FIBER INGREDIENTS Food Applications and Health Benefits
FIBER INGREDIENTS Food Applications and Health Benefits SUSAN SUNGSOO
EDITED BY C H O AND P R I S C I L L A
Boca Raton London New York
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SAMUEL
CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2009 by Taylor and Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Printed in the United States of America on acid-free paper 10 9 8 7 6 5 4 3 2 1 International Standard Book Number: 978-1-4200-4384-6 (Hardback) This book contains information obtained from authentic and highly regarded sources. Reasonable efforts have been made to publish reliable data and information, but the author and publisher cannot assume responsibility for the validity of all materials or the consequences of their use. The authors and publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright. com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging‑in‑Publication Data Fiber ingredients : food applications and health benefits / editors, Susan Sungsoo Cho and Priscilla Samuel. p. ; cm. “A CRC title.” Includes bibliographical references and index. ISBN 978-1-4200-4384-6 (alk. paper) 1. Fiber in human nutrition. 2. Food--Fiber content. I. Cho, Sungsoo. II. Samuel, Priscilla. III. Title. [DNLM: 1. Dietary Fiber--therapeutic use. 2. Food, Fortified. 3. Nutritive Value. 4. Polysaccharides--therapeutic use. WB 427 F443 2009] QP144.F52F53 2009 613.2’63--dc22 Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com
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Contents Preface......................................................................................................... vii About the Editors.........................................................................................ix Contributors..................................................................................................xi 1
Functional and Dietary Fibers: An Introduction........................... 1 Susan Cho
Section I Soluble Fibers 2
Alpha-cyclodextrin.............................................................................. 9 Jonathan David Buckley, Alison Mary Coates, and Peter Ranald Charles Howe
3
Nutriose ® Soluble Fiber............................................................... 19 Catherine Lefranc-Millot, Daniel Wils, Jean-Michel Roturier, Catherine Le Bihan, and Marie-Hélène Saniez-Degrave
4
Inulin................................................................................................... 41 Anne Franck and Douwina Bosscher
5
Fibersol® -2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient................................................................................. 61 Chieko Hashizume and Kazuhiro Okuma
6
Partially Hydrolyzed Guar Gum Dietary Fiber............................ 79 Mahendra P. Kapoor and Lekh R. Juneja
7
Acacia Gum...................................................................................... 121 Sebastien Baray
8
Pectin................................................................................................. 135 Hans Ulrich Endress and Frank Mattes
9
Polydextrose..................................................................................... 173 Julian D. Stowell
v
vi
Contents
Section II Resistant Starch 10
Resistant Starch (RS)...................................................................... 205 E. Terry Finocchiaro, Anne Birkett, and Monika Okoniewska
Section III Conventional Fibers 11
Oat Fiber from Oat Hull................................................................. 249 Jon Bodner and Susan Sungsoo Cho
12
Cellulose........................................................................................... 263 Toru Takahashi
13
Oat β-Glucan.................................................................................... 283 Niina Tapola and Essi Sarkkinen
14
Rice Bran: Production, Composition, Functionality and Food Applications, Physiological Benefits........................... 305 Talwinder S. Kahlon
15
Barley Fiber...................................................................................... 323 Christine E. Fastnaught
16
Sugar Beet Fiber: Production, Characteristics, Food Applications, and Physiological Benefits..................................... 359 Marie-Christine Ralet, Fabienne Guillon, Catherine Renard, and Jean-Francois Thibault
17
Psyllium............................................................................................ 393 Seyed Ali Ziai
Section IV New Development 18
Fruit Fibers....................................................................................... 427 Jürgen Fischer
19
Aleurone Flour: A Novel Wheat Ingredient Rich in Fermentable Fiber, Micronutrients, and Bioavailable Folate.... 439 Michael Fenech, Peter Clifton, Manny Noakes and David Topping
Appendix: Suppliers of Dietary Fiber Ingredients............................. 455 Index........................................................................................................... 467
Preface The Adequate Intake (AI) of total dietary fiber for children, adolescents, and adults was set to 14 g dietary fiber/1000 kcal by the Institute of Medicine, National Academy of Sciences, USA, to reduce the risk of chronic diseases. In many developed countries, fiber is recognized as a shortfall nutrient that is low in daily diet. A majority of Western people do not meet recommended intakes, indicating a need for consuming more fiber-rich foods. Health professionals should recommend foods high in fiber to improve public health. It is imperative that food product developers formulate foods with fiber to improve fiber intake status of the population. In this book, various fiber ingredients available at the marketplace have been reviewed. Each chapter includes characteristics, functionality, and health benefits of each ingredient. The book describes details of claim opportunities for fiber ingredients and fiber-containing foods, such as gastrointestinal health, cardiovascular health, weight management, satiety, glycemic control, and prebiotic effects. This book can be a useful reference for product developers, nutritionists, dieticians, and regulatory agencies.
vii
About the Editors Susan Cho, Ph.D., M.B.A., is the President of NutraSource, a nutrition and food safety consulting firm (www.consult-nutrasource.com; ssch0397@ yahoo.com). She was Director of Nutrition at Kellogg until 2005. She received her Ph.D. (with a major in food science and a minor in biochemistry) and her M.S. in nutrition from the University of Wisconsin–Madison, Madison. She has her M.B.A. from the University of Chicago. Dr. Cho is a well-known expert in dietary fiber research. She has written 4 books and published more than 50 articles in the areas of carbohydrates, fiber, and functional foods. Priscilla Samuel, Ph.D., is Director of Nutrition Sciences, Scientific & Regulatory Affairs with Solae, LLC. She worked previously at Mead Johnson Nutritionals, Quaker Oats, Tropicana, and the Kellogg Company. Under her leadership at Quaker, health claims were obtained for oats soluble fiber internationally, and for Oatrim™ in the U.S. Dr. Samuel holds a Ph.D. in human nutrition with minors in public health and marketing from the University of Tennessee–Knoxville, her M.S. in human nutrition from the University of North Carolina–Greensboro, and her B.S. in nutrition and child development from Bangalore University, India.
ix
Contributors Anne Birkett National Starch Food Innovation Bridgewater, New Jersey, U.S.A.
Christine E. Fastnaught PhoenixAgri Research Fargo, North Dakota, U.S.A.
Jon Bodner JRS USA Schoolcraft, Michigan, U.S.A.
Michael Fenech CSIRO Human Nutrition, Food Science Australia Adelaide, Australia
Douwina Bosscher Orafti Active Food Ingredients Tienen, Belgium
E. Terry Finocchiaro National Starch Food Innovation Bridgewater, New Jersey, U.S.A.
Sebastien Baray Colloïdes Naturels, Inc. Bridgewater, New Jersey, U.S.A.
Jürgen Fischer Herbafood Ingredients Havel, Germany
Jonathan David Buckley School of Health Sciences University of South Australia Adelaide, Australia
Anne Franck Orafti Active Food Ingredients Tienen, Belgium
Susan Cho Nutrasource Clarksville, Maryland, U.S.A.
Fabienne Guillon UR1268 Biopolymères Interactions Assemblages INRA Nantes Cedex 03, France
Peter Clifton CSIRO Human Nutrition, Food Science Australia Adelaide, Australia
Chieko Hashizume Matsutani Chemical Industry Co., Ltd. Itami City, Hyogo, Japan
Hans Ulrich Endress Pektin-Fabrik Neuenbuerg Herbstreith & Fox KG Neuenbuerg, Germany
Peter Howe School of Health Sciences University of South Australia Adelaide, Australia
xi
xii
Contributors
Lekh R. Juneja Interface Solution Division Taiyo Kagaku Co. Ltd. Yokkaichi, Mie, Japan
Kazuhiro Okuma Matsutani Chemical Industry Co., Ltd. Itami City, Hyogo, Japan
Talwinder S. Kahlon Western Regional Research Center USDA, ARS Albany, California, U.S.A.
Marie-Christine Ralet UR1268 Biopolymères Interactions Assemblages INRA Nantes Cedex 03, France
Mahendra P. Kapoor Interface Solution Division Taiyo Kagaku Co. Ltd. Yokkaichi, Mie, Japan
Catherine Renard UR1268 Biopolymères Interactions Assemblages INRA Nantes Cedex 03, France
Catherine Lefranc-Millot Nutrition Management Roquette Freres Lestrem, France Frank Mattes Pektin-Fabrik Neuenbuerg Herbstreith & Fox KG Neuenbuerg, Germany Manny Noakes CSIRO Human Nutrition, Food Science Australia Adelaide, Australia Monika Okoniewska National Starch Food Innovation Bridgewater, New Jersey, U.S.A.
