in children occurring between 12 and 24 months (Figure 41.3 present the usual bar diagram with reference). However, analysis of data on prevalence was undertaken at equal intervals (month wise) and it showed that the maximum underweight is attained at 11 months with the plateau beginning at 12 months itself (Figure 41.3), instead of 24 months, as was reported by earlier workers [2].

41.3 Usual bar diagram with reference.

This was further substantiated through a fitted quadratic regression to the prevalence of underweight data (Figure 41.4). The maximum of the fitted curve was around 12 months. The analysis indicated malnutrition sets in early in life and accelerates during 8–11 months. Maximum malnutrition prevalence is attained already under one year and the prevalence plateaus at 12–35 months. Small area statistics ‘Small area estimation’ is a statistical technique which makes it possible to enhance the precision of subgroup estimates. The technique uses the idea of ‘borrow strength’ from similar other areas to develop more accurate estimates for a given area. There has been a growing demand for reliable small area estimates both from the public and private sectors. In our country, with such large variations, there is an increasing concern about issues of distribution, equity

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41.4 Fitted quadratic regression to the prevalence of underweight data.

and disparity. There may exist sub-groups that are far below the average in certain respects and need upgrading. Deep stratification or nested stratification (stratification within stratification), is very useful tool, if appropriately used. The technique provides a sampling design which requires a much smaller sample size and is intuitively more efficient than the conventional stratified design using only one stratification variable. Deep stratification is a tool which automatically controls variability according to disaggregated groups and even simple random sampling within each stratum usually leads to self weighting design, which is easy to analyse and interpret. There are some concerns with reference to efficacy of surveys with regard to relative margin of error, particularly for sub-group estimates. The subgroups could be related socio-economic, demographic, housing or household characteristics, or even classifications like grades of anemia or undernutrition (mild, moderate and severe). Sample size is usually determined for the overall indicator, keeping in mind the desired precision, complexity of the design and expected nonresponse. The subgroup indicator estimates as above mostly suffer from inadequacy of sample size. The inadequate sample size for each subgroup leads to highly imprecise and unreliable estimates for these subgroups. Disaggregated analysis by subgroups with inadequate sample size leads to erroneous inference. There could be situations where results based on such analysis find place in formulating policies, which may often have far reaching implications.

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".9

Softwares

SPSS (originally, Statistical Package for the Social Sciences) was released in its first version in 1968. It is among the most widely used programs for statistical analysis in social sciences. Statistics included in the base software: ● Descriptive statistics: Cross-tabulation, Frequencies, Descriptives, Explore, Descriptive Ratio Statistics ● Bivariate statistics: Means, t-test, ANOVA, Correlation (bivariate, partial, distances), Non-parametric tests ● Prediction for numerical outcomes – Linear regression ● Prediction for identifying groups – factor analysis, cluster analysis (two-step, K-means, hierarchical), discriminate functions ● Add-on modules provide additional capabilities. The available modules are as follows: ● SPSS Data Validation (added in version 14) – It allows programming of logical checks and reporting of suspicious values. ● SPSS Regression Models – Logistic regression, ordinal regression, multinomial logistic regression, and mixed models. ● SPSS Advanced Models – Multivariate GLM and repeated measures ANOVA (removed from base system in version 14). ● SPSS Classification Tree – It creates classification and decision trees for identifying groups and predicting behaviour. ● SPSS Table – It allows user-defined control of output for reports. ● SPSS Exact Test – It allows statistical testing on small samples. ● SPSS Categories ● SPSS Trends ● SPSS Conjoint ● SPSS Missing Value Analysis – It is simple regression-based imputation. ● SPSS Map ● SPSS Complex Samples (added in Version 12) – It adjusts for stratification and clustering and other sample selection biases. ● Epi Info is public domain statistical software for epidemiology developed by Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia (USA). ● Epi Info has been in existence for over 20 years and is currently available for Microsoft Windows. ● Cranes Software International Ltd. (Cranes), a company that provides Enterprise Statistical Analytics and Engineering Simulation Software Products and Solutions across the globe, announced the launch of SYSTAT 13, the latest version of its flagship statistical software package.

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SYSTAT 13 introduces the following new statistical methods: ● ● ● ● ● ●

●

●

ARCH & GARCH Models in Time Series Best Subsets Regression Confirmatory Factor Analysis Environment Variables in Best Statistics Polynomial Regression Enhancements to existing methods such as ANOVA, Bootstrapping, Cross-tabulation, Fitting Distributions, Hypothesis Testing and more! SYSTAT, a proprietary product from the Cranes® Group of Companies, integrates both basic and advanced statistical tools with dazzling accompanying graphics. Additionally, SYSTAT has newly partnered with Cytel – a 20-year leader in the design and analysis of clinical trials – to bring you SYSTAT 13 with Exact Tests, a new SYSTAT product that contains Cytel’s famous exact-inference testing procedures.

References 1.

(2001). Nutritional status of children in Uttar Pradesh, NFI Bulletin, January 2001. 2. NIGAM AK (2001). Analysis of malnutrition data - Revisited. Invited talk at the International Conference on Statistics, Combinatorics and Related Areas held at Wollongong, Australia. VIR SC

42 Reducing malnutrition: An analysis of the Integrated Child Development Services (ICDS) scheme Deepika N. Chaudhery

Deepika N. Chaudhery, PhD, is the Deputy Regional Director for Asia, Micronutrient Initiative (MI), Asia. Earlier, Dr Chaudhery as Coordinator Programs, MI, Asia, worked in close consultation with country governments in the development, delivery and quality assurance of micronutrient programs in six Asian countries – Afghanistan, Bangladesh, Indonesia, India, Nepal and Pakistan. Prior to this, Dr Chaudhery provided technical and programme management support to micronutrient India programmes as the Chief Executive Officer at the Micronutrient Initiative India Trust. Additionally, she has a vast experience in the field of reproductive and child health, HIV/AIDS and nutrition programmes as CARE India officer and as project officer, Nutrition, with UNICEF (India Country Office) based at Hyderabad.

42.1

Background

Even after 61 years of independence and reforms, under nutrition continues to remain a chronic public health problem in India. According to the most recent National Family and Health Survey (NFHS-3) 2005–06 [1], about 45% children less than 3 years of age are stunted (low weight-for-height) and 40% are underweight (low weight-for-age). Marginal improvement in nutritional status of children between NFHS-3 and NFHS-2 conducted in 1998–99 [2] has been disappointing. Malnutrition, both undernutrition and micronutrient deficiencies, restricts the growth and development of children, resulting in a substantial dip in productivity levels in adulthood. This has a cumulative negative effect on the health parameters and hence the country’s economic development. Among the programs and initiatives which are meant to combat undernutrition is India’s largest community-based outreach program for vulnerable children and women called the Integrated Child Development Services (ICDS) program. A key mandate of ICDS has been to improve nutritional and health standards of children below 6 years of age.

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1155

This chapter provides an overview of the ICDS program; tracks its contribution in improving nutrition and health outcomes; identifies limitations and outlines a way forward. Sections 42.2, 42.3, 42.4 and 42.5 present program design and implementation framework, evolution and current reach. Section 42.6 provides an analysis of limitations and Section 42.7 outlines how nutrition and health outcomes were impacted when innovative approaches were implemented. Section 42.8 proposes a strategy and actions to improve the effectiveness of ICDS as it moves towards universalisation.

42.2

Program background: design and implementation framework

The Department of Women and Child Development (DWCD), Ministry of Human Resource Development (Mo HRD), Government of India (GoI) was rechristened as Ministry of Women and Child Development in 2006. Under the aegis of the MoHRD, the ICDS scheme was launched in 1975. It was introduced in 33 blocks with the objective of contributing to goals of the National Policy for Children and has significantly expanded since then. This Section presents an outline of the design of the ICDS program – its objectives, package of services, infrastructure, human resources, and delivery mechanisms. It is important to note that the ICDS as described in this Section is the envisioned “program design”. What the program actually looks like in different operational contexts is described in Sections 42.2 and 42.3. Key participants of the scheme are children below 6 years, pregnant and lactating mothers and women in the 15–45 years age group. By 2006, ICDS covered about 6118 projects 1 across the country. Poised for universal coverage, as per GoI estimates of 2008 services are being provided to about 562.2 lakh (56.2 m) participants of which 467.2 lakh (46.7m) are children (0–6 years) and 95 lakh (9.5 m) are pregnant and lactating mothers, through a network of about 7.48 lakh (0.75 m) anganwadi centers [3] across the country.

42.2.1 Key objectives of ICDS [4] ● ●

Improve nutritional and health status of children below 6 years of age; Build a foundation for the child’s physical, psychological and emotional development;

1. ICDS project comprises 100 anganwadi centers, one for every village with 1000 population.

1156 ●

●

●

Public health nutrition in developing countries

Reduce incidence of mortality, morbidity, malnutrition and school dropouts; Enhance capability of the mother to look after health, nutritional and development needs of the child through proper community education; and Achieve effective coordination of policy and implementation among various departments to promote child development.

42.2.2 Basket of services under ICDS ●

●

●

●

Nutrition – Supplementary feeding, growth monitoring and promotion, nutrition and health education; Early care and stimulation – For children under 3 years of age and preschool education for children 3–6 years of age; Health – Immunization, support in micronutrient supplementation (vitamin A, iron, folic acid), health check-ups, referral services, and treatment of minor illnesses; Convergence – Of other supportive services such as safe drinking water, environmental sanitation, women’s empowerment, non-formal education and adult literacy.

Nutrition and early childhood care and preschool education related services are the primary responsibility of the Ministry of Women & Child Development whereas health related services fall under the direct purview of the Department of Health & Family Welfare. The anganwadi is the focal point for the delivery of services at the community level, located within the village or slum area it caters to. The anganwadi center (AWC) is expected to serve as a convenient meeting place for women’s groups that create awareness and mobilize joint action for child growth and development.

42.2.3 Composition of the ICDS Team  The anganwadi worker (AWW) who as per policy is recommended to be a local resident of the village, is the nodal frontline worker of the ICDS program. The AWW, assisted by anganwadi helper, operate at the village level. The Supervisor, Child Development Project Officer (CDPO) and District Project Officer (DPO) are at the sector (20 to 25 AWCs), project (a project being about 100 villages/blocks and in rural areas is often an entire block) and district levels, respectively. In larger rural and tribal projects, there is an Additional Child Development Project Officer (ACDPO). The onus of implementing ICDS program activities lies with this team of ICDS functionaries.

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Functionaries of the Department of Health include Auxiliary Nurse Midwife (ANM) and male health workers at village level, Lady Health Visitors (LHVs) at sector level, medical officer-in-charge (MOIC) at block level and Chief Medical officer (CMO) at district level. ANM’s unit of operation is the sub-center that caters to 5,000–8,000 people. The Primary Health Center (PHC) established for every 30,000–50,000 population is managed by the PHC’s MO. The health team works with the ICDS team to deliver services (Fig. 42.1). An AWC was initially meant to cater to a population of 1,000 but now in actual practice ends up servicing 1500 persons or more. In a large village of about 3,000–3,500 population, there are about 2–3 AWCs. Presently, there are an average 125–150 AWCs per project/block, since additional AWCs have been sanctioned, based on increased village and block population. However, in tribal areas the number of AWCs per project is about 700. Box 42.1 Roles and responsibilities of ICDS project staff [15] AWW • Village mapping. •

•

•

• • • •

Supervisor

• Preparing quarterly action plan. Conducting community • Supervising service survey twice a year and delivery and monitoring enlisting beneficiaries. day-to-day AWC activities. Delivering services – • Planning and organizing growth monitoring and induction training of promotion; preschool AWWs and helpers. education; distributing • Supervising and supplementary nutrition; providing continuing assisting health staff in education to AWWs immunization and heath during home visits. check-ups. • Planning and organizing Providing information and sectoral meetings. counseling to families/ • Analyzing skills and communities during home performance of AWWs. visits and group meetings. • Compiling/reviewing Promoting community MPRs and interpreting participation. data. Preparing Monthly • Assessing shortfalls in Progress Report (MPR). achievements; suggesMaintaining the AWC. ing corrective action. Liaising with panchayat, • Coordinating with PHC, primary schools, mahila CHC and different mandals. departments (Education, Information & Broadasting).

CDPO • Recruiting and training staff. • Supervising daily activities of AWC including periodic field visits. • Conducting monthly meetings with Superviors to discuss progress and problems. • Convergence between ICDS, Health, Panchayati Raj Institution (PRI) and local leaders • Maintaining records and registers – MPR; quarerly/annual progress reports • Procuring, storing and maintaining equipment and supplies. • Procuring and distributing supplementary nutrition. • Guiding and continuing education of project staff. • Promoting community participation.

The integrated ICDS package of services is intended to enhance impact of various nutrition, health and child development interventions. The package is delivered by the AWW with support from the helper. The AWW

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42.1 ICDS and Health Systems’: from Central to Village . 1

2 3

4

Villages covered by Lady Health Supervisor (LHV) and Mukhiya Sevika/ Supervisor are not necessarily the same Health sub-centre is recommended to cover about 5,000 population. ANM’s monthly visit to villages is normally based on microplan prepared for immunization coverage - atleast one visit/village/month on the days fixed for immunization. Accredited Social Health Activist (ASHAs)

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1159

needs to survey all families in the community to identify children below 6 years, pregnant and nursing mothers and adolescent girls in the catchment area. To enhance outreach of services and ensure better service utilization, the AWW needs to mobilize community support.

42.3

Key nutrition, early childcare and preschool education and health related services

42.3.1 Nutrition component under ICDS Supplementary feeding – Under the ICDS program, children less than 6 years of age are expected to be given supplementary food (often referred to as supplementary nutrition) which provides 300 calories and 8–10 grams of protein while pregnant and lactating mothers and adolescent girls are to be provided food with 500 calories and 20–25 grams of protein to meet the calorie and protein deficits in Indian diets consumed by poor populations. Children who are severely malnourished are recommended to be provided double the quantity of food. This amounts to 600 calories and 16–20 grams of protein. Supplementary food consists of local grains, oil, and in some areas Ready-To-Eat (RTE) foods. In case of RTE foods, children less than 3 years are given Take-Home Rations (THR) and 3–6 year olds are served on-the-spot. As per the Supreme Court directives, Hot Cooked Meals (HCM) are being provided in many states. In addition, the GoI has recommended that the ICDS supplementary nutrition needs to be fortified with essential micronutrients comprising iron, calcium, vitamin A, thiamin, riboflavin, niacin, folic acid and vitamin C at 50% of the recommended dietary allowance per day [5]. Details are presented in Table 42.1. Besides serving as a nutrition supplement, supplementary food is viewed to serve as an incentive and contact opportunity to attract mothers and their children to avail other nutrition, health and preschool education related services. This food is meant for the child/pregnant/lactating mother and adolescent girls and is not a substitute for home food. Growth monitoring and promotion – Children below 3 years are weighed once a month and those between 3–6 years are weighed quarterly. It is mandated that weights of all children below 6 years be recorded on growth charts at the AWC. This helps to assess the growth pattern of an individual child, detect growth faltering and determine nutritional status. Therefore, each child’s nutritional status is evaluated, gaps identified and remedial steps suggested. Counseling for breastfeeding, complementary feeding and other health care needs is expected to be provided subsequent to the weighing. Counseling on feeding practices is central to “Growth Monitoring and Promotion” for achieving desired impact.

1

1240 22 12 400 400 0.6 0.7 8.0 30 30

687 18.6 4.3 56 161 0.4 0.3 4.7 9 18

RDA – Recommended Dietary Allowance

Energy (kcal) Protein (g) Iron (mg) Vitamin A (mg) Calcium (mg) Thiamin (mg) Riboflavin (mg) Niacin (mg) Vitamin C (mg) Free Folic Acid (mg)

553 3.4 7.7 344 239 0.2 0.4 3.3 21 12

1690 30 18 400 400 0.9 1.0 11.0 40.0 40

978 26.5 6.8 66 66 0.6 0.3 7.4 15.0 26

Intake

RDA

Gap

RDA1

Intake

Age group 1–3 years

Age group 1–3 years

Table 42.1 Recommended Dietary Allowances, nutrient intakes and gaps [5]

712 3.5 11.2 334 334 0.3 0.7 3.6 25 14

Gap 2175 65 38 600 1000 1.1 1.3 14.0 40 400

RDA 1654 45 12 111 352 1.0 0.5 12.4 26 48

Intake

Pregnant women

521 20 26 489 648 0.1 0.8 1.6 14 352

Gap 2425 75 30 950 1000 1.2 1.4 16 80 150

RDA 1852 46.7 11.8 107 320 1.2 0.6 14.4 28 53

Intake

Lactating women

573 28.3 18.2 843 680 0 0.8 1.6 52 97

Gap

1160 Public health nutrition in developing countries

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Mothers, caregivers and families of children who are growth faltered are to be provided support via appropriate information; extra counseling through increased number of home visits; ensuring access to basic health services such as immunization by ANM; and those found severely malnourished are given special care through therapeutic supplementary nutrition (referred as “double ration”) and referral to a health facility. The concept of community-based nutrition surveillance has also been introduced in ICDS projects of selected states. A community chart for nutritional status monitoring is maintained at AWCs since this reflects nutritional status of all children registered with the anganwadi at any point in time and is a useful tool for community dialogue. Nutrition and health education (NHE) – The primary objective is to build the capacity of women in the 15–45 years age group to enable them to take care of their own health, nutrition and development needs as also to their children and families. NHE comprises of basic nutrition and health information related to child care and development including infant and young child feeding practices and environmental sanitation. It is built on local knowledge, attitude, practices and resources to cover all women. Home visits, mother’s meetings, events such as Nutrition and Health Day, immunization sessions, growth monitoring days, and local festivals/ gatherings are contact points to deliver NHE with or without the use of Information Education and Communication (IEC) materials. “Growth promotion” is viewed as a critical component of the larger NHE.

42.3.2 Early childhood care and preschool education (ECCE) As envisaged in ICDS, ECCE focuses on total development of the child (0–6 years). It includes promotion of early stimulation of under-3s through interventions with mothers/caregivers. It’s program for 3–6 year olds in the anganwadi is directed towards providing and ensuring a stimulating environment, with emphasis on necessary inputs for optimal growth and development. Child-centered play-way activities, which build on local culture and practices, using local support materials developed by the AWW, are promoted. Early learning component provides sound foundation for cumulative lifelong learning and development. It prepares children for primary schooling and offers substitute care to younger siblings, freeing older children, especially girls, to attend school. Local level coordination between the AWC and primary schools via convenient timings, location and supportive linkages between the AWW and primary school teacher is promoted [2].

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42.3.3 Health Health related services include immunization, delivery of micronutrient supplements, health check-ups, referral services and treatment of minor illnesses. These are provided by functionaries of the Health Department. ICDS provides support for the operationalization of the National Nutritional Anemia Control Program (NNACP) [6] and the National Policy on Management of Vitamin A Deficiency [7] under the purview of the Department of Health & Family Welfare. In coordination with the AWW, the ANM provides these services at the village level. The NNACP aims at decreasing prevalence and incidence of anemia in young children and women in the reproductive age group, especially pregnant and lactating women. The program focuses on promotion of regular consumption of foods rich in iron, provision of IFA supplements in the form of tablets to “high-risk groups” and identification and treatment of severely anemic cases. The supplementation component recommends IFA in liquid formulation containing 20 mg elemental iron and 100 μg folic acid per day [8] for children aged 6–60 months; 1 big IFA tablet (100 mg elemental iron and 500 μg folic acid) a day for 100 days for pregnant and lactating mothers after the first trimester of pregnancy and 2 big tablets a day for minimum 100 days for severely anemic pregnant mothers and women who are 15–45 years old. The National Policy for Management of Vitamin A Deficiency [7] promotes consumption of Vitamin A rich foods by pregnant and lactating women and by children under 5 years of age, promotion of colostrum feeding, exclusive breastfeeding for the first 6 months of life and continued breastfeeding until at least 2 years of life and administering massive doses of vitamin A. The massive dose component includes 9 mega doses of vitamin A supplement (VAS) for children 6 months to 5 years; first dose of 100,000 IU of vitamin A is recommended to be administered with measles vaccination at 9 months and subsequent 8 doses of 200,000 IU each at every 6 months interval. In the past five years, a biannual service delivery approach is being institutionalised to improve coverage of the 2nd to the 9th dose of VAS.

42.4

Training in ICDS

Training infrastructure includes the National Institute of Public Cooperation and Child Development (NIPCCD) at the national level, its regional centers located at Lucknow, Bangalore, Indore and Guwahati, 18 Mid Level Training Centers (MLTCs) and 283 Anganwadi Training Centers (AWTCs). While CDPOs are trained at NIPCCD, Supervisors’ training is conducted at MLTCs and that of AWWs at AWTCs.

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The curriculum for all levels of functionaries covers a wide range of nutrition, health and child development aspects and includes gender and community mobilization. AWWs are provided induction training for 15 days followed by a job course training and subsequent refresher programs. Job course training for CDPO’s, supervisors and AWWs is for 30 days. Out of the 26 working days 23 days are for institutional training with practical and mock sessions while 3 days are allocated for supervised practice. Participatory techniques are used and classroom teaching is supported by role play, demonstration and exercises (9-11). With the launch of “Udisha” project in 1999 (Box 42.2) under the ICDS, training of functionaries was redefined. “Udisha” was conceptualized as a dynamic and responsive human resource development program with a vibrant training and communication package [8]. It was supported by the World Bank during 1999–2004 and its three main components included regular training, innovative and area specific training and IEC.

42.5 Program evolution This Section describes program evolution in terms of coverage and monetary investment by government and development partners. The ICDS program has evolved over the last 33 years. An expenditure of about Rs 1,190 crore2 was incurred during the first 17 years, following which the government increased spending from Rs 2,271 crore2 under the Eighth Five-Year Plan to Rs 4,557 crore2 under the Ninth Five-Year Plan. The program has been supported by donors, including UNICEF, CARE, World Food Program and the Norwegian Agency for Development Cooperation [12]. The proposed outlay for the Eleventh Five-Year Plan is Rs 41764.80 crores2 [13]. It is proposed that the financial assistance under the program will be on 85:15 sharing between the central and State governments during the Eleventh Five Year Plan followed by 75:25 sharing during the 12th Plan and 50:50 sharing thereafter. World Bank supported ICDS in overlapping phases from 1990 to 2006. This includes Tamil Nadu Integrated Project (TNIP), ICDS – phases I, II and III and ICDS – Andhra Pradesh Economic Restructuring Project with International Development Assistance of about US$ 700 million [3].

42.5.1 World Bank assisted ICDS Phases I, II and III ●

2

ICDS Phase I – Support was provided to the Tamil Nadu Integrated Project (TINP I and TINP II) as an alternative to the standard ICDS program; TINP I was implemented between 1980 and 1989 covering

1 crore = 10 million (Rs. 45 = One US $).

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6 districts. TINP II was operationalised between 1991 and 1998 covering 24 districts in the state of Tamil Nadu. Box 42.2 Udisha - background and key features Udisha was a national initiative for quality improvement in training of ICDS functionaries and caregivers. Udisha was based on a vision that all functionaries of ICDS should be developed into agents of social change. The Department of Women and Child Development conducted a review of the entire training component of ICDS. This review was conducted over a period of two years and focused on training needs assessment, methodologies, syllabus, training resources, procedures, systems and program strategies. From this process ‘emerged’ the basic challenges which were attempted to be addressed by Udisha. Key features ● Revision of syllabus The revised syllabus under Udisha focused on AWW as a communicator, facilitator and a mobiliser and consisted of modules based on participatory methodologies and experiential learning. All modules focussed on a life cycle approach.

Training based on area/region specific needs About 75% of the core syllabus was common for the entire country, and 25% of the syllabus was based on area specific needs. This was developed by individual states to reflect the training needs for functionaries working in that region/area. Training need’s assessment formed an integral part of the process. ●

Integration and coordination of training For better coordination amongst the various players such as trainees as well as trainers/institutions and to avoid duplication and overlapping, task forces were set up at National and State levels to facilitate the process of planning and training in states. The states in turn formulated State Training Action Plan and Training Calendars. The process focused on who, what, where, how and when to be trained. ●

Technical support and institution building Udisha encouraged NIPCCD to develop into a center of excellence and a premier institute of child development. It also envisaged a dynamic collaboration with India's leading institutes such as the National Institute of Nutrition, the National Center for Education, Research and Training and the National Institute of Health and Family Welfare. ●

Monitoring Udisha focused on improving the skills of the ICDS project managers and functionaries in collection, analysis, interpretation and use of data at the community level. ●

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ICDS Phase II – Support was extended to the standard government ICDS program and to additional activities. It operated in 461 new blocks in the states of Bihar, Jharkhand, Madhya Pradesh and Chhattisgarh between 1993 and 2002. ICDS Phase III – Primary emphasis shifted from expanded coverage to improving quality of services. Operations extended to 318 projects in Kerala, Maharashtra, Rajasthan, Tamil Nadu and Uttar Pradesh between the years 1999 and 2006. In addition, a restructured component included coverage of the erstwhile ICDS-II projects between the years 2002 and 2004 and expansion to Orissa and Uttrakhand.