Jean-Michel Roturier Nutrition Management Roquette Freres Lestrem, France Priscilla Samuel Nutrition Department The Solae Company St. Louis, Missouri, U.S.A. Marie-Hélène Saniez-Degrave Nutrition Management Roquette Freres Lestrem, France Essi Sarkkinen Foodfiles Kuopio, Finland
xiii
Contributors Julian D. Stowell Danisco Sweeteners Redhill, Surrey, U.K. Toru Takahashi Mimasaka University Tsuyama City, Japan Niina Tapola Foodfiles Kuopio, Finland Jean-Francois Thibault UR1268 Biopolymères Interactions Assemblages INRA Nantes Cedex 03, France
David Topping CSIRO Human Nutrition, Food Science Australia Adelaide, Australia
Daniel Wils Nutrition Management Roquette Freres Lestrem, France
Seyed Ali Ziai Department of Pharmacology Faculty of Medicine Shaheed Beheshti University of Medical Sciences Tehran, Iran
1 Functional and Dietary Fibers: An Introduction Susan Cho Contents Dietary Fiber Intake Levels around the World....................................................1 What Is Dietary Fiber?.............................................................................................2 Approved Health Claims........................................................................................3 Potential Health Claim............................................................................................4 Potential Structure Function Claims.....................................................................4 High-Fiber Foods/High-Fiber, Low-Fat Foods and Satiety and/or Weight Control....................................................................................4 High-Fiber Foods/High-Fiber, Low-Fat Foods and Glycemic Control...5 Dietary Fiber and Intestinal Regularity......................................................5 References.................................................................................................................5
Dietary Fiber Intake Levels around the World Based on studies done in rural Africa, Burkitt and Trowell proposed that the consumption of diets deficient in fiber is associated with an increased incidence of chronic diseases such as diverticulitis, diabetes, heart disease, and certain types of cancer. In the past 35 years, evidence of the beneficial effects of dietary fiber (DF) in chronic diseases has been accumulated (Bingham et al. 2003; Kokke et al. 2005; Lopez-Miranda et al. 2007; Marlett et al. 2002; Zhang et al. 2006). Reports of various government agencies noted that there has been great interest in the specific effects of dietary fiber on several chronic diseases. Recommendations for adult dietary fiber intake generally are in the range of 20 to 35 grams per day. Children over age 2 should consume an amount equal to or greater than their age plus 5 grams per day (Williams et al. 1995). Despite dietary guidelines (DG), dietary fiber intakes of the general public are well below the recommended levels. In the United States, the average American adult consumes only 14 to 15 grams of dietary fiber a
1
2
Fiber Ingredients: Food Applications and Health Benefits
day (Cho et al. unpublished data). Approximately 75% of Americans do not have adequate dietary fiber intake. Dietary fiber intake levels in the AsiaPacific region and in most industrialized nations in Europe are also far below the recommended levels (Galvin et al. 2001; Lairon et al. 2003; Murakami et al. 2007).
What Is Dietary Fiber? In the early 1970s, Burkitt and Trowell defined DF as plant cell wall polysaccharides and lignin that are not hydrolyzed by human alimentary enzymes (Burkitt et al. 1974; Burkitt and Trowell 1975). Recently, the Institute of Medicine (IOM; 2002) defined total fiber as the sum of functional and dietary fiber, that is, the sum of non-starch polysaccharides (NSP) and non-digestible oligosaccharides. The IOM definition is in line with the definition proposed by Lee and Prosky (1995) based on the survey results of AOAC International. Two international surveys were conducted by the AOAC International in order to fulfill two objectives: (1) to determine if a consensus could be reached on the definition of DF and associated methodologies; and (2) to consider appropriate classification of oligosaccharides that are not hydrolyzed by human alimentary enzymes (Lee and Prosky 1995). The first survey was initiated in December 1992, and 144 professionals participated. A large majority of participants (70%) supported the idea that the DF definition should reflect both chemical and physiological perspectives. The survey results indicated that 65% of people supported the current DF definition as polysaccharides and lignin that are not hydrolyzed by human alimentary enzymes. However, 59% supported a future expansion of the DF definition to include oligosaccharides that are not hydrolyzed by human alimentary enzymes. In December 1993, a follow-up survey was sent out, specifically addressing the issue of a new definition that may include oligosaccharides that are not hydrolyzed by human alimentary enzymes, along with the results from the first survey for confirmation (Lee and Prosky 1995). The second time, 65% of the participants supported the inclusion of these oligosaccharides, while 80% supported the inclusion of resistant starches and lignin in the DF definition beyond NSP. It is noteworthy that only 6% believed that DF includes only NSP or plant cell wall components. Based on these survey results, Cho (formerly Lee) and Prosky have proposed the expansion of the definition of DF to include resistant oligosaccharides, in addition to the currently included NSP, resistant starch, and lignin (Lee and Prosky 1995). This proposal was adopted at the AOAC Workshop on Complex Carbohydrates held in Nashville, Tennessee, in October 1995 (Cho and Prosky 1999).
3
Functional and Dietary Fibers: Introduction
Approved Health Claims The Nutrition Labeling and Education Act (NLEA) of 1990 provides rules regarding health claims used on labels that characterize a relationship between a food, a food component, dietary ingredient, or dietary supplement and risk of a disease. So far, the U.S. Food and Drug Administration (FDA) has approved several health claims related to dietary fiber and risk reduction of chronic diseases, such as coronary heart disease (CHD) and cancer (FDA 1993; FDA 1998). Table 1.1 summarizes approved health claims and model health claims. It should be noted that these health claims have been approved for foods and may or may not be applicable to dietary supplements.
Table 1.1 FDA-Approved Health Claims for Fiber Risk Reduction
Type of Fiber
Model Health Claim
Cancer
Fiber-containing grain products, fruits, and vegetables (101.76)
Low-fat diets rich in fiber-containing grain products, fruits, and vegetables may reduce the risk of some types of cancer, a disease associated with many factors.
CHD
Diets rich in fruits, vegetables, and grain products that contain fiber, particularly soluble fiber (101.77)
Diets low in saturated fat and cholesterol and rich in fruits, vegetables, and grain products that contain some types of dietary fiber, particularly soluble fiber, may reduce the risk of heart disease, a disease associated with many factors.
CHD
Soluble fiber from certain foods (oats and/or psyllium) (101.81)
Soluble fiber from psyllium and foods such as [Product Name], as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease. A serving of [Product Name] supplies __ grams of the ___ grams soluble fiber from psyllium seed husk necessary per day to have this effect. Diets low in saturated fat and cholesterol that include 3 g of soluble fiber from whole oats per day may reduce the risk of heart disease. One serving of this whole-oats product provides ___ grams of this soluble fiber.
4
Fiber Ingredients: Food Applications and Health Benefits
Potential Health Claim In addition to already approved health claims, it may be possible to make a claim for fiber’s role in risk reduction of diabetes. Type 2 diabetes is characterized by sustained high blood sugar levels. It tends to develop when the body can no longer produce enough of the hormone insulin to lower blood sugar to normal levels or cannot properly use the insulin. There are several important risk factors for type 2 diabetes, such as being overweight, being physically inactive, smoking, and some dietary factors. Among dietary factors, a high-fiber diet and foods with a low glycemic index do not quickly raise blood sugar levels and are associated with a lower risk of type 2 diabetes. The 2004 report of the USDA DG Expert Panel (USDA 2004) stated that the “intake of fiber has been inversely associated with type 2 diabetes in a number of epidemiological studies.” In response to the question, What are the major health benefits of fiber-containing foods?, the DG report concluded that “Diets rich in dietary fiber have a number of important health benefits including helping to promote healthy laxation, reducing the risk of type 2 diabetes, and decreasing the risk of coronary heart disease (CHD).” Also the 2002 Institute of Medicine (IOM) report stated that “There is evidence on risk of reduction of diabetes as a secondary endpoint to support a recommended intake level for total fiber that is primarily based on prevention of CHD.” Overall, strong scientific evidence is available to support a relationship between fiber intake and prevention of diabetes.
Potential Structure Function Claims High-Fiber Foods/High-Fiber, Low-Fat Foods and Satiety and/or Weight Control Both observational and clinical studies suggest that intake of certain fiber may be useful in controlling body weight (Lindstrom et al. 2006; Murakami et al. 2007). The 2000 and 2005 Dietary Guidelines for Americans (USDA) stated that high-fiber content of foods, in particular whole grains, help “you feel full with less calories.” In a report defining the term fiber, the NAS stated that high-fiber diets delay stomach emptying, which increases the time energy and nutrients are absorbed from the digestive tract. Additionally, several important review articles provide direct support for high fiber intake and satiety/weight control. However, the 2002 IOM report states that “Although the finding that the overall data on dietary fiber intake are negatively correlated with BMI are suggestive
Functional and Dietary Fibers: Introduction
5
of a role for fiber in weight control, the studies designed to determine how fiber intake might impact overall energy intake have not shown a major effect.” High-Fiber Foods/High-Fiber, Low-Fat Foods and Glycemic Control Both epidemiological and intervention studies suggest that intake of certain fiber may delay glucose uptake and attenuate insulin responses (Lindstrom et al. 2006; Murakami et al. 2007). Various functional and dietary fibers, such as resistant starch, resistant maltodextrins, oat beta-glucans, pectins, hydroxymethylpropyl cellulose (HMPC), psyllium, and guar gum, have been found to be efficacious in significantly reducing glycemic responses (Brouns et al. 2007, Institute of Medicine 2002). Dietary Fiber and Intestinal Regularity This dietary fiber can help relieve constipation by influencing stool consistency, increasing stool bulk, making the stool softer, and decreasing fecal transit time through the bowel (Marlett et al. 2002; IOM 2002). The gastrointestinal tract is highly sensitive to dietary fiber, and consumption of fiber seems to relieve and prevent constipation. The fiber in wheat bran and oat bran seems to be more effective than similar amounts of fiber from fruits and vegetables. The 2002 report of the IOM concluded that functional and dietary fiber increase fecal weights and increase the number of fecal movements per day, and improve the ease with which a stool is passed.
References Bingham SA, Day NE, Luben R, Ferrari P, Slimani N, Norat T, Clavel-Chapelon F, Kesse E, Nieters A, Boeing H, Tjonneland A, Overvad K, Martinez C, Dorronsoro M, Gonzalez CA, Key TJ, Trichopoulou A, Naska A, Vineis P, Tumino R, Krogh V, Bueno-de-Mesquita HB, Peeters PH, Berglund G, Hallmans G, Lund E, Skeie G, Kaaks R, Riboli E (2003) Dietary fiber in food and protection against colorectal cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC): an observational study. Lancet 361:1496–501. Erratum in: Lancet 362:1000. Brouns F, Arrigoni E, Langkilde AM, Verkooijen I, Fässler C, Andersson H, Kettlitz B, van Nieuwenhoven M, Philipsson H, Amado R. (2007) Physiological and metabolic properties of a digestion-resistant maltodextrin, classified as type 3 retrograded resistant starch. J Agrid Food Chem. 55:1574–81. Burkitt DP, Trowell HC (1975) Refined Carbohydrate Foods and Disease: Implications of Dietary Fiber. London, England: Academic Press. Burkitt DP, Walker AR, Painter NS (1974) Dietary fiber and disease. JAMA
229(8):1068–74.
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Fiber Ingredients: Food Applications and Health Benefits
Cho SS, Prosky L (1999) Complex carbohydrates: Definition and analysis. In: Cho SS, Prosky L, Dreher M, eds. Complex Carbohydrates. New York, NY: Marcel Dekker, 131–144. Food and Drug Administration (FDA) (1993) Food labeling: general provisions; nutrition labeling; label format; nutrient claims; ingredient labeling; state and local requirements; and exemptions: final rules. Fed. Register 58:2302–906. Food and Drug Administration (FDA) (1998) Food labeling: health claims; soluble fiber from certain foods and coronary heart disease. Fed Register 63(32):8103. Galvin MA, Kiely M, Harrington KE, Robson PJ, Moore R, Flynn A (2001) The North/ South Ireland Food Consumption Survey: the dietary fibre intake of Irish adults. Public Health Nutr 4(5A):1061–8. Institute of Medicine (2002) Dietary Reference Intakes for Energy, Carbohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC: National Academy Press. Kokke FT, Taminiau JA, Benninga MA (2005) The role of dietary fiber in childhood and its applications in pediatric gastroenterology. Nestle Nutr Workshop Ser Pediatr Program 56:111–20; discussion 120–6. Lairon D, Bertrais S, Vincent S, Arnault N, Galan P, Boutron MC, Hercberg S (2003) Dietary fibre intake and clinical indices in the French Supplementation en Vitamines et Mineraux Antioxydants (SU.VI.MAX) adult cohort. Proc Nutr Soc 62(1):11–55. Lee SC, Prosky L (1992) Dietary fiber analysis for nutrition labeling. Cereal Foods World 37:765–71. Lee SC, Prosky L (1995) International survey on dietary fiber: definition, analysis, and reference materials. J AOAC Int 78:22–36. Lindstrom J, Peltonen M, Eriksson JG, Louheranta A, Fogelholm M, Uusitupa M, Tuomilehto J (2006) High-fibre, low-fat diet predicts long-term weight loss and decreased type 2 diabetes risk: the Finnish Diabetes Prevention Study. Diabetologia 49(5):912–20. Lopez-Miranda J, Williams C, Lairon D (2007) Dietary, physiological, genetic and pathological influences on postprandial lipid metabolism. Br J Nutr 98(3):458–73. Marlett JA, McBurney MI, Slavin JL (2002) Position of the American Dietetic Association: health implications of dietary fiber. J Am Diet Assoc 102:993–1000. Murakami K, Sasaki S, Okubo H, Takahashi Y, Hosoi Y, Itabashi M (2007) Dietary fiber intake, dietary glycemic index and load, and body mass index: a cross-sectional study of 3931 Japanese women aged 18–20 years. Eur J Clin Nutr 61(8):986–95. U.S. Department of Agriculture (2004) Expert Panel Report on Dietary Guidelines. Washington, DC: U.S. Government Printing Office. Williams CL, Bollella M, Wynder EL (1995) A new recommendation for dietary fiber in childhood. Pediatrics 96:985–8. Zhang C, Liu S, Solomon CG, Hu FB (2006) Dietary fiber intake, dietary glycemic load, and the risk for gestational diabetes mellitus. Diabetes Care 29(10):2223–30.
Section I
Soluble Fibers
2 Alpha-Cyclodextrin Jonathan David Buckley, Alison Mary Coates, Peter Ranald, and Charles Howe
Contents Characteristics..........................................................................................................9 Functionality and Food Applications................................................................. 11 Physiological Benefits............................................................................................ 11 Safety/Toxicity........................................................................................................ 13 Conclusions............................................................................................................. 14 References............................................................................................................... 15
Characteristics Alpha-cyclodextrin (α-CD) contains six glucopyranosyl units linked by α-1,4glycosidic bonds and is one of a family of three cyclodextrin molecules (α-, β-, and γ-cyclodextrin) (see Figure 2.1). In nature, the cyclodextrins are produced as a storage form of carbohydrate by some microorganisms, but they can also be produced industrially by the enzymatic degradation of amylose by cyclodextrin-glucosyltransferases (CGTs), a group of amylolytic enzymes belonging to the class of α-amylases. CGTs cleave the helical amylose molecule at regular intervals of 6, 7, or 8 glucose units forming at the same time a ring by an intramolecular glucosyltransferase reaction, resulting in the formation of α-, β-, and γ-cyclodextrin, respectively [1]. More than 80 years ago it was discovered that α-CD is resistant to digestion by the pancreatic juice of dogs [2]. This resistance to hydrolysis by pancreatic amylase was confirmed in subsequent studies, which also identified a resistance to hydrolysis by salivary amylase [3–5]. This resistance to hydrolysis may be partly due to α-CD itself being an inhibitor of pancreatic amylase activity [6]. While the resistance of α-CD to hydrolysis by pancreatic and salivary amylase means that it remains almost undigested in the small intestine, it is completely fermented in the large intestine [7, 8]. 9
10
Fiber Ingredients: Food Applications and Health Benefits OH
OH
O
O O
HO
O O O H H
HO O HO
O OH OH H H O O O
O OH
O
O H
O
HO
O OH
O HO
H O O O
HO
HO
H H O O O
H O
O
O
O HO O HO
OH O OH
OH
OH
HO O
O H
OH
HO HO O
O HO
OH O
OH
O
HO
α-CD
OH O
OH
β-CD OH HO
O
O
O O O H H
O OH OH
O HO O HO
HO O OH
HO
O HO O HO
OH
O
OH
OH O OH O
H H O O O OH H O O
O
OH O
OH
HO
γ-CD Figure 2.1 Chemical structure of the cyclodextrins. (From Biwer et al., Appl. Microbiol. Biotech. 59:609–17, 2002. With kind permission of Springer Science and Business Media.)
As a result of α-CD’s chemical structure (i.e., α-glucan), combined with its non-digestibility and fermentability, it resembles retrograded or crystalline non-granular starch, or so-called “resistant starch” of the RS3 type according to Englyst’s classification [9]. However, unlike resistant starch, it is freely soluble in water (145 g ⋅ l-1) yielding clear low-viscosity solutions [5]; is resistant to heat (i.e., pasteurization); and is stable at pH levels generally encountered in food manufacture. While α-CD resembles resistant starch, its water solubility, resistance to digestion in the small intestine, and fermentability in the
Alpha-cyclodextrin
11
large intestine mean that it is by definition a form of soluble, fermentable, dietary fiber.