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ICDS Phase IV – A five year phase four is planned to be implemented in 8 states - Bihar, Chhattisgarh, Jharkhand, Madhya Pradesh, Maharashtra, Rajasthan, Uttar Pradesh and Andhra Pradesh with support from the World Bank. Objectives of the project are to reduce child malnutrition and improve early child development outcomes among children 3–6 years of age [14]. Following a targeted approach, the project envisages covering 158 high-burden districts from these states for intensive implementation.

As coverage increased, more states and more districts or blocks within states were given sanctions for AWCs and additional staff. During the expansion phase there were innovations supported the World Bank, UNICEF and NGOs, e.g. CARE and the Micronutrient Initiative to increase coverage of nutrition and health related services and behaviors. Under the Eleventh Five Year Plan – to comply with directions of the Supreme Court and to implement the National Common Minimum Program of the Government, the ICDS scheme has been expanded to cover 466 new projects and 188,168 additional AWCs. Based on revised population norms, recommended by the Inter-Ministerial Task Force, the states have given a requirement of 173 additional projects, 107,274 additional AWCs and 25,961 mini-AWCs [13].

42.6

Evidence from program evaluations and program limitations

Evidence from large scale program evaluations, including some select studies that were undertaken to measure impact of ICDS in improving nutrition and health services and behaviors of the target population are described in the Section. This Section also presents program limitations which have impeded progress.

42.6.1 Evidence from large-scale evaluations Three large scale evaluations of the ICDS program were undertaken – two evaluations by NIPCCD, i.e. 1992–93 [15] and 2005–06 evaluation [3] and one by National Council of Applied Economic Research (NCAER) in 2001 [16]. While these showed improvement on some health, nutrition and preschool outcomes, significant gaps were identified in program implementation. Key recommendations were to have on-the-job training that incorporated innovative methods of imparting refresher training; strengthening supervision; focusing on NHE; intensifying implementation of the preschool education component; and improving community participation (Box 42.3).

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Box 42.3 Gaps and recommendations: NIPCCD program evaluation Need to upgrade the physical infrastructural facilities of AWCs. Semi-permanent anganwadi structures need to be progressively replaced by permanent and pucca buildings and handpumps should be installed within the premises wherever possible. Categorical instructions may be issued not to locate AWCs in the areas predominantly inhabited by upper class and upper caste population, as it hinders utilization of services by the lowest castes and poor beneficiaries. ● Need to experiment with some innovative methods of imparting refresher training. The possibility of involving academic and technical institutions in strengthening continuing education needs to be explored. ● It should be mandatory for the Project Officers to organize frequent training workshops at the project level. The concept of establishing a resource centre at CDPO's office needs consideration and a policy decision. ● Supervision needs be strengthened. No Supervisor should have more than 20 AWCs under charge. A double or additional charge is detrimental for the supportive role. There is need therefore, to create a post of a substitute Supervisor in every project. ● Participation of ANMs in providing referral services, health check-up, home visits and NHE session needs to be promoted further. Both AWW and ANM should work in close collaboration in taking care of health needs of women and children. ● Coverage of children under supplementary nutrition, and particularly that of under-threes, should be improved through door-to-door surveys, encouraging consumption of food at the anganwadi and enhancing mothers' awareness about appropriate feeding practices. ● Implementation of NHE was found to be far below the desired level. It is suggested that Supervisors should be given the responsibility to hold formal NHE sessions regularly in AWCs under their charge. Rigorous monitoring by CDPOs and active participation of health functionaries can improve implementation of this component. For group formation and collecting women at one place for NHE sessions, locally popular social/recreational events may be organised. Utilisation of folk media such as nautanki, kathputli, etc, need to be included in the training curricula of functionaries to strengthen their skills in imparting NHE effectively. ● There is need for improving the implementation of pre–school education (PSE) component. Non-availability of material for play and learning is one of the major constraints. Efforts are needed to provide a minimum set of appropriate educational aids and material at every AWC. ● Irregular supply of equipment, food items, play material and medicine kits is one of the major problems in implementation of ICDS. The State Governments should take appropriate measures to streamline supplies for smoother implementation of the program. ● Community participation is a very weak link of the ICDS programme. It is imperative that community representatives should be involved right from the preparatory stage of initiating a project. Effective ways of augmenting participation need to be evolved. AWWs apparently do not have the requisite skills for promoting participation. CDPOs and Supervisors should take appropriate initiative in this regard. ● It was observed that coverage and outreach of services need to be improved in tribal areas, keeping in view the topographical factors. In urban areas also, the services provided were minimal and the situation was worse than that in tribal and rural areas. Steps need to be taken urgently to improve the situation in urban slums. (Source: National Institute of Public Cooperation & Child Development. National Evaluation of the Integrated Child Development Services. New Delhi, 1992) ●

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Based on 1992–93 and 1998–99 NFHS data, it was initially found that ICDS had significant and positive effect on nutritional outcomes, but on more rigorous exploration, little effect was found when children in ICDS villages were compared to children in non-ICDS villages [17]. NFHS 2005–06 [18] assessed utilization of services under ICDS. Key findings are as follows: ●

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81% children under age six living in enumeration areas covered by an AWC, only 28.4% received any services. Most common services included receiving supplementary food (26% children < 6 years of age, 20.5% pregnant women and 16.5% lactating mothers); preschool education (23% for children 3–6 years of age); receiving health check ups (15.8% children under age six, 12.3% pregnant women and 8.5% lactating mothers) and 20% and 18% of children received immunization and growth monitoring services, respectively; Only 10.9% pregnant women and 8.3% lactating mothers received nutrition and health education. Children between 2 and 3 years were more likely to be taken to an AWC than younger and older children; Mothers with no education were least likely to take advantage of services offered by an AWC; and Only 50% of the age eligible children from scheduled tribes in areas covered by an AWC received some kind of service.

These findings clearly indicate a sub-optimal utilization of services under a program that has been operational for several years.

42.6.2 Select studies In addition to large scale evaluations, numerous studies were conducted to assess different aspects of the program. Highlights from few studies over the last decade are given below. Findings reported are variable. On 18 years of completion of ICDS, Ghandhi et al [19] concluded that the program benefited all sections of communities including backward and minorities. There was significant decrease in the prevalent of severely malnourished children from 21% in 1976 to 7% in 1990. Contrary to this, there are assessments which show limited impact of ICDS on the nutritional status of children [20, 21]. Nutritional status of 1286 pre-school children residing in urban, rural and slum areas of Chandigarh revealed that the prevalence of undernutrition was significantly higher among the ICDS beneficiaries (53.8%) than nonICDS beneficiaries (46.9%) [20]. In another report between the years 1981 and 1991, the proportion of children with severe protein energy malnutri-

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tion living in the same 6 villages of Garhi tribal block of South Rajasthan declined from 14.6% to only 11.3% [21]. In a study conducted in Agra district of Uttar Pradesh, supplementary food was received by 20–48% of the pregnant mothers and 35–53.7 % of children and coverage with IFA tablets was in the range of 24–30 % indicating a clear need to strengthen service utilization [22]. An assessment indicated benefit of nutrition supplement provided by ICDS during latter part of pregnancy to undernourished pregnant women in maternal weight gain and birth weight. The ICDS supplemented mothers gained 100 grams more in pregnancy and the birth weight was higher by 58 g (p < 0.05) as compared to un-supplemented ICDS mothers. Birth weight in un-supplemented ICDS areas was 25 grams higher as compared to non ICDS area [23]. An assessment of the impact of non-formal preschool education on mental and cognitive development of rural and urban children showed positive findings [24]. Mean test scores among rural ICDS attendees aged 3–4 years were 73.77 compared to 67.33 for non-attendees. The scores for rural ICDS attendees 4–5 years old was 95.60 compared to 82.20 for non-attendees.

42.6.3 Program Limitations This section analyses program limitations under key areas of program mandate i.e., coverage, capacity, training and supervision, linkage with the health sector, monitoring and community engagement. Program mandate ICDS has six objectives which cover a large program mandate making the scope of work for program functionaries extensive and diverse in nature. Moreover, objectives with reference to nutritional status are not stated in terms of measurable goals. In many cases, efforts have not been rigorous enough to improve coverage with services and changing behaviors. This has contributed to limited impact of ICDS on weight and height of children. ICDS has not adequately focused on right age groups i.e. below 2 years with appropriate evidence based interventions that could improve nutritional status of young children. Emphasis has been on supplementary feeding and the 3–6 years age group. The understanding of links between key services and behaviors, and program impact has not been adequately communicated to district, block and sector levels. There has been little attempt to examine whether the program was moving towards impact or not. While a key focus area of ICDS is to address malnutrition, most of the efforts were directed towards providing supplementary food and addressing severe undernutrition through not a comprehensive approach but only by

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the double ration approach. Child care and feeding practices were given very little attention. Efforts to streamline identification of beneficiaries and ensuring supply and consumption of supplementary food were far from satisfactory. Linkage with the health sector for provision of micronutrient supplements and referral of severely malnourished child has remained poor since the roles of ICDS functionaries were often not clearly defined for these services. AWW was viewed by the government as a worker who would focus on activities to prevent malnutrition and promotive behaviors such as promoting and supporting breastfeeding and complementary feeding. Field observations reveals that she is often busy with supply of supplementary food as well as is drawn into different activities in the village – from conducting surveys for various departments to undertaking work during election duties, preventing her from focusing on her core responsibilities. Coverage Universalization of ICDS is the goal but this remains to be achieved in most states. Many existing AWCs currently cover more than 1000 population and reach of ICDS among urban slums and resettlement colonies continues to be patchy. There is limited flexibility at state and district levels for responding to population redistribution and new settlements. Focus has been essentially on increasing number of projects and AWCs with insufficient attention paid to identifying and reaching excluded families (due to geography and caste) even within current coverage areas. Infrastructure and human resources There are many ICDS projects which report inadequate infrastructure in terms of buildings to house an AWC and equipment such as weighing scales, records and registers. Human resources are also often not as per sanctions. It has been observed that the ICDS Supervisor positions in many states lie vacant for long periods. Staff expertise and capacity A key reason for inadequate focus and sharpness in ICDS efforts in improving nutritional status and child development outcomes is the absence of adequate technical and managerial expertise at various levels. Most ICDS officials and staff come from general academic backgrounds (and hence there are only a few who have received training in nutrition and child development and related disciplines including management) has been a contributory factor.

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Many senior ICDS managers like DPOs and CDPOs think that undernutrition can be overcome by merely “supplementary feeding”. This concept has percolated up to the AWW worker level. Training The ICDS training content and methodology in many cases is not designed in a manner that can help a field functionary to systematically plan for prevention and management of malnutrition in a community. ICDS functionary is not trained to be a good planner and manager of the day to day activities. Village survey is often completed systematically and the data is seldom used as a planning tool. She is therefore often not aware of the number of pregnant mothers and children <6 years in the village. In fact, there is a gap in her understanding of roles and responsibilities for achievement of the objectives. There are no protocols for prevention and treatment of malnutrition in routine ICDS training. However, within the Integrated Management of Neonatal Care Childhood Illnesses (IMNCI), training effort has been made to introduce this concept by health sector in select areas. Training programs provide the same content to all staff, not taking into account capacity and needs. Ongoing training and capacity building through supervisory visits and reviews is inadequate. As a results of training gaps, the AWWs skills in counseling for growth promotion are found to be sub optimal. The AWW is provided with different IEC materials to support growth promotion and disseminate information on ICDS services, however their use is inadequate for reasons that vary from IEC not being well integrated with the training component to some materials having too much of information. Simple tools and job-aids required to guide day-to-day work are usually missing. Supervision Several evaluations on ICDS noted supervision as a missing link in the program. Training has not equipped supervisors to guide and mentor AWWs to achieve each of the objectives. Supervisors’s role has focused primarily on supply and distribution of supplementary nutrition, attendance of children at AWCs and preschool education. Problem seeking and problem solving approach in supervision is inadequate. Limited mobility of supervisory staff restricts their ability to complete even mandatory field visits. Delayed payments of travel allowance to supervisory staff compounds the issue. Monitoring ICDS monitoring indicators and system do not track process outcomes critical to impact nutritional status and early childhood education. Due to

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the pressure of reporting information against various indicators listed in the monitoring format, it is not analyzed at either AWC or project level for program management and decision making. There is no system to check data entry of denominators and numerations and capacity to look at the most critical indicators continues to be weak. Linkage with health sector Three of the six objectives of ICDS are related to health services. However, linkages with the health system are not at the desirable level. In areas, where NGOs such as CARE or others are working to support the ICDS system, these linkages are found to be effective. Operationalisation of biannual vitamin A strategy has also addressed the issue of defining roles and responsibilities of ICDS and health sectors and linking the two systems effectively for achieving the goal. The health system has not been able to accord priority to some critical nutrition interventions such infant and young child feeding. Sector boundaries of ICDS and health are not coterminus which often prevents in the formation of joint sector level operational plans and reviews involving AWWs, ANMs and supervisors of Health and ICDS. Community engagement This is not implemented as envisioned in the program. Mothers’ groups and community volunteers have been tried in some contexts but there is insufficient experience and evidence to indicate if there are approaches that will work in different contexts. Role of Panchayati Raj Institutions (PRIs) in implementing and monitoring ICDS is not clearly defined and their involvement has been sporadic. It is important to recognize these limitations to be able to make modifications as the program moves forward.

42.7

Contribution of ICDS in improving nutrition and health services and behaviors of children and women: evidence from innovative approaches within ICDS

The recognition of the program limitations has been an ongoing process. State Governments with support from agencies such as the World Bank, UNICEF, CARE and the Micronutrient Initiative, through innovative approaches and program variations, have addressed many of these gap areas (highlighted in Section 42.6) to improve program effectiveness. The potential of ICDS to improve nutritional and health outcomes and thereby

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nutritional status is well demonstrated through these innovative approaches. Particularly the “what and how” which led to positive shifts in nutrition and health outcomes as described in this Section. Recently, the Micronutrient Initiative conducted a study of “Best Practices in ICDS” for the World Bank with one of the key objectives to inform the ICDS Reforms/ ICDS IV design. Many of the approaches described in this chapter are reflected in that analysis [25]. Successful innovations characterized by operating at reasonable scale covering a minimum of 100,000 population and resulting in positive nutrition services and behaviors including improvement in nutritional status3 include the Tamil Nadu Integrated Nutrition Project-phase II, Dular, Integrated Nutrition and Health Project-phase II, Keno Parbo Na, Anchal Se Agan Tak, Community Based Maternal and Child Health Nutrition (MCHN) Project, ICDS phase-III, and fortification of supplementary food in West Bengal. These innovations have not addressed the preschool education component of the program. There are innovations under the District Primary Education Program to improve early childhood education which are not covered in this chapter.

42.7.1 Tamil Nadu Integrated Nutrition Project (TINP-I and II) The evolution of the Tamil Nadu Integrated Nutrition Project (TINP) supported by the World Bank in 1980 went beyond supplementary feeding and focused on improving home based caring practices, in order to achieve an impact on moderate levels of undernutrition. There was a steady drop in malnutrition rates for all ages included. The mean weight at 6 months and 36 months in 1990 compared to 1982 was 360 grams (6.5% gain in weight) and 650 grams (6.2% gain in weight) heavier, respectively. These differences were significant in all monthly ages between 6 and 36 months. Percentage of children malnourished (-2SD of NCHS) decreased by 10.12 percentage points between 1982 and 1990. Evaluations indicated a decrease in underweight prevalence of about 1.5 percentage points per year in participating districts, twice the rate of non-participating ones [26]. The success of the TINP-I was founded on several factors including: selective feeding, careful focus on supplementing 3

In ICDS Program, Nutritional status is also described as normal, Grades I, II, III and IV malnutrition. ICDS used Indian Academy of Paediatrics (IAP) classification is on the basis of Harvard growth standards where: normal – >80% of standard weight-for-age; Grade 1 – 71–80%; Grade II – 61–70%; Grade III – 51–60% and Grade IV – <50%. Malnutrition is expressed in standard deviation units (Z-scores) from the median of the reference population in all innovations described in Section 42.4 with the exception of Community Maternal & Child Health & Nutrition Project which uses the IAP classification.

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the dietary intake of young children when their growth faltered and until their growth resumed; favourable worker–Supervisor ratios; clear job descriptions; and a well-focused monitoring system. Based on the experiences of TINP I, TINP-II launched in 1991 was implemented in 318 of the state’s 385 rural blocks. Objective and implementation approaches TINP II modified the strategy to make significant reduction in high prevalence of children suffering from moderate undernutrition, by shifting towards a more preventive focus. Core strategies were regular growth monitoring and promotion, nutrition education and health checks for all children, therapeutic supplementary feeding for moderately and severely underweight children who presented with growth faltering, and high risk pregnant and lactating women. There was more emphasis on training ICDS workers, building supervision and monitoring and creating an efficient management and information system. Information was analyzed and fed back into project implementation. Community participation was enhanced and members were trained to promote growth recording, monthly weighing and spot feeding. Results The program halved the prevalence of severe malnutrition in villages where it was implemented [27] though it did not fully meet the objective of reducing moderate malnutrition. It was suggested that TINP interventions must include greater focus on home level actions and proactive integration with health systems for better results.

42.7.2 Dular This initiative was undertaken in Bihar in 1999 and in Jharkhand in 2001 in collaboration with UNICEF to complement ICDS and build upon its infrastructure [28]. Objectives and implementation approaches Improving prenatal attendance as well as promoting breastfeeding, colostrum feeding and appropriate complementary feeding practices for decreasing malnutrition were key objectives. One of the major goals of this program was to capitalize and develop community resources at the grassroots level. Dular established a community-based tracking system of the health status of women and of children 0–36 months of age by neighbourhood-based local resource persons (LRPs). Dular’s approach seeks to ensure that girls and women of reproductive age have access to

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adequate nutrition, health care, and information about child care throughout their lives – especially while they are pregnant and nursing their young children. See Box 42.4 on implementation approaches. Box 42.4 Implementation strategy of the Dular program ●

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Dular trains local resource groups (LRGs), which comprise of local resource persons (LRPs) (approximately one for every 10 to 15 households), who assist the AWWs in providing services to pregnant women and mothers of newborns in their homes. Focus is on promoting safe delivery, breastfeeding, immunization, and other essential care practices during pregnancy and early childhood. The Dular program is initially introduced to a village through the village contact drive (VCD). ● This event consists of 2 days of training and advocacy, during which the objectives of the strategy are discussed with the community members and information is gathered regarding local beliefs and practices (for example, one of the most problematic common practices in tribal areas is the socalled hell-fasting, a fasting period for the mother commencing just after giving birth) related to women and children's health. ● This information is used to plan project activities appropriate to local conditions that are maintained over a consistent period. LRPs identified during the village contact drive collectively form a LRG, which meets weekly with the AWW to review program progress.

Results An impact evaluation of 744 women and children in Jharkhand showed that women in Dular villages were 4 times more likely to feed their newborns with colostrum than those in non-Dular villages. There was a significant difference in the proportion of women breastfeeding their infants before giving them other foods and liquids between the Dular and non-Dular villages (adjusted probabilities 41.4% and 17.1%, respectively). Young children in Dular areas had 45% lower prevalence of severe malnutrition than those in non-Dular villages.

42.7.3 Integrated Nutrition and Health Project (INHP) – Phase II CARE India implemented a large-scale INHP II in partnership with Ministries of Women and Child Development and the state Health and Family Welfare Departments, local NGOs and Community Based Organizations from October 2001 to September 2006. INHP II was implemented in approximately 95,572 AWCs in 747 ICDS projects across 78 districts in 9 states – Andhra Pradesh (AP), Bihar, Chhattisgarh, Jharkhand, Madhya Pradesh (MP), Orissa, Rajasthan, Uttar Pradesh (UP) and West Bengal.

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Objectives and interventions The objectives of this project was to reduce child malnutrition and infant mortality by providing an integrated and comprehensive approach to supporting ICDS and Reproductive and Child Health (RCH) programs of the GoI. INHP supported a subset of national program interventions that effectively reduce child malnutrition, including antenatal care; home-based newborn care; infant and young child feeding; providing vitamin A supplements for children, supplementary nutrition and child immunization. These services reached around 102 million people including pregnant and lactating women and children less than 2 years of age [29]. Implementers ICDS and RCH functionaries and volunteers4 (in 40% of program areas), were supported by local NGO workers. There was one CARE officer for every 3–4 blocks, supporting and guiding ICDS, RCH and NGO staff on technical/ operational issues. Implementation approaches See Box 42.5 Results An evaluation research was conducted in 2 intervention districts with controls in the two of the nine CARE supported states i.e. states of AP and UP to provide diverse socio-demographic contexts to assess “net impact” of the interventions package. Results from this research are presented in Table 42.2. There were improvements in early initiation of breast feeding, exclusive breastfeeding, timely introduction, quantity, quality and frequency of complementary feeding, responsive feeding, coverage with vitamin A and IFA supplements and contacts by service providers during the critical life cycle periods. There was marked improvement in UP as compared to AP. While the program did not reduce underweight and stunting in the study populations, in UP, the intervention clearly had an effect on wasting. INHP interventions

4

Volunteers are active, interested members of their communities, who serve as promoters and monitors of nutrition and health practices and are called Change Agents. Each change agent accepts responsibility for reaching 15-20 families in his/her neighborhood on a voluntary basis. Each anganwadi center has 5-6 such change agents who act as a link between families and service providers in facilitating change and promoting local problem solving.

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Box 42.5 Implementation approaches in INHP-II It was recognized that malnutrition was near universal and increased between the 6 and 18 months period and only less than 10% infants in this age group were eating even half the recommended quantities of complementary foods in most states. This led to the development and adoption of an Essential Nutrition Action Framework which included guidance on how to deliver these actions at district, block, sector and village levels; a 3-step counseling guide and age specific feeding recommendations. Critical elements of the overall INHP II implementation approach included: ●

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●

●

Mechanism to minimize exclusion (social map to include all eligibles, modified registers for tracking of services and behaviors). Home visits by AWW, volunteers and ANM during the critical period of pregnancy till the child is at least 2 years of age, more between 6 and 11 months to help establish adequate complementary feeding including use of simple tools, e.g. home visit planner to help prioritize these visits and their content (simple calculations showed that this could be accomplished with about 1-2 home visits on a working day by an AWW and the role of the ANM was to reinforce messages during her visits and/or immunization sessions). Strengthen fixed day/fixed site services where AWW and ANM deliver a package of nutrition and health services. This included immunization, antenatal care, distribution of Vitamin A and IFA, nutrition and health education and supplementary nutrition as Take Home Rations (THR) at the AWC and was referred to as Nutrition and Health Day. Strengthened supervisory processes and tools for focused implementation particularly, supervisory checklist, sector meeting checklist which provided guidance on content and processes to be monitored. District and block level planning and joint reviews conducted with participation from ICDS, Health and PRI. Ongoing capacity building on critical interventions and tasks to achieve the desired outcomes and impact. Use of data locally and efforts for Behaviour Change Communication (print and folk media in addition to interpersonal communication) and community mobilization.

protected against wasting among the following groups – all children, boys, infants 0–5 and 6–11 months. Anemia levels decreased slightly (from 88.6% to 86.7%) in intervention areas in UP while in control areas anemia increased (83.1% to 87.4%; p < 0.05) suggesting a protective effect of the intervention [30]. In addition, a program-wide evaluation across 8 states showed an eight percentage point reduction in underweight in children 12–23 months of age from 61% to 53 % over a period of 5 years.

42.7.4 Keno Parbo Na Building on the ICDS infrastructure, an innovative initiative based on Positive Deviance (PD) approach was initiated in 2001 in a phased manner, with UNICEF support, in 4 districts including South 24 Paraganas, Dakshin Dinajpur, Murshidabad and Purulia of West Bengal.