Functionality and Food Applications Due to the steric arrangement of the glucopyranosyl units of α-CD, the inner side of the torus-like molecule is less polar than the outside, which allows for the formation of inclusion complexes with non-polar organic compounds of appropriate size by incorporating them into the cavity of the ring structure [5]. The formation of these inclusion complexes can improve the aqueous solubility, chemical and physical stability, and therefore the bioavailability of the sequestered molecule [10]. The ability of α-CD to form inclusion complexes has attracted the interest of the food industry for some time [11, 12], and α-CD has previously been used in foods to protect volatile compounds from evaporation, and chemically sensitive products from oxidation or photodegradation [13, 14]. It has also been proposed that, because α-CD is tasteless and odorless, water-soluble, and stable under most temperatures and pH conditions generally encountered in food processing, it may be particularly suitable for addition to liquid and semisolid foods and to beverages for the purpose of fiber supplementation [15, 16]. α-CD is currently used in food manufacturing as a carrier for flavors, colors, and sweeteners in foods such as dry mixes, baked goods, and instant teas and coffee, and as a stabilizer for flavors, colors, vitamins, and polyunsaturated fatty acids in dry mixes and dietary supplements (< 1% of the final product), as a flavor modifier in soya milk (< 1%), and as an absorbent (breath freshener) in confectionery (10% to 15% of the final product) [17].
Physiological Benefits Studies in rats have demonstrated that α-CD reduces plasma triglyceride and cholesterol concentrations [18, 19], effects similar to those seen with other dietary fibers and which may provide protection against the development of cardiovascular disease [20, 21] and colorectal cancer [22]. Like other indigestible dietary fibers, α-CD can also be fermented by the microbiota of the large intestine to yield short-chain fatty acids [23], some of which might provide additional protection against colorectal cancer [24]. While α-CD can provide many of the benefits of other dietary fibers in terms of improved blood lipids and increased fecal bulk, its ability to inhibit pancreatic amylase activity [6], and thereby potentially inhibit the hydrolysis of complex carbohydrates in the small intestine, has led to interest in the pos-
12
Fiber Ingredients: Food Applications and Health Benefits
Area under Plasma Glucose Curve (m mol.l–1.min1)
160 140 120 100
* †
80 60 40 20 0
0
2 5 10 Dose of α-cyclodextrin (g)
Figure 2.2 Dose-dependent reduction in plasma glucose following incorporation of α-cyclodextrin into a standard carbohydrate meal. (From Buckley et al., Ann. Nutr. Metab. 50:108–14, 2006. With kind permission of S Karger AG Basel.)
sibility that α-CD can reduce carbohydrate digestion and thereby attenuate the postprandial glycemic response to carbohydrate-containing foods [25]. Postprandial elevations in blood glucose are associated with an increased risk of developing metabolic disease (e.g., diabetes), cardiovascular disease, and some cancers [26–30], and foods that elicit lower postprandial blood glucose excursions, such as low glycemic index foods (i.e., foods that elicit a low postprandial glycemic response per unit of available carbohydrate), reduce the risk of developing these diseases [31–35]. It was recently shown that the addition of α-CD in doses ranging from 0 g to 10 g to a standard meal of boiled white rice containing 50 g of available carbohydrate resulted in a dose-dependent inhibition of the postprandial blood glucose response, as evidenced by a progressive reduction in the area under the postprandial plasma glucose curve [25] (see Figure 2.2). Thus, it appears that the addition of α-CD to carbohydrate-containing foods may effectively reduce their glycemic index, enabling the food industry to produce lower glycemic index versions of existing foods so that people can consume a lower glycemic index diet without having to alter their food choices. While the consumption of a low glycemic diet can reduce the risk of developing cardiovascular disease, diabetes, and certain cancers [31–35], there is also evidence that consuming a low glycemic index diet can reduce body fat [36–39], which is of particular importance given the current global obesity epidemic [40]. More than 20 years ago Suzuki and Sato [41] reported small weight-loss effects of substituting α-CD for carbohydrate in the diet, but the substance used by Suzuki and Sato was actually a mixture of n-dextrin, α-CD, β-cyclodextrin, and γ-cyclodextrin (50:30:15:5) so it was not possible to determine what effects the individual components had contributed to the weight-loss effect. However, recently, Artiss et al. [42] showed that feeding
Alpha-cyclodextrin
13
rats for six weeks ad libitum a high-fat diet containing α-CD (10% w/w of the fat in the diet) reduced weight gain (7.4% lower body weight) and body fat mass (22% lower body fat) compared with rats fed a high-fat diet without α-CD. In fact the weight gain in the rats fed the high-fat diet with α-CD was not different from that of rats fed a low-fat diet. The lower body weight and body fat in the rats that consumed the high-fat diet with α-CD compared with rats fed just the high-fat diet occurred despite there being no difference in energy intake or quantity of food consumed between these two groups. The addition of α-CD to the diet also reduced plasma triglyceride concentrations by 30%, cholesterol by 9%, normalized serum leptin concentrations, and improved insulin sensitivity compared with rats on the high-fat diet without α-CD. While the mechanism of the body fat reduction could not be completely determined, the addition of α-CD to the high-fat diet was associated with a ~20% increase in the fat content of the feces (without steatorrhea), although this increased fecal excretion of fat accounted for only some, not all, of the reduction in body fat accumulation. Based on the amount of weight gain and the amount of fat consumed, the authors were able to calculate that 1 g of α-CD prevented the absorption of the equivalent of some 9 g of dietary fat in this animal model.
Safety/Toxicity The safety of α-CD as a food ingredient was recently assessed by the World Health Organization [43] then subsequently by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) [17] and was given an acceptable daily intake of “not specified.” α-CD was also recently awarded Generally Recognized As Safe (GRAS) status by the Food and Drug Administration in the United States [44] and has been approved for use as a novel food by Food Standards Australia and New Zealand [45]. The approval of α-CD for use as a food in the USA and Australia has been underpinned by safety data from numerous studies that have shown that the only adverse effects associated with the consumption of α-CD are minor gastrointestinal complaints associated with the consumption of any non-digestible, fermentable dietary fiber (e.g., bloating, nausea, flatulence, diarrhea). A number of studies have been conducted to test the maternal and embryonic/fetal safety of α-CD consumption during pregnancy and have found no evidence of any harmful effects. Waalkens-Berendsen et al. [46] showed, using artificially inseminated New Zealand white rabbits, that feeding α-CD at doses of 5%, 10%, and 20% (w/w) of diet during the first 29 days of gestation was well tolerated with no adverse effects on maternal reproductive performance, and no embryotoxic, fetotoxic, or teratogenic effects were found. Similar studies have been carried out in both rats and mice [15, 16, 47–49],
14
Fiber Ingredients: Food Applications and Health Benefits
as well as dogs [49], with no evidence of any maternal toxicity, fetotoxicity, embryotoxicity, teratogenicity, or other adverse effects. Mutagenicity (i.e., carcinogenicity) of α-CD has also been assessed using Ames tests with α-CD concentrations of up to 20 mg and gave negative results [50]. The Ames test is based on the assumption that any substance that is mutagenic (for the bacteria used in the test) may also be carcinogenic. While some substances that cause cancer in laboratory animals do not necessarily give a positive Ames test, the potential for α-CD to damage DNA (and therefore its carcinogenic potential) was also tested using in vivo micronucleus tests on mouse bone marrow and these tests showed no evidence of any chromosomal damage or damage to the mitotic apparatus [51]. It may therefore be concluded that α-CD does not appear to cause DNA damage and is not carcinogenic. The only adverse effect of consuming α-CD, which has been shown consistently, is the occurrence of minor gastrointestinal complaints (bloating, nausea, diarrhea). Lina et al. [16] administered α-CD to rats at dietary rates of 1%, 5%, and 15% for four weeks and persistent diarrhea was the most prominent treatment-related effect in the 15% group, especially in the male animals. In association with this diarrhea, food consumption and food conversion efficiency were decreased. The weight of the full and empty cecum was increased in the 5% and 15% α-CD groups. A similar finding occurred in Beagle dogs that consumed diets consisting of 0, 5%, 10%, or 20% α-CD for 13 weeks [49], with diarrhea occurring in all groups that consumed α-CD. The incidence and severity of the diarrhea increased with increasing doses of α-CD and were more pronounced in males than females. Significant cecal enlargement also occurred in the males in the 10% and 20% α-CD groups. While these studies establish that diarrhea and cecal enlargement occur with the consumption of α-CD, these effects are not specific to α-CD and are known to occur following ingestion of other poorly digestible carbohydrates [52–55]. It is generally accepted that these effects represent a well-recognized physiological response to the presence of high amounts of non-digestible, fermentable carbohydrate in the lower gut and have no relevance to human safety [56, 57].