–6.3

591 86.8 3.5

–11.11

12.21

789 63.5

789 91.8

789 4.6

1831 24.6

2034 35.7 11.1

8.01

1643 22.1

Recommended complementary feeding frequency amongst breastfed children n² 1620 1893 1702 1901 1447 6–8 months (2+times/day) 34.5 56.1 21.6 11.4 35.5 24.1 –3.5 2.3 9–11 months

Introduction of solids at 6–8 months n¹ 1746 2012 % 30.4 49.5 19.1

Comparison (Rangareddy, AP)

9.8

–1.4

2.0

758 78.5

750 44.4

741 59.0

15.0

47.4

54.4

712 62.8

711 96.1

711 2.1

679 70.7

661 93.2

658 10.5

7.9

–2.9

8.4

25.4

1476

1650 52.8

23.1

30.7

3.2

1445

1666 26.8

18.2

1473

1624 56.5

15.0

29.7

Diffe Intervention Comparison -rence (Barabanki, UP) (Unnao, UP) of Baseline Endline Change Baseline Endline Change Change Baseline Endline Change Baseline Endline Change

Intervention (Karimnagar, AP)

Complementary feeding Behaviours (6–23 months old)

Exclusive breastfeeding n¹ 614 549 % 77.0 70.7 616 77.0

611 67.6

591 69.0

Prelacteal feeds n¹ 614 % 61.7

545 49.2 –12.5

610 18.9

Breastfeeding initiated 1 hour after delivery n¹ 614 545 591 % 22.3 36.5 14.2 16.9

8.11

1.0

Difference of change

7.11

–44.51

46.01

Breastfeeding behaviours (0–5 months old) Intervention Comparison Diffe Intervention Comparison Diffe(Karimnagar, AP) (Rangareddy, AP) -rence (Barabanki, UP) (Unnao, UP) rence Baseline Endline Change Baseline Endline Change of Baseline Endline Change Baseline Endline Change of Change change

Table 42.2 Changes in selected infant and young child feeding behaviours, Nutrition Evaluation Research in CARE’s Integrated Nutrition and Health Project - II

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2034 52.2 69.9 74.4 14.0 6.9 4.0

1643 5.1 19.8 37.0

1650 41.2 44.7 57.8

1650 22.4 39.2 53.4

6.9

6.0

6.0

1650

37.8

23.9

36.1 24.9 20.8

20.0 29.8 27.8

5.4

5.5

5.0

29.0

20.8

1666 7.4 19.2 45.4

1666 2.8 14.4 31.1

2.1

2.4

0.8

1666

15.9

4.6 31.3

11.3

1624 21.8 26.7 49.9

1624 10.9 32.9 43.7

3.2

1.0

1.3

1624

n¹ = Total no. of children 0–5 months; n² = Total no. of children 6–23 months; 1Significant at 95% confidence level]

1831 38.2 63.0 70.4 –7.51 –0.5 –0.4

6.5 6.4 3.6

Fed from a separate plate n² 1746 2012 6–8 months 61.1 67.6 9–11 months 75.5 81.9 12–23months 77.8 81.4

1643 2.4 9.4 25.6

0.0 2.8 –4.61

Consumption of 3 or more food groups in the past 24 hours n² 1746 2012 1831 2034 6–8 months 5.1 8.2 3.1 0.8 3.9 3.1 9–11 months 8.2 14.7 6.5 2.9 6.6 3.7 12–23months 15.0 22.1 7.1 4.6 16.3 11.7

1643

8.8

1.5

–4.4

3.1

0.7

31.3

5.7

0.5

40.9

9.7

4.7

9.6

17.3

1.0

26.9

42.4

7.6

4.9

15.4

28.3

Consumption of at least half the recommended quantity of solids n² 1746 2012 1831 2034 6–8 months (100+ g) 26.7 43.2 16.5 16.0 27.6 11.6 9–11 months (150+ g) 18.0 36.6 18.6 8.3 23.2 13.9 12–23months (200+ g) 20.1 44.8 24.7 10.3 35.7 25.4

(3 + times/day) 12.9 12–23months (3 + times/day) 15.5

14.4 7.5 4.5

8.1 18.5 12.6

1.1

–1.4

0.5

15.4

6.7

21.71 17.41 16.31

11.91 11.31 15.21

4.31

6.91

4.51

13.61

14.11

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Objectives and implementation approaches The objective was to reduce and prevent malnutrition among children under 3 years, by focusing on local solutions, resources and practices [31]. This included training of childcare workers; weighing children and determining their nutritional status; identifying pockets of high malnutrition; having discussions/brainstorming sessions to identify best care practices in the community; motivating families to adopt them through participatory learning during Nutritional Counseling and Child Care Sessions. See Box 42.6 for key elements of the strategy. Box 42.6 Keno Parbo Na - key elements of the program strategy ●

●

●

●

●

●

●

Community mobilisation around the Positive Deviance Approach through participatory processes, which involve the formation of village committees and pro-active dialogues between social groups and institutions, using cultural methods such as village picnics, fairs, etc. Convergence and partnership between the service providers, administration and NGOs involved in implementation. Capacity building of childcare functionaries and the community using the "triple A" approach through regular review of activities. Community based management of malnutrition through Nutritional Counselling and Care Sessions (NCCS), emphasizing positive behavioral changes in childcare practices (12 days of spot feeding and 18 days of Take Home Rations for children in grades II, III and IV children) Hands-on training of mothers or caregivers over a 12 day period, on infant feeding like exclusive breast feeding, complementary feeding, healthcare, hygiene, and psycho-social care practices followed by practice sessions at home for a further 18 days. The cycle extends over 6-9 months within which period mothers/caregivers start showing behaviour change. There is also emphasis on vitamin A supplementation, hand washing practices, diarrhoea management, prevention of low birth weight (LBW), early registration of pregnancy, and antenatal care. Action-oriented, realistic and time-bound indicators.

Results An evaluation utilizing a case control design showed a positive effect on key behaviors and services particularly exclusive breastfeeding, timely initiation and frequency of complementary foods and Vitamin A coverage (Table 42.2). Higher percentage of mothers in PD area (69%) received health and nutrition education by AWW mostly at AWCs compared to 27% in control areas. The prevalence of underweight and stunting (45.6% and 25.2%, respectively) was significantly (p<0.01) lower in the PD area compared to control area (63.2% and 37.4%, respectively) in children aged 12–17 months. No gender differentials were observed in underweight or wasting between both groups, though prevalence of stunting reduced significantly among girls in the PD area compared to the control area.

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42.7.5 Anchal Se Agan Tak (ASAT) Objective and implementation approaches A comprehensive strategy to prevent and treat malnutrition was implemented in Rajasthan in 2005 [32]. Enhanced ICDS structures in terms of capacities to deliver quality services and community support at various levels were developed. At the village level, community volunteers called the Gram Sampark Samooh interfaced with families and systems to generate demand for services. Table 42.3 Key outcome indicators under the Positive Deviance project in West Bengal Indicators

Positive Deviance areas

Non-Positive Deviance areas

76.4

44.1**

22.1

65.4**

69.7

61.3*

44.0 40.5

28.8** 50.2*

21.1 52.1 26.8

60.8** 32.9** 6.3**

85.9

68.2**

34.2 50.2

40.7* 33.0**

Breastfeeding practices Percentage distribution of mothers of <12 months children according to breastfeeding practices Time of initiation of breastfeeding <3 hours Pre-lacteal feeds given Percentage distribution of children of <12 months according to breastfeeding practices by current age 4–5 months – solely breast fed Complementary feeding practices Percentage distribution of mothers of 12–23 month children by feeding practices Age of initiation of complementary feeding in months 6 >7 Frequency of other complementary feeds/day 2–3 4–5 >6 Immunization and vitamin A coverage Percentage distribution of children (12–23 months) completely immunized Percentage distribution of children (18–35 months) who received massive dose of vitamin A supplementation One dose Two doses

Positive deviance (intervention areas); Non-Positive Deviance (control areas). *p<0.05, **p<0.01

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A block support team was established in project blocks to assist staff at block and village level to implement the program. In project districts, a District Mobile Monitoring Training Team was constituted to monitor progress and provide on-the-job guidance to the village team. A District Support Team was constituted to improve coordination between sectors, review overall progress, and ensure effective implementation across the district. In addition, a state-level training and monitoring unit was formed. The program focused on household counseling, having a Maternal and Child Health and Nutrition (MCHN) Day, and a fixed Weighing and Counseling Day which was organised a week prior to the MCHN Day. ●

●

●

●

●

Household counselling on various issues related to health and nutrition. Maternal and Child Health and Nutrition (MCHN) Day: A state-wide monthly fixed day event. It focused on immunization, vitamin A supplementation (twice a year), weighing of pregnant women, provision of IFA tablets to pregnant women and adolescent girls, salt testing and counselling on maternal and child issues. It was held at the AWC and was facilitated by the ANM and AWW with assistance from the Sahyogini (village volunteer) and the anganwadi helper. Fixed Weighing and Counselling Day: A state-wide initiative (initiated in February 2006) on a fixed day one week prior to the MCHN Day. All children in the village less than six years of age were weighed. The AWW and Sahyogini facilitate the process. Special Plan of Action (SPOA) initiated in 2005 in 14 blocks. The goal of SPOA was to manage child malnutrition through support of ICDS by training ICDS functionaries, adopting WHO standard protocols, strengthening referral services and counselling families. The strategy focused efforts on interventions and capacity building at the 3 levels: family, community and district hospitals. Training tools and modules were developed to train all functionaries in systematic training sessions.

Results A survey utilizing a case control design was undertaken in 2006 to assess program impact. A higher percentage of women fed the newborn colostrum (47%) in ASAT project areas compared to control areas (18%). Weighing efficiency, exclusive breast feeding rates, timely initiation of complementary feeding were higher in ASAT areas compared to control areas. Diarrhoea episodes were less frequent in ASAT areas compared to control areas. There was more contact of the mothers with AWW and community volunteers in ASAT areas (59.7%) compared to control areas

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(46.8%). There was marginal difference in prevalence of underweight in ASAT areas (50%) compared to control areas (56%). However, stunting was significantly higher in control areas in comparison to the ASAT group (45% compared to 35% in control areas; p<0.01). Factors contributing to success of ASAT include counseling focused on nutrition and health interventions, training and skill building of functionaries to prevent and treat malnutrition and enhanced ICDS structures, e.g. block and district teams.

42.7.6 Community-based Maternal and Child Health Nutrition Project (MCHN Project) This 4-year project (2001–2005) was implemented in 8 blocks of 4 districts in Uttar Pradesh covering a population of 1.33 million in collaboration with UNICEF (Jhansi, Allahabad, Agra, Varanasi, 2 blocks per district). It was based on a multisectoral approach involving Health and ICDS as also Panchayati Raj Institution (PRI) for water and sanitation. The Departments of Social and Preventive Medicine of the Medical colleges provided coordination and technical support [33]. Objectives The aim was to reduce underweight in children less than 2 years by 20%; improve coverage of children with vitamin A supplementation to 80%; ensure 60% women consume minimum 100 IFA tablets and 100% households use iodized salt. The target group referred to as “at risk families” comprised families with children below 2 years, pregnant, lactating women and newly weds and children below 6 years with severe malnutrition. Implementation approaches See Box 42.7. Results A baseline survey was undertaken in 2000 and an endline in 2005. There was a positive shift in behaviors and services. The practice of initiating breastfeeding within an hour of birth increased 5-fold (baseline 4.6%; endline 21.9%); percentage of infants introduced to semi-solid food between 6 and 9 months increased from 18% in baseline to 63% in endline; women receiving more than 90 IFA tablets during index pregnancy increased from 6% to 61% and consumption increased from 9% to 22%. For health, nutrition, water, hygiene and sanitation education as well as

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Box 42.7 Implementation approaches in Community-based Maternal and Child Health Nutrition (MCHN) Project Block officers ●

●

Two block level officers, designated as Block Trainer cum Monitor (BTMs), were appointed in each block for overseeing the overall implementation of project in their respective blocks. They, along with ANM and AWW were involved in identifying community based volunteers; providing support in organising and conducting pre-service and in-service training of a team of trainees comprising community volunteers, health worker (ANM) and ICDS worker (AWW) as well as in organizing quarterly monitoring meetings at the health sub-centre level (comprising 5–7 villages).

Community volunteers ●

●

●

●

●

●

●

●

Community volunteers, referred as Community Health Nutrition Sanitation Mobilisers (CHNSMs) or in local language Bal Parivar Mitra (BPMS) meaning "friend of families with young children" were selected and assigned the tasks of reaching the "at risk families" at least once a fortnight. For the selection of the community volunteers, a social map of each village was prepared by ICDS workers with the help of BTMs and the community members. Three to five primary community clusters were identified on the basis of religion, caste or creed in a village with 1000–1500 population. In each village, effort was made to have a volunteer or a BPM selected from each of the clusters jointly by the ICDS and health frontline workers with the help of BTM and participation of community members. Volunteers with positive attitude on influencing social issues pertaining to women and children and who were vocal, dynamic and respected were selected. Each BPM was responsible for a cluster of 50–60 households but was expected to be working at a time with identified 15–20 "at risk families" in the cluster. The primary responsibility of these volunteers was to visit homes of identified families and counsel them on adoption of appropriate maternal and child care and feeding practices such as promotion of early initiation of breastfeeding, exclusive breastfeeding with emphasis on "no water" for first six months, complementary feeding, increasing food and rest during pregnancy, following appropriate hygiene and sanitation care, use of safe source of drinking water, use of iodised salt. The latter included salt and water testing. ■ Right advice at the right time to the right recipient or family was the principle applied in the interpersonal counseling sessions to be organized by BPMs with the selected risk family. These community volunteers were also responsible for undertaking monitoring and for maintaining records of actions taken. ■ Community volunteers were also in-charge of informing the "at risk families" of the importance of reproductive and child health and nutrition services such as antenatal care, routine immunization to children and vitamin A supplement administration. BPMs also mobilized the "at risk families" to avail of these services which were provided free of charge by frontline workers of primary health care centre and the ICDS. For rehabilitation of severely malnourished, special attention was directed at rapid screening by observation and follow up of severely malnourished children by BPMs. The volunteers were trained to screen severely malnourished children. Imparting training to BPMs was the most critical component of the project implementation since they were the primary persons reaching the "at risk families". Considering low levels of literacy of BPMs, a three-day intensive and easy to understand case-study based training was imparted. Focus was on development of skills for counseling, screening of severely malnourished

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Public health nutrition in developing countries

by observation and linking with service providers. In-service training continued during monitoring sessions. BPMs were given no monetary compensation but social recognition such as a badge to wear, a large name plate to be put on the doors of their house, a cloth bag for carrying monitoring forms and training manual as well as a certificate following completion of training.

Factors that contributed to the success of MCHN: ● ● ● ● ●

● ● ● ●

Emphasis on under 2 years and "at risk families". Emphasis on correct advice to selected "risk families". Community mobilisers were incharge of only 15–20 "risk families" Supplies of IFA tablets and ORS ensured Trainings completed using pictorial monitoring card with emphasis on life cycle approach Monitoring by community mobilisers using pictorial cards A system to link with health established Technical core group established Project facilitator positioned at block levels and district levels

nutritional health services, Community Volunteers referred as Bal Parivar Mitras (BPMs) were the main contact points for counselling “at risk” families, followed by ANM and AWW. There was no emphasis on growth monitoring and promotion but on “right advice at right time to right receipient”. There was considerable decline in percentage of severely malnourished children (baseline: 25%; endline: 14%) as per IAP classification and percentage of children with normal nutritional status improved marginally from 25% to 28%.

42.7.7 ICDS Phase III Phase III of the World Bank assisted ICDS, originally in five states viz. Kerala, Uttar Pradesh, Rajasthan, Maharashtra and Tamil Nadu was expanded to six additional states of Madhya Pradesh, Bihar, Chhattisgarh, Jharkhand, Orissa and Uttaranchal in 2003. It also strengthened the ICDS program in all 35 states/union territories, by improving quality of training of ICDS functionaries through project Udisha [34]. Objectives and approaches The project aimed at accelerating improvement of nutrition status of children 0–6 years and women. It provided additional inputs over and above inputs admissible in the ICDS Scheme, viz. construction of civil works, hardware inputs for better service delivery (adult weighing scales, display boards, outdoor play materials), quality improvement (study tours, Free Expression for Quality Improvement (FREQI)5 , training for IEC etc) and 5

Formation of quality circles to encourage better interaction among AWWs so that they could exchange notes freely, bring them to the notice of the supervisory staff and with their support achieve higher quality of service delivery.

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monitoring and evaluation activities (development of computerized Monitoring Information Systems (MIS), social assessment, operational research studies, baseline/endline surveys). There was emphasis on introducing an Adolescent Girls Scheme to address the life cycle issue of malnutrition. Results Pre-post evaluation (baseline in 2000, endline in 2006) was conducted in five states. Percentage of children under 3 years who were breastfed within 2 hours of birth increased from 37% during baseline to 51% in endline. Only 21% children under 6 months were reported to have been exclusively breastfed which declined from 28% in baseline. Percentage of children 6–9 months receiving solid or semi-solid food and breast milk increased from 38% to 64% and percentage of children between 6 and 36 months who consumed vitamin A rich food increased from 53% to 71%. There was significant improvement in services related to antenatal care of pregnant women, immunization, de-worming and treatment of diarrhoea. Impact of IEC and training led to increased awareness of infant feeding practices among AWWs though knowledge transfer from AWWs to women remained a cause of concern. Overall, underweight significantly decreased from 44.5% to 36%. Malnutrition rates decreased in each state: Kerala 11.1% to 3.5%; Maharashtra 51.8% to 42.6%; Rajasthan 43% to 35.4%; Tamil Nadu 50.9% to 39.5%; and UP 58.1% to 44.7%.

42.7.8 Fortification of supplementary food in West Bengal In 2005, the Department of Women and Child Development in West Bengal with support from the Micronutrient Initiative supported the fortification of the supplementary food (comprising khichdi, a rice and dal mixture) with a premix called vitashakti6 containing iron, vitamin A and folic acid. The key objective of this approach was of increasing iron and vitamin A stores and decreasing the prevalence of iron deficiency, anemia, and vitamin A deficiency. Introduced in the South 24 Parganas district, this approach has now been up-scaled to the entire state by the Government of Bengal. Implementation The premix is added to the cooked food (khichdi) by a spoon measuring 1.25 grams for 5 beneficiaries. The premix is initially mixed with water 6

14 mg microencapsulated ferrous fumerate, vitamin A 500 IU, folic acid 0.05 mg per 0.25 g serving.

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Public health nutrition in developing countries

and then added to the cooked food after it is removed from fire. The premix cost for each beneficiary is only Rs. 0.03/per day. Half-kg packets in a plastic container are provided to the AWCs and each packet can cater to 2000 beneficiaries. It is given to children from the age of 3 to 6 years, pregnant and lactating women. Results A cluster, randomized, double-blind, controlled trial was undertaken in 30 AWCs in the South 24 Parganas district [35]. Children in the age group of 36–66 months were randomly assigned to receive either a fortified or a non-fortified khichdi for a period of 24 weeks. Hemoglobin, serum ferritin, and serum retinol were measured. Prevalence of anemia decreased from 19.1% to 4.1%; mean serum ferritin levels showed a marked increase from 25.1 to 35.5 μg/l and prevalence of iron deficiency anemia showed a decrease from 4.9 to 0.4%. There were no significant differences in serum retinol concentrations or in the prevalence of vitamin A deficiency between the fortified- and non-fortified-khichdi groups. Overall, the prevalence rates of anemia, iron deficiency and iron deficiency anemia were significantly lower in the fortified group compared to the non-fortified group. This demonstrated that fortifying supplementary food can be effective at increasing iron stores and reducing the prevalence of iron deficiency and anemia at the community level. This assumes great importance in a country where about 70% children aged, 6–59 months and 55.3 % of women in the age group of 15–49 years, are suffering from anemia [1]. Common elements cutting across these projects contributing to positive outcomes were focused on: ● ● ●

●

●

●

Critical age group of 0–3 years for achieving nutritional impact; Evidence based interventions; Strengthened capacity and structures at all levels in terms program content and operational “know-how”; Supportive supervision (supervisors guiding and problem solving, use of checklists and frameworks); Implementation approaches (home visits during critical periods of the life cycle; allocation of Nutrition and Health days for service improvement); and Outcome-based monitoring system to track most critical behaviors and services.

Evidence described in this section clearly indicated that with renewed focus and strengthened capacity, the ICDS program can effectively deliver nutrition and health services.

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42.8 Moving forward: revisit and refine key strategies ICDS is one of the largest programs for child development not just in India but in the Asian sub-continent. Contributions that the program has made in improving nutrition and health outcomes in children and women have been discussed in Section 42.7. As ICDS moves towards universalization, it is critical that it revisits its design and implementation strategies by incorporating lessons learned from various innovation effects. Refinements around specific components are essential to achieve higher impact on nutritional status of children.

42.8.1 Recommendations Define objectives and interventions ICDS must clearly state which objectives will it hold itself accountable for. Currently it has a diverse mandate, from early childhood development, reducing child malnutrition, mortality, morbidity; improving adolescent health and nutrition to women’s empowerment. These overlap with objectives of other government departments. Expand coverage Allocate resources needed to ensure that population norms are followed for establishing AWCs. There should be one AWC for 1,000 population with provision for increase. They should take into account special groups and areas (migrants, slums in small towns and isolated hamlets). Focus on younger children for nutrition impact The program should improve nutrition outcomes for under-3s particularly under-2s and strengthen the early childhood education component for 3–6 year olds. Prioritize “doable” evidence-based interventions Nutrition impact can be achieved through a package of “doable” interventions which includes early and exclusive breastfeeding, age appropriate complementary feeding including initiation at 6 months, age specific frequencies and quantities for children 6–24 months old, responsive feeding and feeding during and after illness, vitamin A supplementation, pediatric IFA supplementation beginning 6 months or home-based fortification to address iron deficiency anemia, use of iodized salt, zinc as adjuvant to oral rehydration salts in treatment of diarrhoea and linkages with health facilities for treatment of infections.

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Public health nutrition in developing countries

Focus on effective operational approaches Ensure home visits with “appropriate content” to households at critical periods of the life cycle – on registration of marriage and pregnancy, newborn and infants on first day, first week, 6–8 months, 9–11 months and 12–18 months including contacts during and after sickness on a priority basis. Behavior Change Communication (BCC) support through interpersonal communication, and social mobilisation through print and mass media for transmitting key messages, at an optimal frequency to saturate the system is critical. Develop simple protocols for prevention/management of malnutrition Based on various innovative approaches supported by CARE, UNICEF, and the World Bank, essential nutrition action package (see Box 42.8 for age-specific feeding recommendations) [36] needs to be developed and adapted for use by the AWWs. AWWs need be accorded status of “community nutrition professionals”. While treatment of severe malnutrition is important, equally critical is that it is complemented with intensive program efforts on prevention of malnutrition. Mortality risk is highest in severely malnourished children, but at the same time it must be appreciated that the number of total children who are at risk of death in mild to moderate malnutrition is several times higher than in normally nourished. The prevention strategy must be centered around reducing incidence of low birth weight and not allowing the near 70% of children who are normal in early infancy to become undernourished by focusing on children <2 years and promoting and ensuring appropriate behaviors and services. Institutionalize a system for linkage with health system Roles and responsibilities of ICDS functionaries and management staff must be spelt out clearly with reference to immunisation, antenatal care, management of severe malnutrition and, micronutrient supplements. ICDS needs to play a significant role in undertaking the routine biannual survey, identifying all newborns, children <2 years and pregnant mothers. In addition, ICDS could play a significant role in mobilising community to seek health services and referrals. A system to bring the two sectors (ICDS and Health) for working as a team for achieving nutrition and health outcomes is critical. Training Create strong linkages between training and implementation. Build capacity to focus on how to achieve specific program objectives. While training

•

•

•

•

•

Eat one additional meal Eat different types of food available in the house (meat, fish, eggs, milk, curd; fruits and vegetables; dal and cereals with added oil) Eat food received from the AWC Eat at least one IFA tablets daily for 100 days Rest for 1 to 2 hours during the day

Pregnancy For child • Breastfeed within 1 hour of birth • Only breastfeed; do not give water, other fluids, honey water, ghutti, or food • Breastfeed frequently on-demand day and night • For a newborn who does not feed vigorously; provide expressed breast milk with a clean small katori or cup as long as breastfeeding is not adequately vigorous • Provide frequent feeding for a small newborn every 1–2 hours • Contact the AWW/ANM immediately if your infant is not able to breastfeed

Up to 6 months of age

•

•

•

•

•

Continue frequent, on-demand breastfeeding, day and night Introduce home foods by feeding little at a time 1–2 teaspoons to gradually increasing the quantity and consistency after a first few days Feed soft mashed or thick, pasty home foods 1 small katori at 2 times per day such as mixed rice and dal, khichri, dalia, rice kheer, suji kheer. Add 1/4 to 1/2 teaspoon of oil in each meal In addition give small potato/mashed banana/carrot/papaya/ egg/meat/fish Feed child yourself, interact with child, feed from a separate bowl to assess how much the child has

6 to 8 months

Box 42.8 Age-specific feeding recommendations

•

•

•

•

Continue frequent, on-demand breastfeeding, day and night. Feed soft mashed or thick, pasty home foods 1 small katori 3 times a day such as rice, dal, mashed chapati in dal with vegetables (potatoes, carrots, pumpkin, etc.), green leafy vegetables. Add 1/2 teaspoon of oil in each meal. Give curd, eggs, meat, fish, if available. In addition give seasonal fruits such as papaya, mango, banana, etc. Feed child yourself, interact with child, feed from a separate bowl to assess how much the child has eaten. Do not force feed, but use gentle

9 to 11 months

•

•

•

•

Continue frequent, on-demand breastfeeding, day and night. Feed soft mashed or in small pieces home foods equal to 1 small katori 4 times per day such as rice, dal, chapatti, with vegetables (potatoes, carrots, pumpkin, etc.), green leafy vegetables. Add 1 to 2 teaspoon of oil in each meal. Give curd, eggs, meat, fish, if available. In addition give seasonal fruits such as papaya, mango, banana, etc. Feed child yourself, interact with child, feed from a separate bowl to assess how much the child has eaten. Do not force feed, but use gentle

12 months to 2 years

Reducing malnutrition: An analysis of the Integrated Child…

1189

•

•

•

eaten. Do not force feed, but use gentle persuasion, with stories, songs and toys to keep the baby’s attention. Increase frequency of breastfeeding during illness After illness, feed child 1 small katori of food 3 times until the child regains weight; encourage the child to eat more The infant should gain about 500 g per month •

•

•

•

persuasion, with stories, songs and toys to keep the baby’s attention. Increase frequency of breastfeeding during illness After illness, feed child 1 small katori of food 4 times until the child regains weight; encourage the child to eat more Seek first dose of Vitamin A (1 lakh IU) at 9 months with measles vaccination The child should gain about 300 g per month

•

•

•

•

•

persuasion, with stories, songs and toys to keep the baby’s attention Increase frequency of breastfeeding during illness After illness, feed child 1 small katori of food 5 times until the child regains weight; encourage the child to eat more Seek second dose of Vitamin A (2 lakh IU) at 18 months and third dose at 24 months Give pediatric iron tablets (one tablet daily, crushed with food for 100 days each year)** The child should gain about 200 g per month

For katori size we can assume an average size of 100 ml. However, katori sizes are not uniform. Health workers should estimate volumes of locally used utensils. (Adapted from material developed by WHO, UNICEF, CARE would facilitate in appreciating each others role and in achieving the objectives.)

Increase frequency of breastfeeding during and after illness • The infant should gain about 700 g per month • Mother and baby undergo changes at around 3 months but continue giving only breastmilk For mother • Eat one additional meal • Eat different types of food available in the house • Eat food received from the AWC • Avoid separation from your infant for more than 2–3 hours at a time

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centers continue to undertake induction training, bulk training to be onthe-job by supervisors and CDPOs who are responsible for delivering results. Joint training with health sector for achieving specific objectives has proved to be effective. Strengthening supervision This should be a priority. Provide flexibility in appointments of supervisors to minimize vacancies and ensure mobility and village level support to the AWW. Holding supervisors responsible for specific results, ensuring intensive training of supervisors, and recognizing good performance will bring better results. Monitoring system and related capacities Revisit monitoring system of the ICDS and evolve it around tracking program outcomes. Institute periodic independent assessments for outcomes such as for feeding, caring (exclusive breastfeeding and appropriate complementary feeding), health-seeking behaviors and nutritional status. Use data generated by this system for program management and decision making at different levels. Provide support to the AWW to generate and use information locally, with tools like the home visits planner. Enhance capacities to gather, analyze, interpret and use data at block and district levels by CDPOs and DPOs. Joint review of data with health sector is considered critical for achieving the nutrition and health objectives. Community engagement Explore and build concrete mechanisms to engage civil society and communities. Involve local government (PRI) representatives in review forums of ICDS at block and district levels and build accountability mechanisms for AWWs and Supervisors to PRI members for delivery of services, availability of supplies, home visits and supervisory visits. Form people’s committees for management of AWC functions. Some of these recommendations are being integrated in ICDS Reforms which are underway. The five-year ICDS-IV Project, referred earlier, is planned to be implemented in 8 states with support from the World Bank. Objectives of the project are to reduce child malnutrition through expansion of utilization of nutrition services and awareness and adoption of appropriate feeding and caring behaviors by households of children 0–6 years of age; and improve early child development outcomes and school readiness among children 3–6 years of age [14]. Key reform principles proposed in the ICDS Reforms/ICDS-IV project

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include better targeting, flexibility in terms of management and program implementation with focus on maintaining quality in service delivery, simplified, evidence and outcome-based program design, stronger convergence at the operational level and strong monitoring and evaluation with focus on an outcome-based results framework. In a country where high levels of malnutrition persist, utilizing ICDS program platform effectively to address the serious public health problem of malnutrition is critical. In every village, under the ICDS umberalla, delivery of appropriate evidence-based interventions through effective mechanisms by the AWWs with support from ANMs and ASHAs (Accredited Social Health Activists) of the National Rural Health Mission, and members of community groups will prevent a large majority of children from becoming malnourished.

References  1. 2.

3. 4. 5.

6. 7.

8. 9.

10.

11.

12.

(IIPS) and ORC MACRO (2000). National Family Health Survey (NFHS-2). India. Mumbai: IIPS. 1998–99. INTERNATIONAL INSTITUTE FOR POPULATION SCIENCES ( IIPS ) and MACRO INTERNATIONAL (2007). National Family Health Survey (NFHS-3). India, Volume 1, Mumbai: IIPS. 2005–06. Integrated Child Development Services program website. Available at: http:// wcd.nic.in/icds.htm. Accessed 10 October 2008. INTEGRATED CHILD DEVELOPMENT SERVICES . Department of Women and Child Development, Ministry of Human Resource Development, GoI, New Delhi. F.No. 5-9/2005/ND/Tech Vol(II) dated 24 February 2009. Revised nutritional and feeding norms of supplementary nutrition in the ICDS scheme. Ministry of Women and Child Development, Government of India. Policy on Control of Nutritional Anemia (1991). National Nutritional Anemia Control Program. Ministry of Health & Family Welfare, GoI. Policy on Management of Vitamin A Deficiency (1991). National Program for Prophylaxis Against Blindness in Children Due to Vitamin A Deficiency. MoHFW, GoI. Letter no. Z.28020/50/2003-CH dated 23rd April, 2007, issued by Assistant Commissioner, Child Health, MoHFW, GoI. Syllabus for job training of AWW (2006). Training Division, National Institute of Public Cooperation & Child Development, Ministry of Women & Child Development, GoI. Syllabus for job training course of supervisors (2006). Training Division, National Institute of Public Cooperation & Child Development, Ministry of Women & Child Development, GoI. Syllabus for job training course of Child Development Project Officers/ Additional Child Development Project Officers (2006). Training Division, National Institute of Public Cooperation & Child Development, Ministry of Women & Child Development, GoI. GRAGNOLATI M , SHEKAR M, DAS GUPTA M , BREDENKAMP C , LEE Y (2005). India’s Undernourished Children: A Call for Reform & Action. Washington, DC: World Bank. INTERNATIONAL INSTITUTE FOR POPULATION SCIENCES

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13. Working Group on Development of Children for the Eleventh Five Year Plan (2007–2011), Ministry of Women and Child Development, GoI, Shastri Bhavan, New Delhi. 14. ICDS IV Project (2007). 2008–09 to 2012–13. Handbook. Central Project Management Unit. Ministry of Women & Child Development, GoI. 15. Syllabus for job training of AWW, Supervisor and CDPO (2006). Training Division, National Institute of Public Cooperation & Child Development, Ministry of Women & Child Development, GoI. 16. NATIONAL INSTITUTE OF PUBLIC COOPERATION & CHILD DEVELOPMENT (1992). National Evaluation of the Integrated Child Development Services. New Delhi. 17. NATIONAL COUNCIL OF APPLIED ECONOMIC RESEARCH (2001). Concurrent Evaluation of Integrated Child Development Services. New Delhi. 18. LOKSHIN M , DAS GUPTA M , GRAGNOLATI M, IVANSCHENKO O (2005). Improving child nutrition: Integrated Child Development Services in India. Development & Change, 36, pp. 613–640. 19. INTERNATIONAL INSTITUTE FOR POPULATION SCIENCES AND MACRO INTERNATIONAL (2007). National Family Health Survey (NFHS-3). India : Key findings. Mumbai: IIPS. 2005–06. 20. GANDHI N, TANDON B , KRISHNAMURTHY KS (1995). Integrated Child Development Services Scheme & Nutritional Status of Indian children. Journal of Tropical Pediatrics, 41, pp. 123–128. 21. BHANDARI B , GUPTA AP, MANDOWARA SL, SAHARE P , SINGHAL M (1993). Decadal Changes in Nutritional and Immunization Status of ICDS Beneficiaries. Indian Journal of Maternal & Child Health, 4, pp. 9–10. 22. SWAMI HM , THAKUR JS, BHATIA SP, BHATIA V (2001). Nutritional Status of Pre-school Children in an Integrated Child Development Service Block of Chandigarh. Journal of Indian Medical Association. 99, pp. 554–556. 23. NAYAR D, KAPIL U, NANDAN D (1998). Status of Receipt of ICDS Package of Services by Under 3 children & pregnant women in district Agra. Indian Pediatrics, 35, pp. 459–462. 24. AGARWAL KN, AGARWAL DK, AGARWAL A, RAO S, PRASAD R, AGARWAL S, SINGH TB (2000). Impact of ICDS on Maternal Nutrition & Birth Weight in Rural Varanasi. Indian Pediatrics, 37, pp. 1321–1327. 25. RAIZADA N, SACHAR RK , BHATIA RC, SEHGAL R , SONI RK (1993). Impact of Preschool Education Component of ICDS on Mental & Cognitive Development of Children. Indian Journal of Maternal Health, 4, pp. 4–8. 26. A Review of “Best Practices” in ICDS (2007). Micronutrient Initiative. For the World Bank. 27. HEAVER R (2002). India’s Tamil Nadu Nutrition Program. Lessons and Issues in Management & Capacity. Health, Nutrition and Population Discussion Paper. World Bank, Washington. 28. SHEKAR M (1991). The Tamil Nadu Integrated Nutrition Project: A Review of the Project with Special Emphasis on the Monitoring and Information System. Cornell Food and Nutrition Policy Program, Working Paper No. 14. Ithaca, New York: Cornell University. 30. DUBOWITZ T, LEVINSON D, PERTERMAN JN, VERMA G, JACOB S, SCHULTINK W (2007). Intensifying Efforts to Reduce Child Malnutrition in India: Evaluation of Dular program in Jharkhand, India. Food & Nutrition Bulletin, 28, pp. 226–273. 31. CARE INDIA (2007). Reproductive & Child Health & Nutrition & HIV/AIDS (RACHNA) Program 2001–2006: Summary of Approaches and Results.

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33. 34. 35.

36.

37.

38.

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DREYFUSS M, LI Y , CHAUDHERY D , SINGH V

(2006). Evaluation Research of Nutrition Interventions in INHP II Areas of CARE India: Final Evaluation Report. CARE India, King Georges Medical University and Johns Hopkins Bloomberg School of Public Health. Impact Evaluation of Positive Deviance Program in West Bengal (2007). National Institute of Nutrition. ICMR, Hyderabad. Anchal Se Angan Tak (ASAT) Strategy Evaluation (2006). Tufts University, Friedman School of Nutrition Science & Policy. Draft Report. Community Based Maternal & Child Health Nutrition Project (2006). Evaluation. ORG Centre for Social Research (division of AC Nielsen ORGMARG Pvt. Ltd.), Lucknow, Implementation Completion Report for ICDS-III/WCD project (IDA Credit INN042) (2006). Borrower’s Evaluation Report. Central Project Management Unit, Ministry of Women & Child Development, GoI. VARMA J L , DAS S , SANKAR R , MANNAR MGR , LEVINSON FJ , HAMER DH (2007). Community-level micronutrient fortification of a food supplement in India: a controlled trial in preschool children aged 36–66 months. American Journal of Clinical Nutrition, 85, pp. 1127–33. Strengthening a package of Essential Nutrition Actions in Integrated Child Development Services and Reproductive and Child Health programs (2006). CARE, India. ICDS DIRECTORATE . Accreditation in ICDS. Karnataka and Andhra Pradesh.

National Rural Health Mission

43 National Rural Health Mission Deoki Nandan

Deoki Nandan, MD, FAMS, FIPHA, FIAPSM, FISCD, is currently the Director of the National Institute of Health & Family Welfare, New Delhi. He has worked as Principal/Dean and Chief of hospital, S N Medical College, Agra. He has been actively working in the field of public health for more than 30 years and during this period has been associated as an advisor as well as consultant with many international organizations. He is also a member of many state-level committees and National Technical Expert Committees, specifically for AIDS, IMNCI and Child Health.

"!.1

Introduction

The National Rural Health Mission (NRHM) was launched on 12 th April 2005 throughout India with a commitment of the government to carry out the necessary architectural corrections in the basic health care delivery system. NRHM covers the entire country but has a special focus on eighteen states (of these 8 are EAG states), identified to have weak public health indicators and/or weak health infrastructure. These focused states are Arunachal Pradesh, Assam, Bihar, Chhattisgarh, Himachal Pradesh, Jharkhand, Jammu & Kashmir, Manipur, Mizoram, Meghalaya, Madhya Pradesh, Nagaland, Orissa, Rajasthan, Sikkim, Tripura, Uttaranchal and Uttar Pradesh. While all the Mission activities are the same for all the states/UTs in the country, the high focus states have the following additional support: (i) An Accredited Social Health Worker (ASHA) in all villages with a population of 1000. (ii) Project Management Support at the state and district level.

"!.2

The vision of the mission

The mission seeks to provide effective health care to rural population # Empowered Action Group (EAG) refers to the following 8 states – Bihar, Chattisgarh, Jharkhand, Madhya Pradesh, Orissa, Rajasthan, Uttaranchal and Uttar Pradesh.

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throughout the country with special focus on 18 identified focused states [1]. Further, NRHM seeks to: ● Raise public spending on health from 0.9% to 2–3% of GDP, with improved arrangement for community financing and risk pooling. ● Undertake architectural correction of the health system to enable it to effectively handle increased allocations and promote policies that strengthen public health management and service delivery in the country. ● Revitalize local health traditions and mainstream Ayurveda, Yoga, Unani, Siddha and Homeopathy (AYUSH) into the public health system. ● Integrate the health concerns effectively through decentralized management at the district, with determinants of health like sanitation and hygiene, nutrition, safe drinking water, gender and social concerns. ● Addressed inter-state and inter-district disparities, especially among the 18 high focus states, including unmet needs for public health infrastructure. ● Ensure achievement of time bound goals and report the progress publicly. ● Improve access of rural people, especially poor women and children to equitable, affordable, accountable and effective primary health care.

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Reduction in child and maternal mortality. Universal access to public health care services for food and nutrition, sanitation and hygiene with emphasis on services addressing women’s and children’s health and universal immunization. Prevention and control of communicable and non-communicable diseases, including locally endemic diseases. Access to integrated comprehensive primary health care. Population stabilization, gender and demographic balance. Revitalize local health traditions and mainstream AYUSH. Promotion of healthy life styles.

43.4 ● ●

The objectives of the mission

The expected outcomes from the mission as proposed for reflection in statistical data

Infant Mortality Rate (IMR) reduced to 30/1000 live births by 2012. Maternal mortality reduced to 100/100,000 live births by 2012.

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Total Fertility Rate (TFR) reduced to 2.1 by 2012. Malaria Mortality Reduction Rate – 50% by 2010, additional 10% by 2012. Kala Azar Mortality Reduction Rate – 100% by 2010 and sustaining elimination until 2012. Filarial/Microfilaria Reduction Rate – 70% by 2010, 80% by 2012 and elimination by 2015. Dengue Mortality Reduction Rate – 50% by 2010 and sustaining at that level till 2012. Cataract operation – increasing to 46 lakhs by 2012. Leprosy Prevalence Rate – reduced from 1.8 per 10,000 in 2005 to less that 1 per 10,000 thereafter. Tuberculosis – DOTS services maintain 85% cure rate through entire mission period and also sustain planned case detection rate. Upgrading Community Health Centres to Indian Public Health Standards. Increase utilization of First Referral units from bed occupancy by referred cases of less than 20% to over 75%. Engaging 250,000 female Accredited Social Health Activists (ASHAs) in 18 states.

43.5

Goals, strategies and outcomes of the Mission

The mission seeks to provide universal access to equitable, affordable and quality health care services which is responsive to the needs of the people, reduction of child and maternal deaths, population stabilization, gender and demographic balance. In this process, the mission would help achieve goals set under the National Health Policy and the Millennium Development Goals. To achieve these goals NRHM will ●

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Facilitate increased access and utilization of quality health services by all. Forge a partnership between the Central, State and the Local governments. Set up a platform for involving the Panchayati Raj institutions and community in the management of primary health programmes and infrastructure. Provide an opportunity for promoting equity and social justice. Establish a mechanism to provide flexibility to the states and the community to promote local initiatives. Develop a framework for promoting inter-sectoral convergence for promotive and preventive health care.

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43.5.1 The core strategies of the mission The following core strategies have been adopted to achieve the goals of mission: ●

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Train and enhance the capacity of Panchayati Raj Institutions (PRIs) to own, control and manage public health services. Promote access to improved health care at household level through the female-health activist (ASHA). Health plan for each village through village-health committee of the panchayat. Strengthening sub-centre through better human resource development, clear quality standards, better community support and an untied fund to enable local planning, action and induction of more Multi-Purpose Workers (MPWs). Strengthening existing primary health care centres (PHCs) through better staffing and human resource development policy, clear quality standards, better community support and an untied fund to enable the local management committee to achieve these standards. Provision of 30–50 bedded community health centres (CHC) per lakh population for improved curative care to a normative standard (Indian Public Health Standards – IPHS defining personnel, equipment and management standards, its decentralized administration by a hospital management committee and the provision of adequate funds and powers to enable these committees to function at optimum levels). Preparation and implementation of an inter-sector District Health Plan including drinking water, sanitation, hygiene and nutrition. Integrating vertical health and family welfare programmes at national, state, district and block levels. Technical support to national, state and district health mission, for public health management. Strengthening capacities for data collection, assessment and review for evidence-based planning, monitoring and supervision. Formulation of transparent policies for deployment and career development of human resource for health. Developing capacities for preventive health care at all levels for promoting healthy life style, reduction in consumption of tobacco and alcohol, etc. Promoting non-profit sector particularly in underserved areas.

43.5.2 Supplementary strategies In addition to these core strategies, some of the supplementary strategies of the mission include:

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Regulation of private sector including the informal Rural Medical Practitioners (RMP) to ensure availability of quality service to citizens at reasonable cost. Promotion of public private partnerships for achieving public health goals. Mainstreaming AYUSH, revitalizing local health traditions. Reorienting medical education to support rural health issues including regulation of medical care and medical ethics. Effective and visible risk pooling and social health insurance to provide health security to the poor by ensuring accessible, affordable, accountable and good quality hospital care.

43.6

Institutional mechanisms in the National Rural Health Mission

The following institutional mechanisms have been created to strengthen functioning at various levels: ●

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Village health and sanitation samiti (at village level consisting of panchayat representative/s, ANM/MPW, anganwadi worker, teacher, ASHA, community health volunteers), Hospital Management Committee/Rogi Kalyan Samiti for community management of public hospitals. District Health Mission, under the leadership of Zila Parishad with District Health Head as Convener and all relevant departments, NGOs, private professionals and others represented on it. State Health Mission, chaired by Chief Minister and co-chaired by Health Minister and with the State Health Secretary as Convener representation of related departments, NGOs, private professionals and others. Integration of Departments of Health and Family Welfare, at national and state level. National Mission Steering Group chaired by Union Minister for Health & Family Welfare with Deputy Chairman Planning Commission, Ministers of Panchayat Raj, Rural Development and Human Resource Development and public health professionals as members, to provide policy support and guidance to the Mission. Empowered Programme Committee chaired by Secretary Health and family Welfare, to be the Executive Body of the Mission.

As a part of this strategy, the state and district missions have been set up in all the states and UTs (Figure 43.1). The Departments of Health and Family Welfare have been merged at the level of the Government of India

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(GoI) and similar system is being followed up at state levels. State level NRHM activities have been designed taking into consideration the reform commitments expected by states including enhanced public spending on health, decentralization, promotion of district level planning, etc.

Governing body, State Health Society (SHS)

43.1 Institutional Mechanisms under NRHM.

43.7

Accredited Social Health Activists (ASHA)

The core strategies envisaged to realize the objectives include improved access to health care at household level through local women in the age of 25–40 years known as Accredited Social Health Activist (ASHA). Every village/large habitat is to have an ASHA chosen by and accountable to the Panchayat. She is to serve as a bridge between the anganwadi workers, ANMs and community. As link between the community and the health facility, the ASHAs are expected to be the first person to call for any health related demand. Under the Framework of Implementation [2], it is proposed to have ASHAs in all the 18 high focus states and to support ASHAs in tribal districts of all the remaining states. One of the main approaches of NRHM involves large-scale transfer of knowledge and skills and health information to ASHAs. Each state is imparting

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trainings to them for 23 days in five episodes as per their state specific needs. A set of guidelines have been developed to enable the states to develop and put in place a proper support mechanism for ASHA. These guidelines spell out the role of ASHA vis-à-vis Anganwadi Worker (AWW) of ICDS and the Auxiliary Nurse Midwives (ANM) of health sector [3]. She is to act as an interface between the community and the public health system. Working as an honorary volunteer, she receives performance-based compensation on specified services rendered by her. The NRHM focuses on decentralization for planning at all levels; ASHA would facilitate preparation and implementation of the Village Health Plans along with anganwadi workers, ANMs, functionaries of other departments and self-help groups (SHGs) under the leadership of Village Health Committee of the Panchayat (elected village body). ASHA is also supplied with a drug kit containing generic AYUSH and allopathic formulations for common ailments, which is replenished, periodically. Some of the roles and responsibilities of ASHA are ●

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To create awareness and provide information to community on determinants of health such as nutrition, basic sanitation and hygiene practices, healthy living and working conditions. To provide information on existing health services and the need for timely utilization of health and family welfare services. Counsel women on birth preparedness, RTIs/STDs (Reproductive Tract Infection / Sexually Transmitted Diseases). Mobilize community and facilitate them in accessing available health related services. Work with voluntary health and sanitation committee to develop a comprehensive village plan. Maintain drug kit to provide first aid facilities.

ASHA is viewed as a key person who would provide help to strengthen the services at the outreach level for a sub-centre, PHC or district health centre. In addition, ASHA is expected to provide data regarding the progress made by the village/community for the consolidation of report at PHC by the medical officer for the bi-monthly meetings. The expected outcomes related to ASHAs at community level as envisaged in the Framework for Implementation (2005–2012) are as below: ●

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Availability of trained community level worker at village level, with a drug kit for generic ailments. Health and Nutrition Day at anganwadi level on a fixed day/month

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for provision of immunization; Ante/post natal check ups and services related to mother and child health care, including nutrition. Availability of generic drugs for common ailments at sub-centre and hospital level. Access to good hospital care through assured availability of doctors, drugs and quality services at PHC/CHC level and assured referral– transport–communication systems to reach these facilities in time. Access to Universal Immunization improved through induction of auto disabled syringes, alternate vaccine delivery and improved mobilization services under the programme. Facilities for institutional delivery improved through provision of referral, transport, escort and improved hospital care subsidized under the Janani Surakshya Yojana (JSY) for the below-poverty-line families. Availability of assured health care at reduced financial risk through pilots of community health insurance under the mission. Availability of safe drinking water. Provisions for household toilets. Outreach services to medically under-served remote areas improved through mobile medical units. Awareness about preventive health including nutrition increased.

43.7.1 The integrated role of ASHA and organizing Village Health Nutrition Days Health Days (referred also as Village Health and Nutrition Days or VHND) are organized every month at the anganwadi level in each village in which immunization, ante/post-natal check ups and services related to mother and child health care including nutrition are being provided. Space at each anganwadi centre (AWC) of ICDS (Integrated Child Development Services) is proposed to serve as the hub of health and nutrition activities in the village. The AWC space is also recommended to be utilized for dispensing out-patient services by any health provider and also serve as depot for medicines and contraceptives. It is proposed that NRHM will aim to establish a village level health institution co-located with AWC with a specific physical location. The role of ASHAs under NRHM is very critical for child survival, child health and strengthening immune functions (Figure 43.2). A number of state governments have introduced innovative programmes related to various schemes under NRHM, where ASHAs play a central role such as vitamin A programme using the biannual administration strategy.