Conclusions α-CD is a type of soluble, fermentable dietary fiber that is tasteless, odorless, resistant to heat, stable at pH levels generally encountered in food manufacture, and able to form inclusion complexes with appropriately sized non-polar organic compounds. These properties have allowed it to be used in foods to protect chemically sensitive products from degradation, as an absorbent, and as a carrier for a range of flavors, colors, sweeteners, and fatty acids. While the consumption of α-CD is associated with many of the same physi-
Alpha-cyclodextrin
15
ological benefits that can be achieved from the consumption of other dietary fibers (e.g., blood cholesterol and triglyceride lowering, increased fecal bulk), it is also able to inhibit salivary and pancreatic amylase, and thereby reduce carbohydrate digestion and the postprandial glycemic response to the consumption of carbohydrate-containing foods. Reducing the glycemic response to carbohydrate foods can potentially reduce the risk of developing cardiovascular disease and certain cancers, and α-CD has the potential therefore to allow for the production of healthier carbohydrate-based foods. There is also some evidence that consuming α-CD can reduce body fat accumulation and might therefore also be useful as a treatment for preventing or reducing obesity. As may occur with the consumption of any non-digestible, fermentable dietary fiber, the consumption of α-CD is associated with minor adverse gastrointestinal complaints such as bloating, nausea, and diarrhea, with the incidence being dose related and particularly evident in males. However, α-CD does not exhibit any toxic or teratogenic effects and has been awarded GRAS status by the Food and Drug Administration in the United States, and has been approved for use as a novel food by Food Standards Australia and New Zealand.
References
1. Schmid, G., Cyclodextrin glycosyltransferase production: yield enhancement by overexpression of cloned genes, TIBTECH, 7, 244, 1989. 2. Karrer, P., Polysaccharide. XX. Zur Kenntnis polymerer Kohlenhydrate, Helv. Chim. Acta., 6, 402, 1923. 3. French, D., The Schardinger dextrins, Adv. Carbohydr. Chem., 12, 189, 1957. 4. Kondo, H., Nakatani, H., and Hiromi, K., In vitro action of human and porcine α-amylases on cyclo-maltooligosaccharides, Carbohydr. Res., 204, 207, 1990. 5. Szejtli, J., Chemistry, physical and biological properties of cyclodextrins, in Comprehensive Supramolecular Chemistry, Atwoods, J., Ed., Pergamon, Oxford, 1996, 5. 6. Koukiekolo, R., et al., Mechanism of porcine pancreatic α-amylase. Inhibition of amylose and maltopentaose hydrolysis by α-, β- and γ-cyclodextrins, Eur. J. Biochem., 268, 841, 2001. 7. Andersen, G., et al., The utilization of Schardinger dextrins by the rat, Toxicol. Appl. Pharmacol., 5, 257, 1963. 8. van Ommen, B., de Bie, A., and Bär, A., Disposition of 14C-α-cyclodextrin in germ-free and conventional rats, Regulat. Toxicol Pharmacol., 39, S57, 2004. 9. Englyst, H., Kingman, S., and Cummings, J., Classification and measurement of nutritionally important starch fractions. Eur. J. Clin. Nutr., 46, S33, 1992. 10. Saenger, W., Cyclodextrin inclusion compounds in research and industry, Angew. Chem. Int. Ed. Engl., 19, 344, 1980. 11. Pszczola, D., Production and potential food applications of cyclodextrins, Food Technol., 42, 96, 1988.
16
Fiber Ingredients: Food Applications and Health Benefits
12. Szejtli, J., Cyclodextrins in foods, cosmetics and toiletries, in Proceedings of the First International Symposium on Cyclodextrins, Szejtli, J., Ed., Akademiai Kiado, Budapest, 1982, 469. 13. Allegre, M., and Deratani, A., Cyclodextrin uses: from concept to industrial reality, Agro. Food Ind. Hi. Tech., 5, 9, 1994. 14. Nagatomo, S., Cyclodextrins—expanding the development of their functions and applications, Chem. Econ. Eng. Rev., 17, 28, 1985. 15. Waalkens-Berendsen, D.H., and Bar, A., Embryotoxicity and teratogenicity study with [alpha]-cyclodextrin in rats, Regulat. Toxicol. Pharmacol., 39, 34, 2004. 16. Lina, B.A.R., and Bar, A., Subchronic oral toxicity studies with [alpha]-cyclodextrin in rats, Regulat. Toxicol. Pharmacol., 39, 14, 2004. 17. World Health Organization, Safety evaluation of certain food additives and contaminants: alpha-cyclodextrin, in WHO Food Additives Series: 48; Geneva, 2004. 18. Kaewprasert, S., Okada, M., and Aoyama, Y., Nutritional effects of cyclodextrins on liver and serum lipids and cecal organic acids in rats, J. Nutr. Sci. Vitaminol., 47, 335, 2001. 19. Shizuka, F., Hara, K., and Hashimoto, H., Dietary fiber-like effects of orally administered cyclodextrins in the rat, in Proceedings of the Eighth International Symposium on Cyclodextrins, Szejtli, J., and Szente, L., Eds., Kluwer Academic Publishers, Dordrecht, 1996, 157. 20. Hokanson, J.E., and Austin, M.A., Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies, J. Cardiovasc. Risk, 3, 213, 1996. 21. Di Mascio, R., Marchioli, R., and Tognoni, G., Cholesterol reduction and stroke occurrence: an overview of randomized clinical trials, Cerebrovasc. Dis., 10, 85, 2000. 22. McPherson-Kay, R., Fiber, stool bulk, and bile acid output: Implications for colon cancer risk, Prevent. Med., 16, 540, 1987. 23. Antenucci, R., and Palmer, J., Enzymatic degradation of α- and β-cyclodextrins by bacteroides of the human colon, J. Agric. Food Chem., 32, 1316, 1984. 24. Nkondjock, A., et al., Specific fatty acids and human colorectal cancer: an overview, Cancer Detect. Prevent., 27, 55, 2003. 25. Buckley, J., et al., Dose-dependent inhibition of the post-prandial glycaemic response to a standard carbohydrate meal following incorporation of alphacyclodextrin, Ann. Nutr. Metab., 50, 108, 2006. 26. Augustin, L., et al., Glycemic index, glycemic load and risk of prostate cancer, Int. J. Cancer, 112, 446, 2004. 27. Dickinson, S., and Brand-Miller, J., Glycemic index, postprandial glycemia and cardiovascular disease, Curr. Opin. Lipidol., 16, 69, 2005. 28. Gerich, J., Clinical significance, pathogenesis, and management of postprandial hyperglycemia, Arch. Intern. Med., 163, 1306, 2003. 29. Hodge, A., et al., Glycemic index and dietary fiber and the risk of type 2 diabetes, Diab. Care, 27, 2701, 2004. 30. Silvera, S., et al., Dietary carbohydrates and breast cancer risk: A prospective study of the roles of overall glycemic index and glycemic load, Int. J. Cancer, 17, DOI: 10.1002/ijc.20796, 2004. 31. Brand-Miller, J., Glycemic load and chronic disease, Nutr. Rev., 61, S49, 2003.
Alpha-cyclodextrin
17
32. Frost, G., et al., Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet, Metab. Clin. Exp., 47, 1245, 1998. 33. Opperman, A., et al., Meta-analysis of the health effects of using the glycaemic index in meal-planning, Br. J. Nutr, 92, 367, 2004. 34. Rizkalla, S., Bellisle, F., and Slama, G., Health benefits of low glycaemic index foods, such as pulses, in diabetic patients and healthy individuals, Br. J. Nutr, 88, S255, 2002. 35. Roberts, S., and Pittas, A., The role of glycemic index in type 2 diabetes, Nutr. Clin. Care, 6, 73, 2003. 36. Brand-Miller, J.C., et al., Glycemic index and obesity, Am. J. Clin. Nutr., 76, 281S, 2002. 37. Ludwig, D., Dietary glycemic index and the regulation of body weight, Lipids, 38, 117, 2003. 38. Pawlak, D., Kushner, J., and Ludwig, D., Effects of dietary glycaemic index on adiposity, glucose homeostasis, and plasma lipids in animals, Lancet, 364, 778, 2004. 39. Ebbeling, C., et al., Effects of an ad libitum low-glycemic load diet on cardiovascular disease risk factors in obese young adults, Am. J. Clin. Nutr., 81, 976, 2005. 40. World Health Organization (WHO) International Obesity Task Force (IOTF), Obesity: Preventing and Managing the Global Epidemic, World Health Organization, Geneva, 1998, 276. 41. Suzuki, M., and Sato, A., Nutritional significance of cyclodextrins: indigestibility and hypolipemic effect of a-cyclodextrin, J. Nutr. Sci. Vitaminol., 31, 209, 1985. 42. Artiss, J.D., et al., The effects of a new soluble dietary fiber on weight gain and selected blood parameters in rats, Metabolism, 55, 195, 2006. 43. World Health Organization, Safety evaluation of certain food additives and contaminants (α-cyclodextrin), WHO Food Additives Series, 49, 111, 2002. 44. US Food and Drug Administration, Agency Response Letter GRAS Notice No. GRN 000155 Nutrition, Center for Food Safety and Applied Nutrition, 2004, http://www.cfsan.fda.gov/~rdb/opa-g155.html. 45. Food Standards Australia and New Zealand, Final assessment report, Application A494, Alpha-cyclodextrin as a novel food, 2004. 46. Waalkens-Berendsen, D., Smits-van Prooije, A., and Bar, A., Embryotoxicity and teratogenicity study with α-cyclodextrin in rabbits, Regulat. Toxicol. Pharmacol., 39, S40, 2004. 47. National Technical Information Service, Final report on the developmental toxicity of alpha-cyclodextrin (CAS No. 10016-20-3) in Sprague–Dawley (CD) rats, United States Department of Commerce Technology Administration, Springfield, 1994. 48. National Technical Information Service, Final report on the developmental toxicity of alpha-cyclodextrin (CAS No. 10016-20-3) in Swiss (CD-1) mice, United States Department of Commerce Technology Administration, Springfield, 1994. 49. Lina, B.A.R., and Bar, A., Subchronic (13-week) oral toxicity study of [alpha]cyclodextrin in dogs, Regulat. Toxicol. Pharmacol., 39, 27, 2004. 50. Blijleven, W., Examination of alpha-cyclodextrin for mutagenic activity in the Ames test, TNO-CIVO Institute, Zeist, the Netherlands, 1991. 51. Immel, H., Examination of α-cyclodextrin in the micronucleus test TNO Nutrition and Food Research Institute, Zeist, the Netherlands, 1991.
18
Fiber Ingredients: Food Applications and Health Benefits
52. Til, H., et al., Subchronic toxicity study of lactitol in dogs, J. Am. Coll. Toxicol., 11, 219, 1992. 53. El-Harith, E., Dickerson, J., and Walker, R., Potato starch and caecal hypertrophy in the rat, Food Cosmet. Toxicol., 14, 115, 1976. 54. Sunvold, G., et al., Dietary fiber for dogs. IV. In-vitro fermentation of selected fiber sources by dog fecal inoculum and in-vivo digestion and metabolism of fiber-supplemented diets, J. Anim. Sci., 73, 1099, 1995. 55. World Health Organization, Polydextroses modified, in WHO Food Additive Series No. 16, 144, 1981. 56. Newberne, P., Conner, M., and Estes, P., The influence of food additives and related materials on lower bowel structure and function, Toxicol. Pathol., 16, 184, 1988. 57. World Health Organization, Principles for the safety assessment of food additives and contaminants in food, Environ. Health Criteria, 70, 39, 1987.
3 Nutriose® Soluble Fiber Catherine Lefranc-Millot, Daniel Wils, Jean-Michel Roturier, Catherine Le Bihan, and Marie-Hélène Saniez-Degrave
Contents Introduction............................................................................................................ 19 Production and Description................................................................................. 21 Dietary Fiber Content............................................................................................22 Digestive Tolerance................................................................................................ 25 The Composition of the Fiber...................................................................... 27 The Type of Food Matrix in Which They Are Included......................... 28 The Intestinal Bacterial Adaptation........................................................... 28 Digestion and Absorption in the Small Intestine: Associated Physiological Effects..................................................................................... 28 Glycemic Response................................................................................................ 29 Gut Well-Being....................................................................................................... 31 Caloric Value...........................................................................................................34 Technical and Physicochemical Properties Allowing Various Food Applications................................................................................................... 35 Powder’s Properties...................................................................................... 35 Resistance to Various Industrial Processing............................................. 35 Taste and Mouthfeel.............................................................................................. 36 Safety, Regulation, and Labeling......................................................................... 37 Conclusion............................................................................................................... 37 References............................................................................................................... 38
Introduction The history of dietary fiber consumption is closely associated with the history of human evolution. The human diet has changed from a plant-based non-purified regimen to a few cereal-based purified diets. The first consequence of this change is the decline of dietary fiber consumption. The association of health effects with dietary fiber was described as early as the 4th 19
20
Fiber Ingredients: Food Applications and Health Benefits
century BCE by Hippocrates, when talking about the laxative effect of the coarseness of cereal grains [1]. The long-standing definition of dietary fiber referred to “plant substances undigested by human enzymes” including lignin, cellulose, and hemicelluloses. In the 1970s [2], the definition of dietary fiber was broadened to include soluble substances (non-cell wall derived materials) such as pectin, gums, and mucilage. In other words, dietary fiber consists of both insoluble components of plant origin, and of soluble components, both of them resistant to the action of endogenous human enzymes of the small intestine. Soluble dietary fibers first studied for their physiological effects, as explained previously. Viscous dietary fibers have been distinguished from the non-viscous ones. Yet, the first studied were those extracted from plants, such as oat bran, barley, soy beans, gum arabic, and guar gum. The use of conventional soluble fibers in processed foods has been limited due to their gel-forming properties, leading to excessive viscosity, even though the data suggest a physiological effect on satiety and on lowering cholesterol absorption [3]. On the contrary, non-viscous soluble fibers like oligosaccharides and resistant dextrins can be introduced quite easily in a large number of foods, at rates sufficient enough to promote health through specific effects. These effects are mainly related to promoting colonic fermentation inducing • A decrease of the colon pH, limiting the growth of potentially harmful bacteria • A production of short-chain fatty acids: acetic, propionic, and butyric acids • An increased absorption of minerals (Ca++ and Mg++) • An increase of energy expenditure • Positive impacts on glucose and lipid metabolisms • A probable impact, when included in foodstuffs, toward satiation and satiety [4] As soluble dietary fibers are fermented in the colon, particular attention should be focused on the possible digestive effects that can be encountered following ingestion. These effects are flatulence, rumbling, and sometimes abdominal pain and diarrhea. It is therefore very important to know the highest dose that can be consumed without inducing complaints. In fact, if health effects are targeted, the level of ingestion must be in accordance with the tolerance threshold of the fiber. NUTRIOSE® can be considered a non-viscous soluble dietary fiber. It was designed to be incorporated in a large number of foodstuffs either in solid or liquid form. It has been clearly demonstrated that this resistant dextrin is stable through various food-processing conditions including sterilization or high temperatures, and very low pH.
Nutriose® Soluble Fiber
21
The particular profile of NUTRIOSE® confers to this dietary fiber an outstanding digestive tolerance that is in agreement with its health-promoting effects. Particularly, as a carbohydrate with low content in mono- and disaccharides, this fiber is very apt to meet the WHO’s recommendations concerning diet, nutrition, and the prevention of chronic diseases [5]. All the previously described properties will be developed hereafter.
Production and Description Dextrins have the same basic chemical formula as starch but are a group of low-molecular-weight carbohydrates, composed of shorter chains. They are mixtures of D-glucose polymers, soluble in cold water. Resistant dextrins are partially hydrolyzed starches converted by heating in the presence of small amounts of food-grade acid. Raw material can be potato, wheat, and corn but also pea, sorghum, and cassava root [6]. Production of food-grade dextrins generally consists of a dextrinization step followed by a purification process rising active carbon and exchange resins. During dextrinification or pyroconversion, a dry roasting of starch is applied in highly controlled conditions [7]: Starch is dried to about 5% moisture and a food-grade acid is added; pyroconversion occurs with the heating at high temperature and during cooking. The dextrin is then quickly cooled. Starch molecules are in fact randomly hydrolyzed by acid and high temperature to produce short-chain oligosaccharides that randomly rearrange during cooling. Therefore, in addition to the digestible glycosidic linkages of starch α 1-4 and α 1-6, non-digestible glycosidic bonds, such as β 1-4, β 1-6, α and β 1-3, 1-2 are produced. Resistant dextrins are therefore more ramified than starch. Hydrolysis and recombination are well described [8, 9]. Table 3.1 shows the type and amount of glycosidic linkages found in starch, in standard maltodextrins, and in dextrins. Chromatography can be utilized to further increase the fiber content and tailor the molecular weight distribution. Different kinds of resistant dextrins, making up a range (branded NUTRIOSE® FB when from wheat or NUTRIOSE® FM when from maize), are produced after the chromatographic step used to control the polydispersity of the molecular weight distribution. The cut-off is determined according to the rheological behavior and the high digestive tolerance threshold to be achieved. Figures 3.1a and 3.1b show the respective structural formulas of starch and of NUTRIOSE® 06, a fiber-rich product of the resistant dextrins range. Figures 3.2a and 3.2b represent the molecular weight distribution of NUTRIOSE® 06 and of a standard dextrin. Polydispersity is 1.8 in the chromatographied dextrin versus 4.1 in the native dextrin. The molecular weight is decreased about twofold by the chromatographic step.