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43.2 Integrated role of ASHA. (a)

Task added by GoI in 2009 [4]

43.8

Implementation Framework and Plan of Action for NRHM

The inherent strength of NRHM lies in its implementation of various schemes with rigor and appropriate monitoring strategy. In order to achieve the goals of the NRHM, some of the key features identified in the Implementation Framework and the Plan of Action of the Mission are ●

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Making the public health delivery system fully functional and accountable to the community Human resources management Community involvement Decentralization Rigorous monitoring and evaluation against standards Convergence of health and related programmes from village level upwards Innovations and flexible financing and Interventions for improving the health indicators

43.8.1 Decentralization In line with the above, the Mission seeks to adopt a convergent approach for interventions under the umbrella of the district plan which seeks to integrate all the related initiatives at the village, block and district levels. The District Health Action Plan is the main instrument for planning, inter-sectoral

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convergence, implementation and monitoring of the activities under the Mission. Based on the district plans, annual state plans are developed. The allocation of funds is as per these annual plans. It is also proposed to conduct periodic surveys on an annual basis to track the improvements in the facilities as well as in the reduction in health indicators. The state plans are approved by the Mission at the national level.

43.8.2 Convergent action on other determinants of health One of the key components of NRHM is about effective integration of health concerns with determinants of health like sanitation and hygiene, nutrition and safe drinking water through a district plan for health. The status of health and related indicators depend on many factors such as drinking water, female literacy, nutrition, early childhood development, sanitation, women’s empowerment along with hospitals and functional health systems. NRHM seeks to adopt a convergent approach for these key determinants for interventions under the umbrella of the district plan. Anganwadi Centre under the ICDS at the village level is proposed to be the principal hub for health action (Figure 43.3). The village committees constituted for drinking water, sanitation, ICDS etc. is envisaged to converge under one common village health committee to cover all these activities. Panchayati Raj Institutions (PRIs), the community level institutions are expected to be fully involved in this convergent approach so that the gains of integrated action can be reflected in district plans.

43.3 Convergent action at village level.

Convergence is also envisaged at the level of the Mission Steering Group which has representation of all the concerned Ministries, such as Department of Women and Child Development, Department of Education and with AYUSH. The PRIs organizations (Self-help Groups, Schools, Water, Health

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and Sanitation Committee or Health, Nutrition and Sanitation Committees, Mahila Samakhya Groups, Zila Saksharta Samitis) are expected to provide an opportunity for seeking local levels accountability in the delivery of social sector programmes. There is a provision under the NRHM to provide for School Health Checkups and School Health Education in consultation with the states. As presented in Figures 43.3 and 43.4 (a, b), convergence of all programmes is at the village and facility levels.

43.4a Intersectoral Convergence.

43.4b Intersectoral convergence under NRHM.

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"!.9

Nutrition: a determinant of health

NRHM has proposed service guarantee for health care at sub-health centre, primary health centre and community health centre. These include prevention and control of childhood diseases as well as malnutrition, vitamin A prophylaxis to the children, iron–folic acid to pregnant mothers and children and testing of iodine in salt. These nutrition services are proposed to be coordinated with the ICDS.

43.5 NRHM – five main approaches.

"!.10 Improving the public health delivery system The status of public health infrastructure in the country, particularly in the EAG and north-east states is very weak and has been the cause for concern for many years. It is pertinent that providing the desired quality services especially in the EAG and the north-eastern states will not be possible till

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the infrastructure is sufficiently upgraded. Realizing this, the Mission seeks to establish functional health facilities in the public domain through revitalization of the existing infrastructure and fresh construction or renovation wherever required. The Mission also seeks to improve service delivery by putting in place enabling systems at all levels. This involves simultaneous corrections in manpower planning as well as infrastructure strengthening. The generic public health delivery system envisioned under NRHM from the village to the block level is presented in Fig. 43.6.

43.11 Indian Public Health Standards (IPHS) The Indian Public Health Standards (IPHS) have been set up for all levels to ensure that quality in services is maintained throughout the delivery of health care services. Figure 43.7 presents the human resource requirements at various levels of health infrastructure under NRHM and Fig. 43.8 presents the details of IPHS.

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Lady Health Visitor, Sub-centre centre, Maternal and Child health

43.6 NRHM – Public Health Delivery Systems.

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"!.12 Public health infrastructure Given the general observation that the health infrastructure is in poor condition in most of the states, NRHM has allocated the budget for

43.7 Human resource requirements.

IPHS for CHCs at a Glance

43.8 Indian Public Health Standards (IPHS) at CHCs.

construction, subject to the condition that it should not be more than 33% of the total NRHM outlay in the case of high focus states and 25% in the case of non-high focus states.

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In order to improve public health infrastructure, a number of initiatives have been put forth such as: ● ●

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Providing untied grants at sub-centre, PHC/CHC and district level. Provision for funds for taking up innovative schemes at district/state/ central level. Funds for Rogi Kalyan Samitis (welfare association for sick persons) for managing the health facilities.

The Mission seeks to ensure the availability of requisite equipment and drugs at all the public health care facilities and it is proposed to procure equipment and drugs progressively in a decentralized manner. It is also proposed to improve outreach activities in un-served and underserved areas specially inhabited by vulnerable sections through provision of Mobile Medical Units (MMU) in every district, which would cover anganwadi centres also.

43.13 Improving availability of critical manpower The issues of availability of critical manpower in the rural areas is proposed to be addressed through initiatives like: (i) introduction of a trained voluntary community health worker (ASHA) in every village of the 18 high-focus states; (ii) an additional ANM at each sub-centre; (iii) three staff nurses at the primary health centres (PHC) to make them operational round the clock and additional specialists and paramedical staff at the community health centres (CHC). In north-east States, keeping in view the difficulty in availing services of doctors and specialists, the emphasis is on recruitment, training and skill up-gradation of locally recruited ANMs, nurses, midwives and paramedics. Contractual appointment/local level engagement of medical and paramedical manpower, upgrading and multi-skilling of the existing medical personnel are some other options which are being planned to fill the critical gaps of manpower. A number of innovations like public-private partnership (PPP) for service provision, franchising of service providers, licensing and training of rural medical practitioners (RMP), rationalization of existing manpower are being explored. It is envisaged that stringent monitoring at all levels, involvement of the PRIs and monitoring by the Rogi Kalyan Samitis would ensure presence of doctors and paramedical in the rural areas. Besides compulsory posting of doctors in the rural areas, better cadre management and personnel policies would also help to improve manpower availability.

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"!.1" Capacity building Capacity building at all levels in India has been a huge challenge and therefore various initiatives have been made under the Mission for capacity building of human resources. These are (i) Programme Management Units (PMUs) at the state/district level – PMUs at the state/district level have been set up in order to provide managerial support for monitoring various activities under NRHM and also tracking of funds (Over 500 professionals have already been recruited). Additionally, the successful implementation of the Mission requires health sector reforms and development of human resources. (ii) National Health System Resource Centre (NHSRC) – NHSRC at the Central and State levels (SHSRC) have been set up to provide technical support at the central and state government levels, respectively. (iii) The NRHM also emphasizes the setting up of fully functional block and district level health management systems. Under NRHM, 70% of the resources would be utilized at block and below block levels while only 20% at the district level. Given the large army of ASHAs, ANMs, nurses, rural medical practitioners, the need of the hour is continuous development of the skills of these health personnel. (iv) Strengthening nursing institutions and linking medical colleges – In order to provide skill development support to rural health workers, involving the voluntary sector in skill development, it is proposed to strengthen the nursing and medical institutions of our country. (v) Strengthening of PRIs – It is proposed to gradually shift the central mechanism of the health facilities like sub-centres under the control of panchayats (elected village body) elicited community organization, with a view to make them more accountable.

"!.15 Monitoring and review One of the differences in the monitoring strategy of NRHM is to involve local communities in planning, implementing and monitoring. NRHM proposes an intensive accountability framework through a three pronged process of community based monitoring, external surveys and stringent internal monitoring. Role of Village Health Committees, PHC health monitoring and planning committees have been spelt out for ensuring monitoring at community level.

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1211

"!.16 Flexible financing One of the strengths of the Mission is to increase the share of central and state governments on health care from the current 20–80 to 40–60 sharing in the long run. While under Xth Plan, 100% grants were planned to be provided to states, in the XI th Plan period the states are expected to contribute 15% to make the share of the Central Government 85%. This relative share of the centre and state is projected to be sustained at 75:25. One of the practical problems experienced by the states has been the transfer of funds under different budget heads at different points of time vertically and for many programmes. Such a system has been found to often result in duplication of efforts, and wastage of scarce resources. The strength of Mission is recognised to lie in providing flexible financing options. The Mission attempts to bring all the schemes of the Ministry of Health and Family Welfare within the overarching umbrella of NRHM. From the XI th Plan onwards, the Framework of Implementation has proposed to have a single budget head for the activities under the Mission. The mechanism of flow of funds under the NRHM budget head is proposed through the Integrated Health Society at the state and the district levels.

43.16.1 Related financial mechanisms: provision of untied funds In order to strengthen the sub-centres, each sub-centre will have an Untied Fund for local action at Rs 10,000 per annum. This fund will be deposited in a joint Bank account of the ANM and Sarpanch (Head of village committee or Panchayat ) and operated by the ANM, in consultation with the village health and sanitation committees. A revolving fund is to be set up at the village level for providing referral and transport facilities for emergency deliveries as well as immediate financial needs for hospitalization. The fund is to be operated by the village health and sanitation committee (VHSC). Such fund would also be made available to VHSC for various health activities including IEC, household survey, preparation of health register, organization of meetings at the village level, etc.

43.16.2 Financial Provisions under Janani Suraksha Yojana (JSY) As per JSY, [5] cash assistance for institutional delivery is given to both mothers and ASHAs in the low- and high-performing states, on production of below poverty line (BPL) cards. All pregnant women delivering in the government health centre like sub-centre, PHC/CHC/FRU (First Re-

1212

Advanced public health nutrition

ferral Unit)/general wards of district hospitals and state hospitals or accredited private institutions are eligible to avail of this assistance. In the low-performing states, the assistance is Rs. 1400/- (about US $ 30) for a pregnant woman while in the high-performing states, the assistance is fixed at Rs. 700/- (about $ 15). The JSY has shown significant progress since its inception with a sharp increase in institutional deliveries.

43.17 NRHM progress made The Mission has shown progress in many states in the past three to four year’s time. More than 0.6 million ASHAs have been selected and are at various stages of selection and training. A total of 13,358 (additional PHCs) APHCs, PHCs, CHCs, and other sub-district facilities have been made 24 × 7 functional. The state of Bihar has reported that the average number of patients visiting a PHC every month has gone up from 39 in January 2006 to 3015 in August 2006. In Punjab, with the Alternate Health Delivery involving service providers under PRIs at 1310 subsidiary health centres, out-patient cases have gone up by 290% between June and October 2006. Regarding availability of medicines, states of UP and Jharkhand revised the per capita allocation for drugs in out-patient leading to better availability of drugs at health facilities [6]. Infant mortality rate is reduced to come to 55, down by 2 points in 2007 as compared to a point in earlier years (2003–06) [6]. Significant gains have also been reported in the rates of institutional deliveries which have increased by 66.4 % in MP, 50.2 % in Rajasthan, 47.3 % in Bihar, 43.8% in Orissa, 20.9% in Andhra Pradesh and 12.4% in Uttar Pradesh between District Level Household Survey DLHS-II (2004) and DLHS-III (2007). The status of full immunization has increased from 20.7% to 41.4% in Bihar, 25.7% to 54.1% in Jharkhand, 30.1% to 36.1% in MP, 53.5% to 62.4 % in Orissa, 23.9% to 48.8 % in Rajasthan and 25.8 % to 30.3 % in UP between DLHS II and DLHS III. The success of NRHM depends to a large extent on many factors. One of these factors is the performance of ASHA or the link worker in the community and her linkages with the health system [3]. For the effective implementation of NRHM, each link worker must be fully aware of the facilities available in the area of operation and also what types of services are available at each facility. Support provided by the district and state nodal officers to immediately respond to local needs is another factor responsible for the successful functioning of NRHM, as the inputs provided by these officers include immediately responding to referrals made by ASHA, upgrading health facilities and infrastructure as per IPHS standards, timely provision of drugs and taking care of logistics as well as organizing campaigns and publicity activities with respect to availability of various services and schemes.

National Rural Health Mission

1213

References 1. National Rural Health Mission (2005–2012) Document, Ministry of Health and Family Welfare, Government of India. 2. Framework for Implementation (2005–2012). National Rural Health MissionMeeting people’s health needs in rural areas’, Ministry of Health and Family Welfare, Government of India. 3. Guidelines for Operationalising Support Mechanism for ASHA. Department of Family Welfare. Ministry of Health & Family Welfare. Government of India. 2006. 4. TEWARI , B .K. State Level Awareness Meeting on NIDDCP, State Government of Chattisgarh, 31st October 2009, Raipur, Chhattisgarh. 5. JANANI SURAKSHA YOJANA (2006). Features & frequently asked questions & answers’. Government of India. http://mohfw.nic.in/dofw/JSY 6. NRHM-The Progress so far. http://mohfw.nic.in/nrhm 7. District Level Household and Facility Survey: Reproductive and Child Health Project. www.rchiips.org/ARCH-1.html

Index

α-carotene, 407 α-error, 1145 β-carotene, 406 β-error, 1138, 1145 γ-carotene, 407 20 Point Programme, 581 24 hour recalls, 35 Abdominal adiposity (high waist–hip ratio (WHR), 103 Abdominal obesity, 970 prevalence in Indians, 102 Abnormalities, 507 congenital, 334 iron deficiency, 623–624 metabolic, 963 Universal Salt Iodization (USI), 562 zinc deficiency, 739 Above-the-poverty-line households (APL), 867 Absolute margin of error, 1144 Absorption spectroscopy, 755 Academy for Educational Development (AED), 1104 Access to food, 996 to services, 1069 Accredited Social Health Activists (ASHA), 199, 597, 1070, 1195, 1200, 1203 Accurate anthropometric measurement, 109 measuring length/height, 109, 10 Aconitase, 611 switch, 612 Acquired Immune Deficiency Syndrome (AIDS), 372, 686 Acquired immunity, 744 Acrodermatitis enteropathica, 739

1214

Action-based behaviors, 1104 Active or responsive feeding, 227 Activity energy expenditure (AEE), 342, 384 Activity implementation plan, 1015 Activity-based costing, 1127 Acute diarrhea, 275 dietary management of, 285 oral zinc supplementation, 5 Acute diarrheal diseases, 279 Acute diarrheal episodes, 275 Acute malnutrition, 310 Acute phase response, 375 Acute Respiratory Infection (ARI), 487 control programme, 169 Additional Child Development Project Officer (ACDPO), 1156 Adenosine tri phosphate (ATP), 610 Adenosyl homocysteine, 629 Adenosyl methionine, 629 Adequate complementary feeding between 6 and 24 months, 226 Adequate prolactin receptors, 182 Adequately iodized salt, 602 Adhesion, 803 Adhyaksh, 1071 Adipocytes, 345 Adiponectin, 346 Adipose tissue, 343 Adiposity, 976 rebound, 347 Adolescence marriage, 69 Adolescent boys and girls iron requirements, 692, 693 Adolescent girls, 715, 872, 873 public health nutrition, 76, 269, 617, 1039, 1040, 1159 iron deficiency, 713–717, 721, 724–729 Adolescent girls Scheme, 1185

Index Adolescent nutrition, 976 Adolescent nutritional dwarfism, 737 Adolescent pregnancy, 719 Adult life, obesity in, 101, thrifty gene hypothesis, 101 Advancing age, 939 Aerobic capacity, 697, 698 Aflatoxins, 322, 970 Age-independent anthropometric indices, 146 Ageing, 932, 933, 957 development agenda, 950, 952 in India, 934, 939 population, 934 society, 934 Age-related eye disease study, 754 Agglomeration, 827 Agricultural extension, 1088 agents, 200 Agriculture, 844 in India, 851, 852 Agriculture Organization/World Health Organization (FAO/WHO), 1087 AIDS patients, zinc supplementation, 390 Albendazole, 306, 460, 705 Albright hereditary osteodystrophy, 357 Albumin, 506 Alcohol, 971, 975 abuse, 940 Alkaline phosphatase, 756 All India Institute of Public Health and Hygiene, 597 Allergic reactions, 36 Allium vegetables, 971 Allocation subsidized quota, 586 Allyl sulphides, 948 Alopecia, 739 Alternative and Innovative Education Centres, 872 Alternative hypothesis (HI), 1137 Alzheimer’s disease, 945 Ambispective cohort study, 12 Amelioration, 671 Amenorrhea, 189, 690 Amoxicillin, 306 AMP (adenosine monophosphate), 417 Amylase rich flour (ARF), 245, 260 Analytical cross-sectional studies, 6 Analyzing information, 1047 Anchal Se Agan Tak (ASAT), 1172, 1180

1215

Ancylostoma duodenale, 685 Anemia, 32, 388, 643 global prevalence, 677–679 in India, 679–680 functional effects of, 697–701 prevention and control, 701–705 Anemia in children and cognitive functions, 699–700 consequences of, 647–649 preventive measures, 649–657 under three years, 645–647 Anencephaly, 630 Anganwadi centers, 1155 Anganwadi helper, 1156, 1181 Anganwadi Training Centers (AWTCs), 1162 Anganwadi worker (AWW), 873, 1156 Anganwadis, 95, 96, 873 Angiotensinogen, 341 Angular stomatitis, 311 ANM (auxillary nurse mid-wife), 96, 1071, 1099, 1157 Annaprashan Vidhi, 227 Annaprashan ceremony, 243 Annapurna scheme, 866, 870 Anorexia, 293, 946 Antenatal care (ANC) services, 76 Antenatal clinic, 13 Anthropometric assessment, 34 indicators, 108 indices, 116 methods, 36 techniques, 109, 131 Anthropometry, 108, 910 fruitless, 109 Anti malarials, 705 Anti-retroviral therapy, 687 Anti-ageing, 948 Anti-anemic, 626 Anti-angiogenic, 948 Antibody, 374 Anti-caking agent, 589 Anti-carcinogen, 948 Anti-depressants, 356 Anti-diarrheals, 789 Anti-hypertensive drug, 968 Anti-infective vitamin, 416 Anti-nutritional factors, 758 Anti-poverty programmes, 865

1216

Public health nutrition in developing countries

Antioxidant, 414, 418, 946, 948 enzymes, 375 nutrients, 947 Antiretroviral (ARV) drugs, 376 therapy (ART), 376 treatment, 375 Antyodaya families, 867 ration cards, 867 Antyodaya Anna Yojana (AAY), 866, 867 Anuka, 833 Apoptosis, 345, 738, 744 Appetite, 382 test, 319 Apple shaped distribution, 149 Applied Nutrition Programs (ANP), 1088 Aquaculture, 763 ARF preparations, 260, 261 developmental technology in India, 261, 266 Arterial lesions, 966 Arterial stiffness, 963 Arthritis, 948, 957 Articulation, 999 Artificial feeding, 399 Ascaris lumbricoides, 685 Ascorbic acid, 616, 683 ASHRAYA project, 906 Aspiration pneumonia, 942 Assessment of needs, 1078 Asymptomatic HIV infection, 686 Atherogenic agent, 947 Atheromatous disease, 947 Atherosclerosis, 966 Atherosclerotic, 966 Atherothrombotic, 963 Atomic absorption spectroscopy, 755 Atrophy, 280 Attributable fraction (exposed), 10 Attributable risk, 11 Audio-visual aids, 1088 media, 1109 Autodiagnosis, 168 Autoimmune Graves disease, 507 Autoimmune thyroid diseases, 554 Autoimmunity, 507 Ayurveda, 1196 AYUSH, 1196

B lymphocyte, 744 B12 deficiency, 631 Baby Friendly Hospital Initiative (BFHI), 193, 196 Baby Zinc, 761 Baby-Friendly communities, 202 crèches, 202 Bactericidal activity, 700 Bal Parivar Mitra (BPMS), 1110, 1183, 1184 Bal-ahar, 263 Bal-Amul, 263 Balanced malt food, 263 Bardet-Biedl syndrome, 357 Bargara salt, 582–583, 601 Barker’s hypothesis, 969 Basal iron loss, 614 Basal metabolic rate (BMR), 342, 925, 944 Basic care, 157, 158 newborn’s vulnerability to hypothermia, 158, 159 preventing hypothermia, 159 Baso lateral membrane, 687 BCM (body cell mass), 394 B-complex vitamins fortification, 808–809 Beadlets, 828 Begging bowl, 862 Behavior adoption, 1098 Behavior change, 1085 intervention, 1085 messages, 1118 Behavior change communication (BCC), 209, 211, 1074, 1088, 1118, 1176 programs, 1115 Behavior modification, 813 Behaviours, 1097 Below poverty line (BPL), 864, 866, 891 cards, 1211 Benefit–cost ratio, 772 Biannual strategy, 486 Biannual vitamin A strategy, 1171 Bi-directional interaction, 743 Bifidus factor, 185 Bilateral pitting edema grade, 302 Bioavailability, 408, 681, 923 of iron, 717 Bioconversion, 408 Biodiesel, 861

Index Biofortification, 850 Biofuel, 851 feedstocks, 861 market, 861 Biological activity, 418 Biological markers, 17 Biomarker, 505, 775 Birth asphyxia, 160, 161, 163 Birth weight, 57 Bitot spots, 415, 798 Blanket SFP, 917 Bleaching, 415 Blinding, 21 Blister packaging, 728 Block core trainers, 495 development officer (BDO), 1071 health plan, 1071 level action plans, 1069 medical officer, 1071 Panchayat Samiti, 1071 Pramukh, 1071 Program Managers of Health Unit (BPMU), 1071 Trainer cum Monitor (BTMs), 1183 Blood lipids (Dyslipedaemia), 966 Blood loss, 685 Blood transfusions, 373, 388 Blood volume, 715 Body calcium, 940 Body composition, 939 Body Fat (BF), 101, 146, 147, 959 Body mass index (BMI), 36, 131, 147, 149, 346, 894, 912, 959, 968 cut-offs, 136 Body weight, 342 Bone density, 940, 942 Bone fractures, 942 Bone health, 940 Bone mineral density, 946 Bone resorption, 741 Born at term, 160 Borrow strength, 1150 Bottle feeding, 206, 239 Botulism, 181 Bovine hemoglobin concentrate, 805 BP100, 321 BPL families, 892 Breast engorgement, 183 Breast milk, 186

1217

quantity of, 187 requirement, 187 retinol concentration, 426 volume of, 187 Breastfeeding, 176, 178, 1159. See also Lactation cycle. benefits for neonatal health, 161 benefits of, 178 campaign, 1090 community-based programme, 207, 211, 211, 214 counseling course, 201 early cessation of, 177 economic benefits of, 179 initiation, 180 patterns in India, 191, 192, 197 ten steps for successful, 194 Breastfeeding behaviours behavioural modifications, 203 of mothers, 203 Breast-milk substitutes, 177 International code of marketing, 198 Brush border receptors, 683 Bullous-pustular dermatitis, 739 Calcium, 946 Calorie co-efficients, 886 deprivation extent, 854 Cancer, 3, 942, 957, 959 Capacity building, 906, 1075, 1104, 1176, 1179, 1210 Carbohydrate intolerance, 275 Carbonic anhydrase, 756 Carcinogens, 971 Cardiomyopathy, 965 Cardiovascular disease (CAD), 43, 385, 957, 964 Carotene, 406 Carotenoids, 406, 946, 948, 971 Carrier-mediated process, 741 Cataract, 946, 957 operation, 1197 Catch up growth, 301, 347, 384 Catchment area, 1159 Catch-up formula, 919 Catechins, 948 Catecholamines, 354 Causality, 1123 Cause–effect

1218

Public health nutrition in developing countries

questions, 1050 relationship, 4, 990 CD4 cell counts, 686 CD4+ T cells, 373 CD8 cytotoxic lymphocytes, 373 CD8+ T cell, 374 Cell division, 629 Cell mediated immunity, 700 immune responses, 389 Cellular binding protein (CRBPII), 410 Cellular differentiation, 416 Cellular iron, molecular regulation of, 621, 623 Central Council of Health and Family Welfare, 576 Central/android obesity, 149, 347 Centre for Research on the Epidemiology of Disasters (CRED), 901 Cephalopelvic disproportion, 721 Cereal pulse based diets, 693 Cerebellar folds, 668 Cerebral palsy, 334 Cervical cancers, 960 Chapatti diagram, 1078 Chemoprophylaxis, 686 Chief Medical officer (CMO), 1157 Child Development Project Officer (CDPO), 1156 Child growth micronutrient interventions, 43 Child health and nutrition months, 489 Child health day approach, 779 Child health months, 460 Child In Need Institute (CINI), 836 Child mortality, 43, 51, 201, 282, 283, 984 common causes, 170 Iodine deficiency, 541 impact, 797 protein energy malnutrition, 295, 299 public health nutrition, 752, 764, 786, 910 rates, 153, 154, 201, 777, 791, 910, 1051 under five mortality rate, 153, 278 Vitamin A and zinc deficiencies, 445, 447, 456, 775–777 Vitamin A supplementation, 791 Child nutrition, evidence-based interventions, 293