22
Fiber Ingredients: Food Applications and Health Benefits
Table 3.1 Results of Interlaboratory Study for the AOAC 2001.03 Method
Mean g/100 g D.S.a Sr RSDr % rb SR RSDR % Rc
NUTRIOSE® FB06
70% Fiber Dextrin
70% Fiber Dextrin
60% Fiber Dextrin
NUTRIOSE® FM06
95 % Fiber Dextrin
84.7
72.3
72.8
59.9
84.4
97.3
0.61 0.71 1.70 2.80 3.29 7.85
1.42 1.96 3.96 2.76 3.82 7.73
0.46 0.67 1.30 1.46 2.00 4.08
0.89 1.48 2.48 1.52 4.26 2.54
1.06 1.25 2.96 2.57 3.05 7.21
1.43 1.47 4.01 2.80 2.88 7.83
Note: D.S.: dry substance. Average of values obtained from the interlaboratory study. b 2.8 x Sr. c 2.8 x SR. a
At the end of the process, demineralization resins and activated carbon are used to purify the product before spray drying. The final products are fine powders entirely soluble in cold water.
Dietary Fiber Content As proposed in the 1980s, dietary fibers are the remnant of the edible part of plants resistant to human digestion in the small intestine. This resistance to digestion is the basic principle used for analytical methods. Several methods have been developed for dietary fiber determination, but the first consensual official method was the enzymatic-gravimetric AOAC 985.29 [10]. The result obtained depends on the fiber fraction after enzymatic degradation by amylase, amyloglucosidase, and protease, and being insoluble in a mixture of four parts alcohol and one part water. The precipitated residue is collected after filtration, then dried, and weighed. In the early 2000s, the definition of dietary fiber was reviewed and enlarged by the American Association of Cereal Chemists (AACC) and received support from the scientific community. Oligosaccharides, which are resistant short-chain polysaccharides with a degree of polymerization conventionally between 3 and 10, are included in the definition. Such oligosaccharides do not precipitate in alcohol solution because of their low molecular weight and thus cannot be quantified with the historical AOAC 985.29 and 991.43 methods.
23
Nutriose® Soluble Fiber CH2OH O
CH2OH
O
OH
O
OH
O
OH
O O
OH
O OH CH2
OH CH2OH
O
OH
O
OH CH2OH
CH2OH
O
OH
O
OH CH2OH O
CH2OH
O
OH
OH
O
OH
O
O
OH
OH
O
OH
O
OH CH2OH
O
CH2OH
O
O OH
OH CH2OH
O
OH
O
CH2
O
OH
O
OH
CH2OH
O O
OH
OH
OH
CH2OH
O
OH
O
O
OH OH
OH
1a: Starch (a) Starch CH2OH O
OH
CH2OH
O
OH
O
OH
O O OH CH2 OH
O
O
O O OH CH2
HO
®
OH
OH
O
OH CH2OH
CH2OH OH
CH2OH O
O
O O OH
OH
OH
O
OH CH2OH OH
O
O
CH2OH
O
O
OH
O
CH2OH OH
CH2OH OH
OH
O
O OH CH2
O O
O
O
OH
HO
OH
CH2 O
O OH CH2OH O OH
O O OH
O OH
1b: NURIOSE 06 (b) Nutriose® 06 Figure 3.1 Respective structural formulas of starch (a) and NUTRIOSE® 06 (b) one type of resistant dextrin of the NUTRIOSE® range.
In 2001, an enzymatic-gravimetric-HPLC method was proposed to the AOAC for the determination of total dietary fiber (TDF) in foods containing resistant maltodextrin (reference AOAC 2001–03) [11]. This method, which also determines low-molecular-weight resistant oligosaccharides using HPLC, is an improvement of the conventional AOAC 985.29 method, which does not take into account these molecules. Briefly, the principle is: The digestible part of the sample is first converted to glucose using enzymatic hydrolysis. The high-molecular-mass soluble dietary fiber is then precipitated in ethanol and weighed. After filtration, a liquid chromatography determination is conducted on the filtrate to obtain
24
Fiber Ingredients: Food Applications and Health Benefits MW = 9610
®
TACKIDEX DF 165 Mn = 2440
105
104
103
Masses Molaires (Daltons) (a)
MW = 5000
®
NUTRIOSE 06
Mn = 2650
105
104
103
Masses Molaires (Daltons) (b) Figure 3.2 Molecular weights distribution of a raw dextrin (a) and of a food dextrin (b).
the quantity of low-molecular-weight resistant oligosaccharides that have not precipitated in the alcohol preparation. Both values are summed for obtaining the total dietary fiber content. An interlaboratory study has been set up for evaluating the performance and the appropriateness of the AOAC 2001–03 methods on different kinds of foodstuffs having variable fiber content from 60% to 95% (see Table 3.1).
Nutriose® Soluble Fiber
25
Six products analyzed in duplicate were tested. Seven laboratories from the United States (two laboratories), Italy, the Netherlands, Japan, Germany, and France have participated. The repeatability standard deviations (RSDr) are 0.7% to 2.0% and the reproducibility standard deviations (RSDR) 2.9% to 4.2%. These results are in accordance with literature data [10] where RSDr and RSDR are respectively 1.3% to 6.1% and 1.8% to 9.4% (see Table 3.1 and Figure 3.3). According to these reference methods, the total fiber content of NUTRIOSE® 06 is 85% per dry substance including 50% of fibers insoluble in ethanol [11] and 35% resistant oligosaccharides.
Digestive Tolerance The beneficial effect of fiber can be of interest only if its digestive tolerance threshold is fully compatible with the recommended daily intake inducing the claimed beneficial effect. This is especially so in the case of the resistant dextrin described in this chapter, which exhibits an outstanding tolerance. The digestive tolerance can be defined as the individual’s ability to tolerate digestive troubles induced after ingestion of a foodstuff. The digestive tolerance threshold is the highest ingested dose inducing no major gastrointestinal trouble in specific clinical studies in comparison with a placebo. It has to be clearly distinguished from the mean laxative threshold, which is the dose inducing diarrhea in half of the subjects and which is sometimes used to characterize tolerance of other fibers. Soluble fibers are mainly fermented in the colon, therefore offering prebiotic benefits. The fermentation results in the production of gas (mainly CO2, CH4, and H2) naturally excreted in both breath air and flatulence. With consumption of high doses of fermentable carbohydrates, the quantity of produced gas can exceed the capacity of breath excretion; therefore tolerance threshold knowledge is needed in order to confirm that the required physiological impact on the body (like the prebiotic effect for example) is obtained at a dose that doesn’t induce digestive discomfort. The digestive tolerance of our indigestible dextrin was very precisely studied, following acute as well as chronic administration protocols, after or without a progressive adaptation period [12, 13]. In one study publishing the outcomes of a short-term digestive tolerance trial in 20 healthy volunteers [12], successive periods of one-week administration of increasing amounts of 10, 15, 30, 45, 60, and 80 grams indigestible dextrin or placebo per day were tested. The placebo was a standard maltodextrin of equivalent molecular weight. None of the doses of the food dextrin, even 80 g/d, resulted in diarrhea. Only increased (“more serious”) flatulence was observed with the highest dosages of 60 and 80 g/d. Increased frequency of bloating was recorded the last day with 80 g/d. In this study, tolerance,
110 105 100 95 90 85 80 75 70 65 60 55 50 45 40 35 30 25 20 15 10 5 0
Product n°2
Black bars: Low molecular weight fiber
Product n°1
Product n°3
Product n°5
Gray bars: High molecular weight fiber (alcohol precipitated)
Product n°4
Product n°6
Figure 3.3 Histogram of the results: inter-laboratory study for the 2001-03 AOAC fiber determination. Products: n°1, NUTRIOSE® FB 06; n°2 and 3, 70% fiber dextrin; n°4, 60 % fiber dextrin; n°5, NUTRIOSE FM 06; n°6, 95 % fiber dextrin. Black bars: HPLC determination. Gray bars: alcohol precipitated.