Child survival, 51, 776 Vitamin A and zinc supplements for, 772, 775 Child Survival and Safe Motherhood Programmes (CSSM), 169, 483 Childhood diarrhea, 776 Childhood malnutrition, 223 status, 300 Children under two in South Asia nutritional status of, 253, 55 Chi-square test, 1148 CHOICE method, 1127 Cholesterol, 9 Chronic degenerative brain disease, 941 diseases, 970 episode, 275 gonadotrophin (CG), 507 infection, 939 inflammatory disorders, 688 malnutrition, 36, 912 recurrent infections, 685 Chronic energy deficiency (CED), 69, 895 among women, 72, 73 Chronic obstructive pulmonary diseases (COPD), 957 Chylomicrons, 410 Class-mean imputations, 1148 Climate change, 859 Climate shifts, 859 Clinical assessment, 34 signs, 910 trials, 1141 zinc deficiency, 737 Cluster WHO Methodology for coverage evaluation surveys (CES), 1143 Cobalamin, 630 Cochrane Group, 42 Codex Alimentarius, 800, 805, 916 standard for food grade salt, 805 Cognition, 941 Cognitive deficits, 647, 669 Cognitive development, 676 Cognitive function, 941 Cohort, 9 studies, 9, 29, 1141 Cold storages, 875 Colon cancer, 946 Color masking compounds, 827

Index Colostrum, 180, 184, 186, 438 immune protection to a neonate, 185 feeding, 1162 Commercial barley malt (CBM), 264 Commercial breast milk substitutes, 177 Common wisdoms, 570 Community based management, 1179 Community Based Maternal and Child Health Nutrition (MCHN), 1110, 1172, 1182 Community -based care, 319 -based monitoring, 1022, 1033 -based nutrition surveillance, 1161 -based tracking system, 1173 -based workers, 210 -based nutrition model, 1106 chart, 1161 engagement, 1171, 1191 gatherings, 1102 health screening, 977 health workers (CHWs), 748 intervention trials, 32 monitoring, 1070 nutrition professionals, 1188 participation, 1074, 1088, 1157, 1173 reviews, 1022 survey, 1157 volunteers, 1110 Community health centre, primary health centre (PHC), 316, 1198 Community Health Nutrition Sanitation Mobilisers (CHNSMs), 1183 Community mobilization, 297, 1179 programmes, 203 Community needs assessment (CNA), 1000 Community-based organisation (CBOs), 1071 Community-based therapeutic care (CTC), 303, 320, 321, 918 Complementary feeding, 187, 206, 223, 225, 226, 1159 adequacy and frequency of, 228 calcium and vitamin A densities, 231 developmental technology in India, 261, 266 diverse food habits, 242 energy and other nutrient intake, 228, 230

1219

faulty practices, causes of, 232, 235 feeding during and after illness, 238 food restrictions due to cultural beliefs, 234 home based, 242–246 improving acceptability, 266 issues and guidelines, 226–227 low-cost, 241 macroand micro-nutrient requirements, 230 measuring the status, 238–239 micronutrient densities, WHO/ UNICEF [21] recommendations, 230–231 nutrient content, 236, 237 recommended protein and other micronutrient intakes, 230 responsive feeding, 237, 238 satisfactory, desirable features for, 235 status – global and India, 240–241 timely initiation, 227 vitamin–mineral supplements, 237 Complementary feeding index (CFI), 238 Complementary food supplement (CFS), 833 Complementary foods, 224, 225 Complementary nutrition, 257 Complete Rural Village Scheme, 868 Comprehensive breastfeeding programme, elements of, 195f Concealed randomization/allocation concealment, 21 Conceptual framework for analysis, 996 of food security, 847 Concomitant illnesses, 166 Conditional cash transfer (CCT), 76, 299, 876 programmes, 874 Confidence intervals, 42 Confounder, 41 Confounding bias, 18 Confounding factors, 1123 Confounding, 3, 41 Conjunctival impression cytology (CIC), 423 Conjunctival xerosis, 423, 798 Consolidated Standards of Reporting Trials (CONSORT), 30 Constipation, 942

1220

Public health nutrition in developing countries

Consumer expenditure survey, 105, 855 Consumption unit, 886 Contamination, 322 Continuum of care, 156 Controlled trials crossover studies, 22 parallel design, 22 Convention on the Rights of the Child, 193 Convulsions, 320 Coping strategies, 900 Corn soya, 263 Corneal ulceration, 332 Corneal xerosis, 423 Corn–Soya–Blend (CSB), 266 Corn–soya–milk, 257 Coronary heart disease, 942 Cortisol, 354 Coupling, 505 c–reactive protein (CRP), 625 Cretinism, 508, 539, 800 Critical development periods, 674 Critical manpower, 1209 Critical moisture content, 806 Critical phases of life, 774 Cross-product ratio, 17 Crude mortality rate (CMR), 912 Crypotoxanthin, 407 Crystalline ascorbic acid, 683 Cumulative incidence rate, 7 Cyanmethemoglobin, 695 Cyclic compounds, 971 Cyclooxygenase (COX), 611 Cysteine-rich intestinal protein, 741 Cystic fibrosis, 739 Cytochrome b5, 611 Cytochrome P, 450, 611 Cytochromes, 610 Cytokines, 341, 941 Cytopenias, 686 Cytotoxic T-lymphocytes, 754 Dai’s (trained birth attendant), 1099 Daily living tasks, 941 Dark green leafy vegetables (DGLV), 450 Darrow’s solution, 330 Day-care nutritional centres, 303 DBS Tg assays, 518 Deaf-mutism, 508 Death rate, 336 Deep vein thrombosis, 965

Deficient iron stores, 624 Degenerative diseases, 178 Degree of variability, 1144 Dehydration, 280, 302, 320 Delayed growth, 912 Demand driven approach, 289 Dementia, 939, 941 Demographic balance, 1196 shift, 935 transition, 932, 960 Demographic Health Surveys (DHS), 27, 987, 1119 Demyelination, 635 Dendric cells, 373 Dengue mortality reduction rate, 1197 Deoxyribonucleotide diphsophates (dNDPs), 612 Deoxythymidine, 633 Department of Health & Family Welfare, 1162 Department of Women and Child Development (DWCD), 1155 Depression, 941 Desolation, 938 Desquamated gastro intestinal cells, 692 Deuterated retinol dilution technique, 425 Deworming, 73, 299, 459, 731, 1185 children, 299, 300 Dexa-scan, 108 Dextrinization, 242 Dextrostix, 332 Diabetes, 940 coronary artery disease, 956 mellitus, 341, 887, 968 Diarrhea, 274, 381, 745 basic prevention strategies, 286 causes of, 276 feeding during, culture-specific beliefs influence, 284 impairment of appetite, 280 management of, 280–285, 752 prevention of, 285–290 Diarrhea Disease Control Programme, 169, 282 Diarrhea Treatment Kit (DTK), 759, 787, 790 Diarrhea, prevention strategies breastfeeding, 286

Index safe water, use of, 287 hand washing, 287 food safety, 288 hygienic sanitary environment, 288 measles immunization, 288 Diarrheal diseases, 274 Diastolic blood pressure (DBP), 958 Diet quality, 844 Diet records, 34 Diet related NCDs, risk factors, 963, 964 Dietary approaches to stop hypertension (DASH), 968 Dietary assessment, 33 diversification, 723, 774, 813, 844 diversity, 239 inadequacies, 680 intake, 25 iron, bioavailability of, 616, 617 methods, 34 Dietary folate equivalent’s (DFE), 627, 628 Dietary guidelines for Americans (2005), 949 for older persons, 949 Dietary zinc, 739 deficiency, 743 Dietary zinc intake essentials, 758 of young children, 739 Diet–disease interactions, 30 Dihydrofolates, 626 Dihydroxyphenylalanine (DOPA), 612 Diiodotyrosines (DITs), 505 Directorate General of Health Services (DGHS), 577 Disability adjusted life years (DALY), 176, 957 Disaggregated analysis, 1149, 1151 Disaster management, 928 Disaster preparedness, 903, 904, 905 Disease free (controls), 29 Disseminated Candida, 311 Distal outcomes, 990 District Health Action Plan (DHAP), 1068, 1069, 1072, 1203 development of, 1075–1077 District Health Care System, 1067 District Level Household Surveys (DLHS), 987

1221

District Mobile Monitoring Training Team, 1181 District Planning Committee (DPC), 1067 District Planning Development Cycle, 1072, 1074 District planning process, 1069, 1072 District Planning Team (DPT), 1072, 1075 District Programme Managers, 1072 District Project Officer (DPO), 1156 Disuse atrophy, 939 Diuretics, 948 Divalent metal ion transporter, 687 Divalent metal transporter-1(DMT-1), 619 Diverticulosis, 971 Docosahexaenoic acid (DHA), 945 Domiciliary care, 304 Dose-response, 1009 Double fortified salt, 702, 826 Double ration approach, 1169 Double-blinded randomized control trial (RCT), 4, 5 case-control study, 5 Down’s syndrome, 334 Dried blood spot (DBS), 518 Drinkable consistency, 261 Drip feed, 564 addition, 805 Drop floats, 694 Drought, 859, 898 Drought Prone Areas Programme (DPAP), 874 Drug kit, 1201 A, 484 Drugs, 378 Dry food rations, 916 Dry milk solids, 383 Dry mix, 564 Dry mixing, 803 Dual energy X-ray absorbiometry (DEXA), 108, 147 Dual nutrition burden fat fold thickness, 87–89 in India, 87–90 in women, 86–87 Duchenne muscular dystrophy, 357 Dular’s approach, 202, 1172, 1173 Duodenal cytochrome b (Dcytb), 619, 687 Dysentery, 275 Dysgeusia, 941, 942 Dyspnea, 686

1222

Public health nutrition in developing countries

Early breastfeeding, 166 initiation of, 176 Early childhood care and preschool education (ECCE), 1161 Early learning, 1161 Early neonatal period, 151 Early warnings, 905 system (EWS), 907 Earthquakes, 898 Economic insecurity, 938, 954 Edema, 293 Edible oils, fortification of, 828 Education and literacy impact, 797 Education Guarantee Scheme (EGC), 872 Education in Nutrition, 1088, 1109 Education initiatives, 973 Efavirenz, 376 Effect theory, 991 Efficacy, 786, 1009 of an intervention, 23 studies, 1118 Efficiency analysis, 1057 assessment, 1057 Eicosapentaenoic acid (EPA), 945 Elaidic acid, 945 Embryogenesis, 416 Emergency thresholds, 911 Emergency treatment wall chart, 330 Emotional irritability, 941 Emotional support, 329 Empirical consumer research, 1089 Empowered Action Group (EAG), 1195 Empowered programme committee, 1199 Encapsulated ferrous fumarate (EFF), 827 Endemic cretinism, 509, 539 Endocrine, 355, 621 disruptors, 355 Endogenous zinc, 757 Endothelial damage, 966 Endothelium, 966 Endurance tests, 697, 698 Energy balance, 342, 960, 975 maintenance of, 342 Energy density (ED), 236, 243, 352 Energy gap, 228 Energy intake, 228, 229, 341 regulation of, 343 Enhancers, 682 Enterocytes, 618, 688

Environmental hygiene, 882 Environmental sanitation, 61 Epidemics, 898 Epidemiologic studies experimental studies, 4 observational studies, 4 Epidemiologic transition, 43 Epidemiological reasoning, 3 systematic error, 3 Epidemiological transition, 964 Epidemiology, 1 Epigenetics, 351 Erythrocyte protoporphyrin, 625, 696 concentration, 674 Erythrocyte zinc content, 755, 755 Erythroid marrow, 696 Erythropoiesis, 617, 686, 688 Erythropoietic need, 618 Essential fatty acids, 393 Essential newborn care (ENBC), 156, 166, 167 Essential nutrition, 1176 Estimated average requirement (EAR), 37, 512, 742 Estimating average or proportion, 1143 Estrogen deficiency, 943 Etiology, 2, 677 Euthyroid, 508 Evaluation design matrix, 1050 Evidence-based decision-making, 1114 Ex-ante analysis, 1057 Exchangeable zinc pool (EZP), 757 Exclusive breastfeeding, 67, 166, 1162 indicator, 188 for 6 months, 188, 190 practices, 187–189 under 6 months, 176 Exclusively breast fed infant breast milk consumption, 187 Expanded immunization coverage, 772 Expanded Program for Immunisation (EPI), 458, 779 Ex-post analysis, 1057 Extended family, 938 External monitoring, 550 Extremely low birth weight, 155 Extrusion, 263, 830 Eye disorders, 959 Eye lesions, 422

Index Fair Price Shops (FPS), 866 Family diet, 242 Family foods, 921 Family planning programme, 80 Family pot, 234, 243, 305 Fasting glucose level, 967 Fat mass, 940 Fat oxidation, 344 Fat soluble A activity, 405 Fatigue, 686 Fat-redistribution syndrome, 377 Faulty dentures, 941 Fe/Zn ratio, 743 Feeding practices, 175 Feeding the under-2, 259, 260 outreach of supplementary foods, 267, 271 Fels Longitudinal Study, 137 Feminization, 936 of old age, 936 Fenton chemistry, 622 Fermentation, 703 Fermenting, 242 Ferri reductase, 687 Ferric pyrophosphate (MGFePP), 827 Ferrihemoglobin, 610 Ferritin, 608, 613, 688 mRNA, 622 Ferrohemoglobin, 610 Ferroportin, 687, 688 Ferroportin-1 (FPN-1), 620 Ferrous fumarate, 692, 805 Ferrous gluconate, 692 Ferrous sulfate, 705 Fertility, 960 decline, 934 Fetal brain, growth and development of, 668 Fetal programming, 351 Fetal-growth restriction, 293, 295 FFM (fat free mass), 394 Fibrinogen, 969 Filarial/Microfilaria reduction rate, 1197 Finger foods, 236 First rice, 227 First stage units (FSU), 887 First World Assembly on Ageing, 950 Fish oil, 966 Fitness and nutritional composition, 917 Fixed WIFS day, 731

1223

Flatulence, 942 Flavin Adenine Dehyrdogenase (FAD), 36 Flavonoids, 948, 971 Floods, 536, 859, 898, 899, 901, 904, 906 Flour fortification, 812 Fluid and electrolyte imbalance, 918 Fluid balance, 948 Fluid intelligence, 669 Folate, 606, 626, 963 availability, 627 conjugase, 628 content, 627 deficiency, 675, 947 nutritional status, 630 trap, 629 Folic acid, 607, 626 and anemia, 629, 630 deficiency, 629, 675 supplementation, 699 Follicle-stimulating hormone (FSH), 507 Food -based approach, 949 access, 845 adequacy, 852 aid, 901, 902 assistance, 901 availability, 848 balance sheets, 29 consistency, 236 diaries, 35 fads, 234 gap, 888 grain security, 855 insecure, 844 label, 972 labeling, 972 prices, 851, 858 rations, 903 security, 335, 672, 845, 851, 855, 859, 872, 874, 882 stability, 847 systems, 845 use, 845, 849 utilization, 848 vehicle, 702 Food and Civil Supplies Department, 577 Food and Nutrition Board, 235 Food and nutrition security, 845, 850 underlying factors, 858, 865 Food Corporation of India (FCI), 872

1224

Public health nutrition in developing countries

Food folate, 627, 628 digestion and absorption, 628 functions, 628, 629 Food fortification, 298, 701, 795, 799, 800, 802, 809, 810 fortificants, 804 global experiences, 810–813 in India, 813–825 industrially processed foods, 814–816 innovative experiments, 831–835 monitoring and evaluation, 837 planning of, 809–810 regulations and standards, 837–839 technical considerations, 802 technology, 803, 804 Food fortification cycle, 809, 810 Food frequency questionnaires (FFQ), 34, 35 Food Insecurity and Vulnerability Information and Mapping Systems (FIVIMS), 849 Food insecurity/hunger per se, 68, 178, 875 global perspective, 852–854 Indian perspective, 854–856, 865–876 Food Security Act, 869 Food security, 846, 881 in India, 882–885 Food-based Dietary Guidelines (FBDG), 1093, 1094 Food-based dietary guidelines for older persons, 950 Food-for-Work (FFW), 874 Food-health-care, 296 Food-secure household, 846 Fortificant, 525, 702, 800, 923 Fortification programme, 1043 Fortified food, 702 Fortified blended foods, 812 Fortified Khichdi (FK), 818 Four P(s), 1014, 1092 Fracture risk, 940 Fragile X syndrome, 357 Frail, 935 Free Expression for Quality Improvement (FREQI), 1184 Free fatty acid, 346 Free radicals, 386, 389 Free folate, 628 Frontline worker, 1156 Full-term infants, 691

Functional iron, 697 Functional proteins, 681 Gait, 941 Galactopoiesis, 179, 181, 182 Gallstones, 940, 957 Gangrene, 959 Gastric capacity, 230 Gastric pepsin, 942 Gastro intestinal tract, 681 Gender equality, 984 impact, 797 Gender equity, 51 Gene expression, 351 General feeding programmes, 914 Generic AYUSH, 1201 Genetic anemia, 677 Genetic modification, 701 Genetics, 957 Geo-climatic conditions, 901 Geriatric (s), 3, 943 nutrition, 943 units, 954 Germination, 260, 703 Gerontologic nutrition, 943 Gerontology, 943 Gestation, 680 age, 57, 691 Gestational diabetes mellitus, 351 Ghrelin, 343 Girl to girl approach, 732 Glacial melting, 859 Global acute malnutrition (GAM), 911 Global Burden of Disease (GBD), 958 Global Hunger Index (GHI), 854, 880 Global warming, 859 Glucocorticoids, 356 Glucose intolerance (Insulin resistance), 103, 967 metabolism, 355 tolerance, 351 Glutamate carboxypeptidase, 628 Glutathione, 386 perodixase, 389 S-transferases, 971 Glycemic index, 354, 962 Goitre, 507, 541, 800 rate, 508

Index size, 514 surveys, 514 Goitrogens, 537 Golden rice, 701 Grain banks, 870 Gram panchayat, 870, 1071 Gram Pradhan, 1071 Gram Sampark Samooh, 1180 Gramin mela (rural fair), 1109 Grass-root workers, 172 Green leafy vegetables (GLVs), 243, 246 Greying of nations, 933, 934 Growth charts, 136, 137, 626, 1159 Growth failure, 738 Growth faltering, 224, 757, 1159 Growth monitoring, 300, 1156 and promotion, 1159 days, 1161 Growth pattern, 1159 Growth promotion, 1161 Growth spurt, 692, 716 Gynecoid fat distribution, 149 Haemoglobinopathies, 643 Hair zinc, 756 concentrations, 756 Half saline, 330 Hand milling, 825 Hands-on training of mothers or caregivers, 1179 Hanging scale (Salter-type or spring balance), 113 Haptocorrin-B12 complex, 632 Hb assays, 680 HDL cholesterol, 968 Health Days/Village Health and Nutrition Days (VHND), 1201, 1202 Health care, 1159 check-up, 873, 1156 clinics, 303 education, 976 management systems, 1210 Mission, 1072 plan, 1198 planning, 1068 security, 1199 services, 1197 Healthier choice, 975

1225

Healthy term infants iron reserves, 231 Hearing loss, 941 Heart disease, 341, 957 Height-for-age index, 119 Helminthic and protozoal infestations, 680 Helminthic infestations, 685 HelpAge India, 953 Hematinic effect, 665, 668 Hematinics, 675 Hematocrit, 644, 694 status, 723 Hematopoiesis, 663 Heme, 609, 681 carrier protein, 619 enzymes, 610 iron, 681, 682, 706 iron absorption, 619, 688 oxygenase, 688 proteins, 609 Hemochromatosis, 688 Hemocue, 695 Hemoglobin (Hb), 608, 610, 675, 696 Hemoglobin cut-off values, 676 Hemoglobin levels, estimation of, 694, 697 Hemolysis, 686 Hemolytic anemia, 687 Hemopoiesis, 417, 676 Hemopoietic factor, 608 Hemosiderin, 608 iron, 613 Hepatic insulin resistance index, 346 Hepatocytes, 411 Hepatomegaly, 292 Hepatosplenomegaly, 737 Hepcidin, 620, 621, 688, 706 Hephaestin, 687, 688 protein, 620 Heterogeneity, 749 HFE (hemo chromatosis gene), 688 Hidden hunger, 796, 845 High blood pressure, 967, 969 High Level Committee on Long Term Grain policy, 863 High performance liquid chromatography (HPLC), 425, 441 High profile disasters, 898 High-energy biscuits, 916 High-risk groups, 1162 High-yield value (HYV), 863

1226

Public health nutrition in developing countries

Hip fractures, 940 HIV. See Human immunodeficiency virus. HIV infection, 686. See also People Living with HIV (PLHIV). in humans, 372 mother to child transmission, 95 HIV lipodystrophy (HIVL), 380 HIV viral load, 387 HIV virus, 5 HIV/AIDS, 984 HIV-associated symptoms, 376 HIV-infected children, supplementation of vitamin A, 387 HIV-infected individuals, 376 HJV (hemo juvelin), 688 Holistic Health Framework (HHF), 360 Holo-RBP, 412 Home available fluids (HAF), 280 Home -based rehabilitation, 323 -based caring practices, 1172 or community-based approach, 314 fortificants, 237, 244, 298, 813, 833 Home visits, 1108, 1157, 1161, 1176 planner, 1191 Homeopathy, 1196 Homeostasis, 612, 687 Homeostatic mechanism, 675 Homeostatic regulation, 342 Homocysteine (Hcy), 629, 947, 963 Homogeneous groups, 1142 Hook worm infestation, 685, 719 Horticulture programme, 1043 Hospital Management Committee, 1199 Hot cooked meals (HCM), 1159 Hot-deck imputation, 1148 Household counseling, 1181 food insecurity, 61 viability, 902 Human immunodeficiency virus (HIV), 372, 685 Human milk, 966 composition of, 184, 186 Human resources, 1016 requirements, 1203, 1208 management, 1203 Humoral, 389 Hunger, 844, 845 -gather society diets, 957

trap, 844 Hybrid study designs, 23 Hydrogenation, 946 Hygiene, 276 and health services, 996 Hyper vitaminosis A, 463 Hyperammonemia, 739 Hyperinsulinemia, 103, 940 Hyperlipidemias, 149 Hyper-osmolar foods, 285 Hypertension, 103, 341, 507, 887, 939, 957, 958, 967 Hypertriglyceridemia, 103 Hypochlorhydria, 946 Hypoglycaemia, 918, 328 Hypogonadism, 737, 739 Hypo-proliferative anemia, 633 Hyporetinolemia, 439 Hyposmia, 941 Hypothalamus, 180 Hypothermia, 328, 918 Hypothyroidism, 506, 516, 538 Hypovolaemic, 329 Hypoxia, 688

ICCIDD (International Council for Control of Iodine Deficiency Disorders), 542 ICDS. See Integrated Child Development Services. ICDS Centre, 873 frontline workers/anganwadi workers, 96 monitoring, 1170 program, evaluations of, 1165 reforms, 1191 training, 1170 ICN Plan of action, 1093, 1094 ID. See Iron deficiency. IDA. See Iron deficiency anemia. IDA among adolescent girls, 715, 720 antenatal care (ANC) services, 731 consequences of, 721, 723 in India and prevention efforts, 730, 731 iron-folic acid (IFA) supplements, 725 prevention and control of, 723, 729 IDD. See iodine deficiency disorders. IDD cells, 577

Index IDD elimination, 526 programme, 528, 533 Idiopathic intra-cranial hypertension, 356 IEC (Information, education and communications), 823 IFA supplements, 1162 IFA tablet, 1162 Immune function, 676, 940 Immune system, 373, 375 Immunization, 163, 873, 1156, 1161 contacts, 77 outreach sessions, 316 sessions, 1161 sites, 493 Immunocompetence, 946 Immunoglobulin, 182 Immunologic mechanisms, 744 Immunosuppression, 686 Impaired, 351 glucose tolerance (IGT), 959 thermo regulation, 700–701 work capacity, 796 Imputation, 1148 based upon regression, 1148 Inappropriate feeding practice, 192 Incaparina, 263 Incidence, 7, 28 density, 7, 14 Inconsistencies, 1148 India capacity building, 1210 dietary consumption pattern, 885–886 district planning committees, 1067 draft district plan, 1067 GHI score, 880 households, socioeconomic status of, 891–892 intra-family distribution of dietary energy, 889–891 NSSO consumption expenditure surveys, 891 nutrient intake trends, 886–889 nutritional status – trends in children and adults, 892–896 public health infrastructure, 1208–1209 rural areas, critical manpower, 1209 disasters, types of, 927 disaster management, 927–929 India Clinical Epidemiology Network (IndiaCLEN), 170

1227

India State Hunger Index (ISHI), 854, 881 India VAD programme policy, 483 biannual fixed month strategy, 487–498 CSSM programme, 483–484 VAD elimination programme, 488 Indian Academy of Pediatrics (IAP), 788 classification, 145–146 Indian Multi-purpose Food (IMPF), 814 Indian Public Health Standards (IPHS), 1198, 1207 Indian Recommended Dietary Allowances (RDA) for infants aged 6–12 months, 229, 231 Indian Standards Institution (ISI), 815 Indian State Hunger Index (ISHI), 881 Indicators of achievement, 1038 Indices, 36 Indira Awaas Yojana, 874 Individual food security, 883 Individualism, 938 Indoles, 948, 971 Infancy and early childhood, iron requirements, 690, 692 body mass index, 347 infant’s iron needs, 231 poor vitamin A status, 231 Infant and young child feeding, 190 Infant and Young Child feeding Index (ICFI), 238 appropriate feeding practices and reducing malnutrition, 225 framework, 490 Infant botulism, 181 Infant feeding practices of mothers and caregivers direct/ proximate factors, 203, 204f Infant Foods Regulation of Production, Supply and Distribution Amendment Bill, 196 Infant Milk Substitutes, Feeding Bottles and Infant Foods Regulation of Production, Supply and Distribution Amendment Bill, 2003 (IMSAB), 196 Infant Mortality Rate (IMR), 63, 1196 Infants and young children, complementary feeding, 223, 226 undernutrition in India, 223, 224 Infection with HIV and appropriate support, 391, 402

1228

Public health nutrition in developing countries

causes of, 373 CD+ t cell count, 374 immune-system maintenance, 375 nutrition status, 377–383 nutritional deficiencies, 374 opportunistic infections, 377 treatment for, 375–377 Infectious diseases, 961 Inferential statistics, 1058 Infestations, 672 protozoal infestations, 681 parasitic infestations, 685 Inflammatory arthritis, 971 Inflammatory peptides, 341 Influenza, 374 Information Education and Communication (IEC), 289, 1088 materials, 1161 Informed consent, 20 Injecting drug users (IDUs), 372 Inositol Phosphates (Phytates), 971 Inpatient (hospital) care, 301–303 In-patient care, 317 Inpatient facility based management, 920 Insoluble complexes, 683 Institutional Mechanisms under NRHM, 1200 Insulin, 967 resistance, 149, 347, 940, 956, 967 sensitivity index, 346 Integrated Child Development Services (ICDS) scheme, 22, 95, 96, 873, 1154 basket of services, 1156 key objectives, 1155–1156 nutrition component under, 1159–1162 program background, 1155 program evaluations and program limitations, 1165–1171 program evolution, 1163–1165 team-composition of, 1156–1159 training in, 1162–1163 Integrated Disease Surveillance Programme (IDSP), 1076 Integrated Food Laws, 839 Integrated Management of Childhood Illness (IMCI), 170, 199 Integrated Management of Neonatal Care Childhood Illnesses (IMNCI), 1170 Integrated Nutrition and Health Project (INHP), 1174, 1176

Integrated Programme for Older Persons, 953 Intelligence quotient, 532 Intention to treat, 32 Interaction or effect modification, 41 Internal consistency checks, 1136 International Association for the Study of Obesity (IASO), 361 International Association of Gerontology, 951 International Center for Tropical Agriculture (CIAT), 859 International Code of Marketing of Breastmilk Substitutes, 193 International commodity prices, 851 International Food Policy Research Institute (IFPRI), 860, 880 International Maize and Wheat Improvement Center (CIMMYT), 859 International Obesity Task Force (IOTF), 361, 895 International Research on Infant Supplementation Initiative (IRIS), 670 International unit (IU), 408, 815 International Zinc Consultative Group, 742 Interpersonal communication (IPC), 203, 213, 1108, 1109 Interpersonal counseling sessions, 1183 Intestinal lumen, 684 Intestinal motility, 942 Intra uterine growth retardation, 969 Intra-abdominal fat, 149 Intracellular folates, 626, 627 Intrauterine growth rate, 57 growth restriction (IUGR), 57, 71 reprogramming, 295 undernutrition, 957 Intrinsic factor (IF), 631 Involution, 179, 182 Iodated salt, 589 Iodide, 503, 504 trapping, 504–505 Iodinated water, 541 Iodine, 502 /Creatinine ratio, 515 absorption, 503–504 content, 589 in biological functions, 509–510 induced hyperthyroidism (IIH), 526

Index induced hypothyroidism, 540 metabolism, 507 nutrition for human populations, 510 nutrition, 554 nutriture, 558 supplementation, 524 Iodine deficiency (ID), 502 in food, 536 in women, 541 Iodine deficiency disorders (IDD), 506, 509, 1042 control program, 524, 535–537, 549– 556 controlling of, 524–533 elimination in India, 597–602 elimination of, 542 public health problem, 537–542, 556– 558 Iodine fortification, 525, 805 with salt, 542, 545 Iodine requirement and intake, 504, 511–513 estimated average requirement (EAR), 512 in pregnancy and lactation, 511, 514 Iodine status impact indicator, 514–518 during pregnancy, 517–518 Iodization, 502 of salt, 543 Iodized oil, 525 injections, 541 supplement, 558 Iodized salt, 523 intervention, 546 supply, 585 Iodometric titration, 551 Iodopsin, 414 Iodothyronines, 506 IRE-binding proteins (IRE-BPs), 621 Iron, 607, 608, 946 binding capacity, 674 bioavailability, 616, 681, 706 carrier protein, 688 day, 728 dietary sources and recommended intake, 627 distribution, 608–609 fortificants, 805 fortification, 724, 743

1229

functional compartment, 609 homeostasis, 618, 684, 687, 706 intestinal absorption at enterocyte, 619 lack, 695 losses, 614 metabolism, 625 molar ratio, 683 premix, 827 recommended daily allowance (RDA), 617–618 recycling in body, 614 storage compartment, 613 transport compartment, 614 uptake in cells, 621 Iron absorption, 237, 684, 687 influencing factors, 617 Iron balance, 645 in children, 645 Iron deficiency (ID), 638, 643, 674, 713, 818 among adolescent girls, 713, 715 Iron deficiency anemia (IDA), 608, 625, 638, 644, 674, 818, 946. See also Nutritional anemia. in pre-school children, 640–642 in young children, 638–642 prevention and control, 650–653 Iron deficiency anemia, prevention and control dietary iron, increasing bioavailability of, 702–703 food fortification, 701–702 nutrient supplements, 703–705 Iron deficient erythropoiesis, 624, 696 intestine, 626 stores, 695 Iron dependent enzymes, 697 Iron flux, 688 Iron folic acid, (IFA), 69, 77, 79 Nutrition–Health Education (NHE) services, 1087 supplement, 73–74, 650–655, 703, 724–726, 1114 tablets, 726, 732, 1090, 1092 Iron regulating protein (IRP), 688 Iron Responsive Element (IRE), 621, 688 Iron supplementation, 699 Iron toxicity, 625, 626 Ischemic heart disease (CHD), 103, 964, 965

1230

Public health nutrition in developing countries

Isocaloric, 264 Isoflavones, 971 Iso-osmolar, 284 Isothiocyanates, 948, 971 Isotope dilution technique, 426 IV infusions, 327 Janani Suraksha Yojana (JSY), 1202, 1211 Jawahar Gram Samridhi Yojana, 874 Jawahar Rozgar Yojana (JRY), 874 Joint FAO/WHO Expert Consultation (2004) on Diet, 970 Joint food, 1087 Junk food, 960

Kala Azar mortality reduction rate, 1197 Kangaroo mother care, 157, 159, 332, 333 Kano Parbo Na, 1107, 1172, 1176, 1184 Keratin, 416 Keratomalacia, 423 Khichdi, 1185 Kidney damage, 959 Kupffer cells, 613 Kwashiorkor, 146, 292, 293, 303, 456, 655, 909 classical, 145 marasmic, 146, 293, 303, 909 Labile iron, 623 Lactation, 179 Lactation cycle, 179, 184. See also Breastfeeding. increase in milk volume, 182 Lactoferrin, 182 Lactoge, 263 Lactogenesis, 179, 180, 181 Lactose, 383 -free, 285 -intolerant people, 383 intolerance, 382, 383 Lacunae, 665 Lady Health Visitor (LHV), 1157, 1207 Lady health workers, 199 Late neonatal period, 151 Latent periods, 16 Laubina, 263 LBW children, 69 nutritional status, 70 Lean body mass, 360, 378, 715

LEAP-1 (liver expressed antimicrobial peptide), 620 Lecithinretinol, 410 Length/height boards, 109 Length-for-age, 116 Leprosy prevalence rate, 1197 Leptin, 343, 966 Leucocyte subsets, 756 zinc content, 755–756 Leucopenia, 686 Leutanizing hormone (LH), 507 Level playing field, 837 Life cycle approach, 997, 1164, 1184 cycle framework, 988 expectancy, 935 expectancy at birth, 879 span, 960 Lifesaving interventions, 320 Lifestyle changes, 956 Lignans, 971 Likert scale, 822 Linear growth retardation, 109 Linolenic acid, 945 Lipid micelles, 410 Lipids, 945 Lipodystrophy, 381 Lipogenic, 345 Lipoprotein, 946 Lipoxygenases, 612 Lipsey and Freeman program theory, 989 Liquefaction, 264 Live births, 151 Livelihood security, 869, 902 Liver apo-RBP, 412 Liver biopsy, 422 Local health traditions, 1196 Lopinavir, 376 Low birth weight (LBW), 57, 293, 346, 969. See also Neonatal mortality. anemia per se, 73 incidence of, 65 inter-generational cycle of, 64 metabolic syndrome in utero, 101 Low density lipoprotein (LDL), 412, 968 Low glycemic index, 962 Low income group (LIG), 257 Low weight for height, 310 Low zinc bioavailability, 737

Index Lower gestational duration, 700 Lozenges, 831 Lugol, 525 Luminal and mucosal overload, 726 Lumpy foods, 244 Lutein, 419 Lycopene, 413, 419, 420 Lymphocyte, 700, 744 Lymphopenia, 686 Lysine hydroxylase, 613 Macro malnutrition, 795 Macronutrients, 280, 960, 963 Macrophages, 373 Macrophage infiltration, 966 Macular degeneration, 946 Macular pigments, 419 Magnetic resonance imaging (MRI), 108 Mahila mandals, 1109 Major infectious disease impact, 797 Mal-absorption syndrome, 9 Malaria, 685, 984 mortality reduction rate, 1197 prevention and treatment and peacekeeping, 772 prophylaxis, 705 Malarial non-hyperendemic region, 667 parasites, 680 parasitosis, 686 prophylaxis, 705 Male health workers, 1157 Malnourishing, 275 Malnutrition, 43, 50, 898, 984, 1154. See also Nutrition, Undernutrition. conceptual framework of, 64f cycle of, 899 diarrhea, role of, 279 in infants, 175–176 WHO Classification of, 146 Malnutrition drama, 252 Malnutrition in children, 293. See also Undernutrition in children. breastfeeding promotion, 295 complimentary feeding, 295–296 nutritional education, 296–297 Malting, 244 Mammary gland, 179 Mammogenesis, 179 Management Information System (MIS),

1231

1058, 1064 Management of Nutrition in Major Emergencies, 921 Managing for Development Results (MfDR), 983 Manmade disasters, 898 Manpower planning, 1207 Mapping vulnerability, 859 Marasmic children, 293 Mastitis, 183 Maternal and child care practices, 996 Maternal and Child health (MCH), 1088, 1207 programme, 603, 1207 Maternal and Child Health Nutrition (MCHN), 1110 day, 1181 project, 202, 172, 1183 Maternal and child undernutrition, 983 Maternal and neonatal health outcomes, 71 Maternal body size, 69 Maternal health, 51, 984 impact, 797 Maternal HIV infection, 95 Maternal hypothyroxinaemia, 512 Maternal iron, 700 Maternal iron deficiency, 646 Maternal mortality, 700, 1196 Maternal night blindness, 442 Maternal nutrition, 974 Maternal nutritional status, deterioration in, 71 Maternal obesity, 351 Maternal undernutrition, 71, 72, 86, 105 anemia, iron deficiency, 73 building iron stores, 73 chronic energy deficiency (CED), 86 early conception, 71 micronutrient deficiency, 73, 74 mother–child dyad, 86 multiple micronutrient supplementation, 74 nutritional status, improving, 72 poor height and low BMI, 71 prenatal dietary supplementation, 72 susceptibility to infections, 86 undernourished girls, 71 Maternal VAD, 476 Maternal zinc, 753 Mature milk, 184, 186

1232

Public health nutrition in developing countries

MCT (medium-chain triglycerides), 393 Meal frequency, 236 Measles, 439 Measuring malnutrition, 910 Meat, fish and poultry (MFP), 702 Mebendazole, 306, 460, 705 Median urinary iodine concentration (UI), 516 Medical nutrition therapy (MNT), 336, 943 Medical officer-in-charge (MOIC), 1157 Megaloblastic anemia, 629, 633, 675 Megaloblastosis, 686 Menarche, 721, 726 Meningitis, 161, 649 Menopause, 946 Menstrual cycle, 726 Menstrual losses, 692 Menstruation, 717 Mental Development Index (MDI), 753 Mental functions, 676 Mental impairment, 941 Mental lethargy, 739 Mental retardation, 502 Mesozeaxanthin, 419 Metabolic alterations, 378 Metabolic diseases, 341 Metabolic disturbance, 319 Metabolic programming, 956 Metabolic syndrome, 959, 967 Metalloenzymes, 738 Metallothionein, 741, 757 gene, 738 Methemoglobin, 610 Methionine synthase, 629, 633 Methylation, 963 Methylmalonyl CoA, 633 mutase, 633 Methyl-THF, 629 Micro feeder, 824 Micro thrombi, 966 Micro-credit programmes for women, 205 Microcredit scheme, 953s Microcytic anemia, 675 Microencapsulate, 656 Micronized ferric pyrophosphate, 830 Micronized ground ferric pyrophosphate, 830 Micronutrient day, 457 Micronutrient deficiencies, 43, 44, 50, 51, 69, 329, 773, 887, 944. See also

Nutritional deficiencies or excesses. complimentary feeding, context to, 295 early childhood, 233 natural and manmade disasters, 899, 903, 909 public health nutrition, 324, 664, 665, 796–798, 799, 813, 817, 821, 823, 962, 970 Micronutrient malnutrition (MNM), 50, 795, 800, 844, 899 Micronutrient premix, 802, 822 Micronutrient sprinkles, 237, 243 Micronutrient supplementation, 298, 299, 1156 Microvilli, 684 Mid-day meal programme, 872 Mid-arm circumference (MAC), 394, 912 Mid-arm /mid-upper arm (MUAC) circumference, 113, 131, 304, 314, 315 Middle-income group (MIG), 257 Mild-moderate malnutrition, 307 Milk coming in, 181 Milk dilated alveoli, 183 Milk ejection, 181 Milky sweet porridge, 268 Minimal dietary iron absorption, 646 Minimum acceptable diet, 239 Minimum dietary diversity, 239 Minimum meal frequency, 239 Minimum wages, 868 Ministry of Social Justice and Empowerment, Government of India, 953 Ministry of Women and Child Development, 1155 Mitochondria, 697 Mitogens, 700 Mixed diet, 681 Mixed feeding, 397 MND. See Micronutrient deficiencies. Mobile Medicare Unit Programme, 953 Mobile video van, 1109 Moderate acute malnutrition, 310, 911 Moderate anemia, 676 Modified adult diet, 244 Modified family foods, 244 Modified Relative Dose Response (MRDR), 425 Monitoring Information Systems (MIS), 1185 Monitoring system design, 1034

Index Monitrices, 1106 Monoiodotyrosines (MITs), 505 Mononucleosis, 374 Monosodium glutamate (MSG), 452 Monotonous diets, 717 Monounsaturated fats, 393 Monounsaturated fatty acids, 945 Monthly per capita expenditures (MPCEs), 891 Mortality, 28, 960 acute malnutrition, 311–312 average daily mortality rate, 152 child, 153, 170, 171, 172, 201, 295 HIV transmission, 389, 396, 398 in children, due to diarrhea, 276–279, 282, 387 iron toxicity, 649 malnutrition deficiencies, 899, 905, 908–910 peonatal, 151, 152–153 perinatal, 541, 700, 706 pregnant mothers, 721–722 reduction efforts, 932, 960, 964, 972, 984, 1005, 1074, 1156, 1175, 1197, 1212 under-5 rates in children, 208, 209 Vitamin A deficiency in children, 434, 435, 445–447, 453, 456, 775 Zinc deficiency in children, 745, 748, 750, 751–752, 775 Mother & Child Day (MCD), 1109 Mother child dyad, 68 Mother-to-child transmission (MTCT), 373, 386 Motor development, 753 mRNA sequence, 621 Mucosal block, 725, 726 Mucosal cells, 683 Multi-micronutrient fortified beverage, 762 seasoning powder, 762 Multi-nodulargoiter, 510 Multiparous, 679 Multiple fortification, 804 Multiple Indicator Cluster Surveys (MICS), 570 Multiple micronutrient powders (MNPs), 1118 Multiple micronutrient supplementation, 32, 74, 298, 664, 668

1233

and iron in child mental development, effect on, 668–669 in child growth, 670–672 Multiple morbidities, 942 Multi-Purpose Workers (MPWs), 1198 Muscle wasting, 385 Myeloid lineage, 633 Myoglobin, 681, 715 Myo-inositol oxygenase, 613 Myristic acid, 970 Myxedematous manifestations, 508 Nanogram, 697 Naso-gastric tube feeding, 919 National (polio) immunization day (NID), 1062 National Agency for Food and Drug Administration and Control (NFDAC), 546 National Aids Control Organisation (NACO), 372 National AIDS Control Programme (NACP), 394 National Anemia Consultative Meeting of Government of India, 730 National Anemia Control Program, 690 National Cancer Control Programme (1984), 972 National Centre for Disease Control or NCDC, 597 National Centre for Health Statistics (NCHS), 55, 892 National Commission for Enterprises in the Unorganised Sector (NCEUS), 865 National Commission on Farmers, 864 National Commission on Macroeconomics and Health, 278 National Consensus Workshop on Management, 336 National Council for Older Persons (NCOP), 952, 952 National Council of Applied Economic Research (NCAER), 1165 National Dairy Development Board (NDDB), 875 National Disaster Management Authority (NDMA), 906, 928 National Disease Control Programs, 1074 National Evaluation of the Integrated Child Development Services 1992, 1166

1234

Public health nutrition in developing countries

National Family Benefit Scheme (NFBS), 870 National Family Health Survey (NFHS), 154 National Food for Work Programme (NFFW), 866, 868 National Food Security Mission (NFSM), 874, 884 National Goitre Control Programme (NGCP), 566, 575 National Guidelines on Infant and Young Child Feeding, 197 National Health and Family Survey (NFHS), 27 National Health Policy, 1197 National Health Survey of India, 278 National Health System Resource Centre (NHSRC), 1210 National Healthy Lifestyle Campaign, 976 National Immunisation Day (NID), 457, 779 National Immunization Schedule, 231 National Institute of Communicable Diseases, 597 National Institute of Health and Family Welfare (NIHFW), 597 National Institute of Nutrition (NIN), 1998, 256, 257 National Institute of Public Cooperation and Child Development (NIPCCD), 1162 National Iodine Deficiency Disorders Control Programme (NIDDCP), 575. See also Universal salt iodization (USI). IDD elimination, challenges, 602–603 iodine levels, monitoring of, 586–590 iodine nutrition, status of, 601–602 iodization, cost of, 584 iodized salt, transport and supply of, 584–586 salt-iodization programme, 580–582 National Maternity Benefit Scheme (NMBS), 870 National Mission Steering Group, 1199 National Neonatology Forum, 170 National Nutrition Monitoring Bureau (NNMB), 87, 886, 887, 958 National Nutrition Policy, 813 National Nutrition Programmes, 887

National Nutritional Anemia Prophylaxis Program (NNAPP) National Old Age Pension Scheme (NAOPS), 870 National Oral Rehydration Therapy Programme, 282 National Plan of Action on Nutrition, 813, 865 National Policy for Children, 1155 National Policy for Older Persons, 951 National Policy for Social Assistance, 870 National Policy on Management of Vitamin A Deficiency, 1162 National Programme of Nutritional Support to Primary Education (NP– NSPE), 872 National Prophylaxis Programme for Prevention of Blindness Due to Vitamin A deficiency (NPPVAD), 480, 778 National Reference Laboratories, 597 National Rural Health Mission (NRHM), 96, 865, 1068, 1195, 1196 goals, strategies and outcomes, 1197– 1199 institutional mechanisms, 1199, 1200 inter-sectoral convergence under, 1205f implementation framework and plan of action, 1203–1206 main approaches, 1206f monitoring strategy of, 1210 progress, 1212 National Sample Survey (NSS), 864 National Sample Survey Organisation (NSSO), 98, 882, 887, 1076 National Social Assistance Programme (NSAP), 869 National Vitamin A Plus Campaign, 779 National Workplace Health Promotion Programme, 973 Natural disasters, 901 Natural killer cells, 400 Natural or man-made disasters, 899 Natural or manmade disasters, nutritional emergencies, 899, 900 capacity building, 906–907 disaster preparedness, 905–906 early warning systems (EWSs), 907– 908 food aid, 901–903

Index food insecurity and malnutrition, 908– 913 food security, 925–927 humanitarian aid organization, 907 micronutrient requirements, 923–925 nutritional interventions, 913–921 nutritional requirements, 921–925 vulnerability of communities, 904 Nausea, 382 NCHS growth references, 137 Needs-based interventions, 210 Negative energy balance, 692, 940 Negative predictive value, 40 Neonatal Health Research Initiative (NHRI), 170 Neonatal health, 156 in India, 168 Neonatal hypothyroidism, 540 Neonatal intensive care unit (NICU), 160, 161 Neonatal mortality, 152, 154. See also Low birth weight (LBW) in India, 154 direct and underlying determinants, 155 distribution of causes, 155 rate (NMR), 153, 154 Neonatal period, 151 average daily mortality rate, 152 Neonate, 151, 175 gastric capacity, 160 Neoplastic diseases, 940 Nestum, 263 Neural tube birth defects, 801 Neural tube defects (NTD), 630, 727 Neural tube formation, 668 Neurochemicals, 341 Neurofibrillary tangles, 941 Neurogenesis, 668 Neurological damage, 508 functions, 941 problems, 389 Neuromuscular integrity, 946 Neuronal migration, 668 Neuropathy, 635 Neuropsychologic functioning, 753 Neuropsychological behavior, 668 Neurotransmitters, 612, 668 Neutropenia, 686 Neutrophils, 755

1235

Nevirapine, 376 Newborn illness, 164 nutritional status of, 159–160 NHE. See Nutrition–health education. Night blindness (XN), 415, 442, 445 during latter pregnancy, 424 during pregnancy, 476 Nitric oxide synthase (NOS), 611 Nodular goiters, 558 Non alcoholic fatty liver disease, 356 Non-alcoholic steatohepatitis, 356 Non-communicable chronic disorders (NCD), 956–957 Non-communicable diseases (NCDs), 956 prevention and control of, 971, 974 Non-fat dry milk powder, 383 Non-food factors, 882 Non-formal preschool education, 873 Non-fortified-khichdi, 1186 Non-heme, 609 absorption, inhibitors of, 617 iron, 609, 681 Non-heme iron, 682, 706 absorption, 616–617, 619 proteins, 611 Non-heme proteins, 681 Non-Insulin Dependent Diabetes Mellitus (NIDDM), 149 Non-modifiable factors, 963 Non-operation flood area, 884 Non-parametric tests, 1152 Non-personnel costs, 1018 Non-pregnant and non-lactating women (NPNL), 90, 91 Non-provitamin A carotenoids, 419 Non-randomized trials, 22 Non-responder, 326 Non-response, 1148 Non-repinephrine, 612, 688 Non-specific immunity, 744 Normal hemoglobin concentration, 675 NRHM. See National Rural Health Mission. Nuclear family, 938 Nucleic acid metabolism, 628 Null Hypothesis (HO), 1137–1139 Nutri-candies, 831 Nutri-delight, 837 Nutrient bioavailability, 777

1236

Public health nutrition in developing countries

Nutrient malabsorption, 378 Nutrients, intrafamily distribution of, 889 Nutriplus programme, 395 Nutriset’s Plumpy net, 322 Nutrition, 3, 1156. See also Malnutrition, Undernutrition. and ageing, 943–949 and food supplies, 1074 Nutrition–electrolytic balance, 327 Nutrition–health education (NHE), 873, 1085, 1087, 1156, 1161 design and implementation, 1094–1103 programs, evaluation of, 1103 successful program experiences, 1104– 1112 to behavior change communication (BCC), 1087–1094 Nutrition-health practices, 1086 Nutrition & Health Day (NHD), 1109, 1161, 1176 Nutrition and Health Examination Surveys (NHANES), 27 Nutrition and Iodine Deficiency Disorders, 577 Nutrition anthropology, 1085 Nutrition certificates, 212 Nutrition communication message, 1099 Nutrition Communication Project (NCP), 1104 Nutrition Counselling and Childcare Sessions (NCCS), 1107 Nutrition education/social marketing programs, 1043, 1087 Nutrition feeding, continuation of, 283 Nutrition Foundation of India, 102 Nutrition Guidelines; MSF, 1995, 914 Nutrition health counseling, 324 Nutrition interventions, 33 Nutrition life cycle framework, 997 Nutrition problem, 987 Nutrition program planning, 987 logical model, 991–993 program theory, 988–989 results framework, 994–997 Rossi, Lipsey and Freeman model, 989– 991 steps, 997–1018 Nutrition Rehabilitation Centre (NRC), 334 Nutrition rehabilitation units, 301

Nutrition security, 844, 884 Nutrition surveillance, 913 Nutrition surveys, 33 Nutrition transition, 960 Nutritional multimix supplements, 298 Nutritional Anemia Control Program (NNACP), 1162 Nutritional anemia, 674, 675, 677. See also Iron deficiency anemia. causes of, 680–687 low iron bioavailability, 681–685 low iron intake, 681 Nutritional assessment, 33 Nutritional counseling, 172 Nutritional Counselling and Care Sessions (NCCS), 1179 Nutritional deficiencies or excesses, 33, 311. See also Micronutrient deficiencies. clinical manifestations, 36 Nutritional education, 296 Nutritional emergencies, 900 Nutritional epidemiology, 25, 33 developing countries, challenges faced, 43–44 non systematic measurement error, 41 random error, 41 study design, 37 systematic error, 41 Nutritional indicators, 37 Nutritional intervention, 257 Nutritional iron deficiency, 623 developmental stages, 623, 625 Nutritional oedema, 912 Nutritional Programme for Adolescent Girls (NPAG), 870 Nutritional rehabilitation, 264, 302 Nutritional sciences, 25 Nutritional screening, 33 Nutritional status, 1159 Nutritional status, infants, 175 caregiver, role of, 178 inappropriate feeding practices, 176 optimal nourishment, 175 Nutritional surveillance, 33 Nutritious diet, 976 Obesity, 3, 341, 956, 958, 964 types of, 149 Obesity genome map, 351

Index Obesity in children assessment of, 348–350 body mass index (BMI), 348–349 consequences of, 355 dietary factors, 352–353 environmental factors, 351–352 epidemic of, 343–344 fat gain, 346 genetic and gene–environment interactions, 350–351 management and treatment, 360–361 physical inactivity, 353–354 prevention, 357–360 prevention and management of, 341– 361 risk factors, 350–355 skin-fold thickness, 350 waist circumference, 350 Obesogenic environment, 352, 976 Objectively Verifiable Indicators (OVIs), 1006, 1073 Obligatory iron loss, 615 Obstetric care umbilical cord, delayed clamping, 655– 656 Ocular signs, 422 Old age, 932 Old age care, 953 government initiatives, 953 voluntary sector initiatives, 953–954 Old age pension, 954 Older persons, dietary guidelines for, 949– 950 Oligospermia, 739 Omega-3 fatty acids, 380 Omega-3 polyunsaturated fatty acids, 945 Omega-6 polyunsaturated fatty acids, 945 Opportunistic infections (OI), 373, 384, 687 Optimal breastfeeding of children, 177 Optimal infant and young child feeding practices, 177 sociocultural constraints, 177 Optimal therapeutic feeding, 314 Optional indicator, 1044 ORS. See Oral rehydration salts. Oral cancers, 960 Oral candida, 311 Oral glucose, 346 Oral health, 941

1237

Oral iron supplementation, 723 Oral rehydration salts (ORS), 206, 280, 747, 761 osmolarity, 786 use rates in India, 788, 789 Oral rehydration therapy (ORT), 280, 786 Organogenesis, 416 Organosulfur, 971 Osmolarity ORS solution, 785, 787 Osteoarthritis, 940 Osteomalaecia, 940 Osteopenia, 940 Osteoporosis, 311, 942 Otitis media, 334 Overnutrition, 50, 146 dietary intake changes, 97–98 health consequences, 102–104 interventions to reduce, 104 physical activity, 98 responsible factors, 97–101 women during reproductive age, 86 Over-the-counter (OTC) formulation, 788 Overweight, 341, 958, 964 Oxidative energy production, 697 Oxidative phosphorylation, 610 Oxidative processes, 681 Oxidative stress, 375, 941, 963 Oxyhemoglobin methods, 695 Oxytocin, 180 secretion, 183 P value, 1137, 1139 Pack house, 875 Palliative care, 394 Para-health professionals, 975 Parasitic infestations, 685 Parathyroid hormone, 806 Parivar Seva Sansthan, 731 Parkinson disease, 939 Participatory Learning for Action (PLA), 1077 Participatory mapping, 1078, 1080 Participatory monitoring, 1022 Participatory Rapid Assessment, 290 Participatory Rural Appraisal (PRA), 1076 Passive diffusion, 741 Passive immunization, 185 Pathogens, 276 Pathological ageing, 942, 943 Patient Welfare Committees, 1070

1238

Public health nutrition in developing countries

Payasam, 268 PDI (Psychomotor Development Index), 753 Pedal oedema, 920 Peer counselors, 199 Peer reinforcement, 1107 Pensionable age, 933 People Living with HIV (PLHIV), 372, 377. See also HIV infection. dietary guidelines, 391–393 fat requirements, 385–386 fluids, 393–402 micronutrients, requirements of, 386– 390 nutritional requirements for, 383–390 protein requirements, 385 Peptide hormone, 688 Peptide YY (PYY), 343 Perinatal mortality, 168, 700 Periodic deworming, 654 Peripheral neuropathy, 959 Pernicious anemia, 629 Persistent diarrhea, 275, 760 Peruvita, 263 Photophobia, 311 Physical work capacity, 676 Physiological ageing, 939, 941 Phytate–zinc molar ratio, 758 Phytoestrogen, 971 Phytonutrients, 957, 960, 971 Pituitary gland, 180 Placenta, 160, 161 Plaque, 941, 966 Plasma ferritin, 696 Plasma insulin, 346 Plasma lipoprotein profile, 946 Plasma/serum zinc concentrations, 755 Plasmodium falsiparum, 705 PLHIV. See People Living with HIV. Plump nut/peanut butter’, 321, 919 Point of use fortification, 817 Polycystic ovarian syndrome, 965 Polymorphonuclear leucocytes, 755 Polyunsaturated fats, 393 Poor man’s meat, 851 Population ageing, 932 Population attributable fraction, 10 Population attributable risk/PAR/ population attributable fraction, 11 Population based surveys, 1059

Population excess risk, 10 Population proportional to size (PPS) sampling, 601 Population stabilization, 1196 Poshak, 262 Positive energy balance, 343, 940, 965 Positive predictive value, 40 Post natal check, 1202 Post partum, 700 Post-exposure prophylaxis, 375 Potassium iodate (KIO3), 525, 826 Poverty, 66, 864 and hunger impact, 797 Powdered millets, 245 Prader-Willi syndrome, 343 Predominant breastfeeding, 176 Pregnancy iron loss, 614, 615 effects of anemia, 700 iron requirements, 689, 690 zinc supplementation in, 753, 754 Pregnancy, nutritional anemia, 674 iron deficiency, 674 Pregnant and lactating women, nutritional status, 86, 90, 97 deterioration, associated factors, 93–95 dietary intake, 90, 95–97 fat fold thickness (FFT), 92 micronutrient deficiencies, 74 mother-child dyad, effect of conception, 94–95 nutrient intake, 91 pre-pregnancy weight, 92 work status, effect of, 93 Pregnant women anemia, dietary intervention, 20 Prelacteal feeding, 181 Premature deliveries, 686, 969 Premature infants iron reserves, 231 Pre-pregnancy weight gain, 69 Pressure ulcers, 946 Preterm and/or low birth weight newborn, 164, 165 Pre-term delivery (gestational age), 155 Pretest sites, 1100 Prevention and Control of Diabetes (1987), 972 Prevention of Food Adulteration (PFA) Act, 578

Index Prevention of Food Adulteration Act Central, 576 Primary education, universalization of, 872 Primary health care (PHC), 76, 198, 592, 782–783, 882, 1196. See also Public health nutrition programme. centres , 1071, 1157, 1198 facilities, 208 network, 598 Primary prevention, community-based programmes for, 976–977 Prophylactic doses, 456 Prostate cancers, 960 Protective proteins, 182 Proteins, 945 Protein balance, 940 Protein energy malnutrition nutritional treatment, 305–307 prevention and management of, 292– 307 Protein size, 265 Protein transcription, 738 Provitamin A, 406 Provitamin A carotenoids, 436, 437 bioefficacy of, 408 Pseudo folate deficiency, 633 Pteroyl glutamate, 626 Pteroylglutamic acid, 626 Ptyalin, 942 Public health, 2, 982 Public health nutrition, 44, 983 analysis of data, 1147–1151 designing a research study, 1135–1137 nutritional guidelines, 46 research designs, 1140–1141 research methods in, 1133–1135 sample size, determination of, 1143– 1147 sampling, 1141–1143 softwares, 1152–1153 Public health delivery system, 1203 Public health nutrition programme, 982, 1031. See also Primary health care. conducting evaluation, phases of, 1047–1048 designing monitoring system, 1034– 1044 evaluation of, 1044–1046 evaluation, designing of, 1049–1055 evaluation, quantitative and qualitative

1239

techniques, 1058–1064 evaluation, types of, 1048–1049 monitoring, 1031–1034 programme efficiency analysis, 1056– 1057 Public health program planning, 982 Public health science, 982 Puffy eyelids, 331 Pulmonary embolus, 965 Pupillary dark adaptation, 424 Pyrimidine, 628 Quality of care, 1069 Quality of life, 939, 940, 960 Radio iodine uptake (RAIU), 503, 509 Radioactive iodine, 503, 504 Rapid weight gain, 347 Rashtriya Krishi Vikas Yojana, 874, 875 Ration cards, 866 Ration size, 914 RBC folate, 630 RBC Protoporphyrin, 696 REACH (Regular Events to Advance Child Health), 779 Ready to eat (RTE), 242 infant foods or nutritious snacks, 244 infant premixes or instant infant foods, 245 foods, 916, 1159 therapeutic food (RUTF), 304, 305, 918 Recommended dietary allowances (RDA), 67 Recommended dietary intake (RDI), 890, 923 Red blood cell, 387 Registered medical practitioner (RMP), 305 Rehydration therapy, 280, 330 Renal clearance rate (RCR), 503, 515 Renal iodine clearance (RIC), 511 Reproductive and Child Health (RCH) programme, 169, 483 Respiratory chain proteins, 697 Respiratory infections, 775 Respiratory rate, 331 Resting Metabolic Rate (RMR), 101, 342 Reticuloendothelial system (RES), 618 Retinoid X receptors (RXR), 416 Retinol activity equivalent (RAE), 408

1240

Public health nutrition in developing countries

Retinol binding protein, 411 Retinol palmitate, 410, 806 Retroperitoneal fat, 149 Rheumatoid arthritis, 939 Rhodopsin, 414, 743 Ribonucleotide diphosphates, 612 Right to Food Act, 337 Rogi Kalyan Samiti, 1070, 1199, 1209 RTE. See Ready to eat. Safe delivery, 1174 Safe drinking water, 882 Sahyogini, 1181 Salt fortification efforts in India, 825, 828 micronutrient Initiative (MI), 827 Salt iodization, 531 Salt iodization units, 590 Salt quality, 589 Salt testing kits (STKs), 550 SAM. See Severe acute malnutrition. Sampoorna Gramin Rozgar Yojana, 868 Sangkap Pinoy Seal program, 836 Saturated fats, 960 Saturated fatty acids (SFA), 966 Saving Newborn Lives, 170 School child-to-community approach, 595 School health checkups, 1205 School Health hducation, 1205 Seasonal dehydrated GLV, 245 Secondary folate deficiency, 686 Sedentary life style, 98, 892 Selective feeding programmes (SFP), 914, 917 Sensory losses, 941 Sensory stimulation, 329 Septic shock, 329 Serum ferritin, 624, 674 Serum folate, 630 Serum methylmalonic acid, 635 Serum retinol (SR), 439, 818 binding protein (RBP), 425 Serum transferrin receptor (sTfR), 625 Serum triglycerides, 968 Serum vitamin B12, 635 Severe acute malnutrition (SAM), 52, 310, 311, 911 and mortality, 311–312 community-based management, 314 hospital-based management of, 313 management of, 313–335

Severe anemia, 676 Severe malnutrition, 385 Severe protein energy malnutrition, 675 Severely malnourished children, inpatient care of, 303 Sexually transmitted diseases, 1201 Sickle cell disease, 739 Skeletal calcium, 940 Skin abnormalities, 738 Skin-to-skin care, 169 Sleep apnea, 341 Small for gestational age (SGA), 57, 72, 752 Social isolation, 937, 941 Social security benefits, 954 Sodium hexametaphosphate (SHMP), 826 Sodium Iron Ethylene Diamine Tetra Acetate (NaFeEDTA), 805 Sodium thiosulfate, 551 Sodium-iodide symporter (NIS), 504 Spot testing kits, 550 Sprinkles, 247, 656, 658, 762 Standing Committee for Nutrition (SCN), 176, 247 Staple foods, 702, 802 Starvation, 850, 898 State AIDS Control Societies (SACS), 377 State Health Mission, 1199 Steatorrhea, 393 Still births, 540, 686 Storage iron, 697 Stress, 976 Stroke, 942, 957 Stunted children, 348 Subacute combined degeneration, 635 Subcutaneous fat, 149 Successful lactation, 179 Suckling reflex, 180, 187 Suckling stimulus, 183 Sugar fortification, 828, 829 Sugar sweetened soft drinks, 970 Supplementary food, fortification of, 1172 Supplemental iron, 691 Supplementary feeding, 1156, 1159 Supplementary feeding programmes (SFP), 335, 917 Supplementary nutrition, 873 Supplementation, 799, 923 Synaptic signaling, 738 Synaptogenesis, 668

Index Synthetic folic acid, 627 Systolic blood pressure (SBP), 958 T cells, 373 T lymphocytes, 744 T8 Killer Cells, 400 Tactile sensations, 180 Take-home rations (THR) or take home delivery systems (THDS), 258, 917, 1159 Targeted Public Distribution System (TPDS), 823, 866, 867 Therapeutic feeding, 314 Therapeutic feeding centre (TFC), 321, 335 Therapeutic feeding programmes (TFP), 917 admission and discharge criteria, 316, 18 Therapeutic milk F-75, 317 Therapeutic milk F-100, 317 Therapeutic supplementary nutrition, 1161 Therapeutic zinc supplementation, 785 Thermic effect of a meal (TEM), 342 Throid hormones (TH) in plasma, 506, 507 release, 506 storage and availability of, 505, 507 Thrombocytopenia, 686 Thyroglobulin (Tg), 502, 505, 517, 528 Thyroid binding, 506 binding globulin (TBG), 506 clearance rate (TCR), 503, 515 Function Test (TFT), 597 gland, 502 hormone (TH), 502, 538, 701 iodine clearance, 509 peroxidase (TPO), 507 size enlargemen, 514 stimulating hormone (TSH), 502, 507, 528, 538 Thyrotoxicosis, 805 Thyrotrophin, 507 Timely complementary feeding rate, 206 Timely contraceptive care, 86 Timely initiation of breastfeeding (TIBF), 211 Total Daily Energy Expenditure (TDEE ), 101 Total Daily Energy Intake (TDEI ), 101

1241

Total energy expenditure (TEE), 384 Total Fertility, 1197 Total Goitre Rate (TGR), 529 Total Sanitation Campaign (TSC), 288, 289 Transcobolamin, 632 Trans-fatty acids, 945 Transferrin, 609 -iron complexes, 621 receptor, 621, 674 saturation (TS), 625, 674, 696 Transfusion, 328 Transgenerational effects, 292 Transitional milk, 184, 186 Transitional societies, 43 life expectancy, 44 Transitory food insecurity, 900 Transmembrane transporter, 687 Transport facilities, 1211 Trials for Improved Practices (TIPS), 1085, 1099 Tricarboxylic acid cycle (TCA), 611 Triceps skin-fold thickness, 147 Triple blind, 21 Tsunamis, 898 Tuberculosis, 1197 Type-1 diabetes, 356 Udisha project, 1163, 1164, 1184 Ulceration, 435, 466 Ultra rice, 830 Ultrasonography, 553 Under five mortality rate (U5MR), 63, 153, 428, 487, 774, 779 Undernourished children, 68 Undernutrition, 50, 1154. See also Malnutrition, Nutrition–overnutrition linkages, 101 infection cycle, 64f Undernutrition in children, 75, 80. See also Malnutrition in children. faulty complementary feeding practices, 232–233 inappropriate feeding practices, 233 mother’s effect on, 71 prevention of, 79t risk factors, regression analysis, 66 Underweight, 51, 1154 UNICEF conceptual model for childhood malnutrition, 1094 UNICEF nutrition framework, 995

1242

Public health nutrition in developing countries

United Nations Demographic Estimations, 933 United Nations Development Programme (UNDP), 928 United Nations International Conference on Population and Development, 951 United Nations International Multiple Micronutrient Preparation (UNIMMAP), 75 United Nations International Year of the Older Persons, 951 United Nations Millennium Development Goals (MDGs), 169 United Nations Office on Ageing, 951 United Nations Principles for Older Persons, 951 United Nations Social Development Conference, Copenhagen, 951 Universal immunization, 1196 programme (UIP), 169 Universal primary education, 984 Universal salt iodization (USI), 502, 523, 545–549, 562, 563. See also National Iodine Deficiency Disorders Control Programme (NIDDCP). effective programme, 567–568 iodized salt, production of, 580–583 in India, innovative efforts, 592–596 Unsanitary conditions, 685 Upgrading Community Health Centres, 1197 Urban agglomeration, 960 Urban health extension, 304 Urban-affluent population energy balance studies, 100, 101 Urbanization, 938, 1087 Urinary Iodine (UI), 515, 528 concentration, 515, 516 excretion (UIE), 502, 515, 529 Utilization of food, 861, 862 Utilization of services, 1069 VADD. See Vitamin A deficiency disorders. VAD. See Vitamin A deficiency. VAS. See Vitamin A supplement. Valid value check, 1136 Value addition effect, 728 Vascular disease, 947 Vascular disorders, 959 Vegetables and fruits in diet, 969, 971

Very low birth weight, 155 Very low density lipoproteins (VLDL), 412 Village Banks, 202 Village contact drive (VCD), 1174 Village Health & Sanitation Committee (VHSC), 290, 1070, 1211 Village Health Committee (VHC), 1070 Village Health Nutrition Days, 1202 Village health plan, 1071 Village health planning, 1070, 1072 Village mapping, 1157 Village or Community Grain Bank Scheme, 870 Village ownership, 1075 Village planning, 1066, 1077, 1082 to district level plan, 1082, 1083f Village support groups, 202 Village transect walk, 1078 Village-health committee, 1198 Viremia, 374 Visceral subcutaneous fat ratio (VSR), 149 Visible goiter, 553 Vision loss, 941 Visual aid, 1102 Visual cycle, 415 Vita shakti, 817, 818, 1185 Vitamin A, 386, 405, 432 prevention and control programme in India, 473 subclinical deficiency in India, 474 Vitamin A capsules (VAC), 457, 482 Vitamin A deficiency (VAD), 405, 433, 773 blindness due to, 778 breastfeeding, promotion of, 448–449 child feeding practices, 437–438 consequences of, 432–435 dietary diversification, 449–451 epidemiology of, 435–441 food fortification, 451–452 food-based approaches, 777–778 high dose vitamin A supplement, 452– 466 in India, elimination of, 498 keratin-producing cells, 433 prevention and control of, 476–477 prevention, intervention strategies, 447–466 protein energy malnutrition, 439 public health problem, 441–443 public health significance, 443–446

Index status in India, 473–476 Vitamin A deficiency disorders (VADD), 434, 474 Vitamin A extenders, 784 Vitamin A fortification, 448, 806 Vitamin A metabolism, 405 â-carotene, 418 11-cis retinal, 414–415 11-cis-retinaldehyde, 414 and storage, 409–414 fat-soluble A, 405 nuclear retinoid receptors, 416 occurrence and sources, 406 recommended dietary allowances (RDA), 420–422 retinal pigment epithelium, 414 Vitamin A months, 457, 780 Vitamin A plus, 460 Vitamin A rich foods, 435 Vitamin A status, assessment of, 422, 428 Vitamin A deficiency, 422, 423 Vitamin A supplement (VAS), 445, 452, 453, 466, 777, 1162, 1179 breastfeeding mothers, post-partum, 784 delivery strategy, 456–460 economic analysis, 790–792 elimination of, 465–466 health-systems-based provision, 778 high potency, 453 monitoring programme, 462–464 program for preschool children in India, 778–779 programme in India, 477–487 progress in coverage, 464–465 promotion and training, 460–462 syrup, 484 trials, 785–790 Vitamin A syrup, 482 Vitamin A toxicity, 463 Vitamin A week, 457 Vitamin B12/ cobalamin, 389, 607, 630, 635, 962 absorption and transport, 631–632 biochemical function, 633–635 dietary deficiency, 632 dietary sources and recommended intake, 631 dietary, bioavailability of, 632 malabsorption, 633

1243

neurological manifestations, 635 status, assessment of, 635 structure of, 631f Vitamin B12 deficiency, 5, 638 Vitamin C, 947 fortification, 808 Vitamin D, 946, 947 deficiency, 9 fortification, 806, 808 Vitamin E, 389, 946, 947 fortification, 808 Vitamin-A-deficient children, 387 Vitamin–mineral premixes, 262 Waist circumference, 968 Waist–hip ratio (WHR), 149, 895, 959, 967 Warmi project, 168 Wasting, 378, 910 Wasting syndrome, 378 Water, 948 fluoridation, 33 testing, 1183 Watery diarrhea, 331 WAZ (weight for age), 670 Weaknesses, 1063 Weaning, 226 food formulations, 263t foods, 226 period, 226 Weekly Distribution Day, 834 Weekly iron folate supplementation (WIFS), 704 Weighing and Counseling Day, 1181 Weighing, 1159 scales, 110 Weight for age (WFA), 912 Weight-for-height (WFH) index, 119, 131, 910 Weight-for-age, 1154 index, 116 Weight-for-length, 116 Wet-on-the-spot feeding, 917 Whip worms, 685 WHO child growth references, 137, 138 WHO Classification of Undernutrition, 135 WHO growth charts, 138 WHO Model List of Essential Medicines, 786 WHO Multicentre Growth Reference Study (MGRS), 55, 892

1244

Public health nutrition in developing countries

Widowerhood, 937 Widowhood, 937 Wolff-Chaikoff effect, 506 Women of childbearing age, 678 World Breastfeeding Trend’s Initiative India report, 240 World Conference on Human Rights, Vienna Assembly, 951 World Fit for Children, 545 World Food, 852 World Food Program (WFP), 812 World Food Security, 882 World Health Organization (WHO), 37, 38 World Health Report 2002, 970 World Summit for Children, New York, 1990, 799 Xanthine oxidase, 682 Xerophthalmia, 422, 434, 435 Xerosis, 415, 433 Xerostomia, 941 Year of the Older Persons, India, 951 Yoga, 976, 1196

Zeaxanthin, 413, 419 Zidovudine, 376 Zinc, 390, 737, 946 biological functions of, 737–738 epidemiology, 738–739 functional indices of, 756–757 and immune response, 744 in the elderly, effect on immune response, 754 interaction with other trace elements, 743–744 physiology of, 740–744

Zinc absorption, 741 Zinc balance, 741, 744 Zinc contamination, 755 Zinc deficiency, 773, 946 clinical manifestations of, 739 diagnosis of, 755–756 growth faltering, 757 Zinc depletion, 756 Zinc dispersible tablets, 788 Zinc fingers, 738 Zinc fortification, 762 Zinc homeostasis, 741–742 Zinc metalloenzymes, 756 Zinc reduced diarrheal morbidity, 299 Zinc requirements, 742 Zinc sulfate, 747 Zinc supplementation, 281, 282, 745, 764, 776 and morbidity, therapeutic effects of, 745–748 and physical growth, 745 economic analysis, 790–792 preventive effects of, 748–753 preventive, 762 programs, 758–763 research trials, 785–786 Zinc tablets, 747 Zinc Task Force, 786 Zinc to iron ratio, 743 Zinc toxicity, 754, 755 Zinc transporters, 741, 742 Zinc-folate interaction, 744 ZIP proteins (zinc importer proteins), 741 Zn availability, 946 Zn–Fe interaction, 743 ZnT(zinc transporter proteins), 741 Z-score/standard deviation unit (SD), 134, 135, 911