Fiber Content % DS
26 Fiber Ingredients: Food Applications and Health Benefits
Nutriose® Soluble Fiber
27
defined as abdominal discomfort threshold, was consequently determined as being 45 g/d for healthy adults. To explore the long-term digestive tolerance, the soluble dietary fiber was tested on 48 volunteers [13]. After a one-week run-in period, about 16 volunteers per group received for four weeks either 30 g/d or 45 g/d of the resistant dextrin or the placebo, a standard maltodextrin. No serious adverse event occurred. No diarrhea was reported, and both food dextrin dosages were well-tolerated. It has been also demonstrated that ingestion of 100 g of the soluble fiber did not cause severe digestive disorders [14], due to a progressive adaptation and distribution in six equal doses per day. Only excessive flatus was recorded after intakes above 50 g/d. It is possible to conclude from these previously reported studies that the mean laxative threshold dose of NUTRIOSE® 06 is above 100 g/d. According to these experimental data, the digestive tolerance threshold has been set, as a “no symptom” dose, at 45 g/d. Different factors can explain this outstanding digestive tolerance for this resistant dextrin. The Composition of the Fiber Low-digestible carbohydrates differ concerning their degrees of absorption, fermentation, and osmotic effect, influencing their metabolism and/or their tolerance [15]: • Absorption and Fermentation Rates: The larger the part fermented, the greater the risk of discomfort. Resistant dextrins like this one, which are partially digested (15%) in the small intestine, are very well tolerated. • Molecular Weight and Fermentation Rate: Smaller molecules give higher osmotic pressure in the colon and slower fermenting compounds are more easily tolerated than faster ones. The higher degree of polymerization of this resistant glucose polymer compared to that of other non-digestible carbohydrates, and hence lower osmotic pressure and slower fermentation, may thus explain its high tolerance threshold even at high dosages. • Way of Fermentation: This food dextrin is fermented throughout the colon, allowing the short-chain fatty acids (SCFA) produced to be progressively absorbed and thus inducing few osmotic effects. On the contrary, dietary fibers like fructans can be quickly fermented in the proximal colon. They consequently induce a rapid decrease in pH, due to lactic acid and SCFA production, leading to possible osmotic effects and laxativity.
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Fiber Ingredients: Food Applications and Health Benefits
The Type of Food Matrix in Which They Are Included Liquid food products, such as beverages and ice cream, are more likely to induce a discomfort than a solid product (bread, biscuit, cookies), partly because of the rate of gastric emptying (faster with liquid food and slower with solid food). However, in the short-term tolerance study [12], the tolerance threshold of this resistant dextrin was assessed on the basis of unfavorable conditions (i.e., incorporated in grape juice or fruit yogurt). As previously mentioned, the tolerance was very good, at doses up to 45 g/d. The Intestinal Bacterial Adaptation The colonic flora can evolve depending on the type of indigestible carbohydrate present in the environment. An improvement of the tolerance can be observed in cases of daily consumption of the same dosage, with decreasing symptoms over the course of time. In the short-term tolerance study, subjects ingesting daily 60 grams of resistant dextrin for six days experience flatulence as more severe than those of the maltodextrin group. Surprisingly, this was no longer the case during the last 24 hours, suggesting an adaptation to the food dextrin [12]. In this study, flatulence occurred more frequently in the 30, 60, and 80 g/d food dextrin groups (p < 0.05), bloating occurring more often during the last day with 80 g/d resistant dextrin (p < 0.05), with none of the doses resulting in diarrhea, even at more than 80 g/d. Adaptation was observed with a decrease in the symptoms’ intensity after 20 days. During the long-term tolerance study [13], both doses of 30 and 45 g/d were very well tolerated with no diarrhea reported due to resistant dextrin supplementation. In the course of the study, some habituation and adaptation of gastrointestinal symptoms were found.
Digestion and Absorption in the Small Intestine: Associated Physiological Effects Invasive tests can be used to quantify the intestinal digestibility in humans. These methods are mainly developed in ileostomized patients or using technical intubations in healthy subjects. Not only may these methods lead to biased results due to the non-physiological conditions of testing, but also, and mainly, they are ethically difficult to manage because of pain-generating situations. The intestinal digestibility of NUTRIOSE® 06 was consequently assessed through in vitro techniques and in vivo animal studies. It allowed evaluating
Nutriose® Soluble Fiber
29
the percentage of resistant dextrin ingested that could resist the action of human digestive enzymes. In vitro tests were used based on previous publications [16, 17]. These kinds of tests consist in exposition of the dietary fiber to different enzymes that simulate the small intestine digestion. As the resistant dextrin is a glucose polymer, hydrolysis of the fiber is assessed by the dosage of the glucose that is delivered through the action of the enzymes. TNO intestinal model allows the measurement of the small intestine digestibility in a more complex system that is quite well recognized by the scientific world [18]. A digestibility test by intestinal infusion in rats was implemented. This test, based on a continuous circulation of the dextrin solution between the duodenum and the ileum in situ in the abdominal cavity of anaesthetized animals, allows the estimation of the intestinal hydrolysis by assaying the amount of residual food dextrin after a two-hour infusion [19]. The results of the studies obtained with the three previously described models indicated a small intestine digestibility in the range of 8.7% to 19% for this indigestible dextrin. In this context, a mean digestibility of 15% was set.
Glycemic Response The rate of absorption of the resistant dextrin at the different stages of the gastrointestinal tract plays a major role in determining its metabolic effect. This soluble fiber is weakly digested in the small intestine (15% of the ingested dose evaluated in vitro) and largely fermented in the colon. This weak absorption in the small intestine induces a low glycemic response (GR = 25) and a low insulinemic response (IR = 13) (see Figures 3.4 and 3.5) as demonstrated by following the FAO/WHO methodological recommendations [20]. The low IR of the food dextrin probably contributes to a better feeling of satiety than after glucose ingestion. As another consequence of this weakly insulogenic effect, no postprandial hypoglycemia is observed on the blood glucose curve after 120 minutes as can be the case after glucose ingestion (Figure 3.4). Finally, incorporation of this soluble fiber as an ingredient of a foodstuff can reduce the glycemic response of a meal. For example, the dextrin was incorporated into pasta, beverages, and biscuits [21]. The glycemic responses to all these foodstuffs were low according to the classification previously proposed [22] and fully agree with the WHO recommendations [20].
30
Fiber Ingredients: Food Applications and Health Benefits 10
Glycaemia (mmol/L)
9 8
®
NUTRIOSE FB 06 Dextrose
7 6 5 4 3
0
30
60
90
120
150
180
210
240
Time (minutes) Figure 3.4 Evolution of glycemia after ingestion of 50 g dextrose or 50 g NUTRIOSE® FB in 250 mL potable water (after overnight fasting).
50 45
Insulinaemia (mUI/L)
40 35 30
®
NUTRIOSE FB 06 Dextrose
25 20 15 10 5 0
0
30
60
90
120
150
180
210
240
Time (minutes) Figure 3.5 Evolution of insulinemia after ingestion of 50 g dextrose or 50 g NUTRIOSE® FB in 250 mL potable water (after overnight fasting).
31
Nutriose® Soluble Fiber
Gut Well-Being Soluble dietary fibers reach the colon almost unchanged where they can induce “prebiotic effects” characterized by (a) an increase in “beneficial bacteria” and/or a decrease in “harmful bacteria,” (b) a decrease in intestinal pH, (c) production of short-chain fatty acids (SCFAs), and (d) changes in bacterial enzymes concentrations [23]. NUTRIOSE® 06, as a resistant dextrin, is mostly resistant to digestion in the small intestine and largely fermented in the colon. It is a soluble dietary fiber [24]. It also shows [5] an outstanding digestive tolerance, allowing its consumption in amounts fully compatible with beneficial changes in the gut ecosystem, described hereafter. The resistant dextrin induces an increase of the colonic saccharolytic flora and a decrease in potentially harmful Clostridium perfringens in human feces. These effects have been noticed in two different clinical studies. In the first study (study 1) [unpublished results], 48 volunteers were randomly included and distributed into four parallel groups. During the 14-day study, the first group consumed 20 g/d glucose (placebo) and the three others respectively 10, 15, or 20 g/d of the food dextrin. At the end of the experiment, an increase in the saccharolytic flora was observed with 10 g/d resistant dextrin consumption (p < 0.05; Table 3.2). A decrease of the genus Clostridium perfringens was seen following 15 g/d consumption (p < 0.05; Table 3.2). In the second study (study 2) [13], 43 volunteers randomly assigned to three parallel groups (placebo, 30, and 45 g/d resistant dextrin) completed the clinical trial. A significant increase in the mean Lactobacilli numbers was observed after a 35-day consumption of 45 g/d food dextrin (p < 0.05; Table 3.2). During the study, a decrease in the genus Clostridium perfringens was observed again, confirming the beneficial effect previously described on potentially harmful bacteria. The soluble fiber is able to induce a decrease in the fecal pH of human volunteers. In the two previously described trials, pH measurements were Table 3.2 Significant Differences (p < 0.05) Observed in Many Types of Flora Quantified in Human Feces before and after Administration of NUTRIOSE® at Different Doses and during Different Durations. Amount of NUTRIOSE® Administered; Duration of the Diet
Type of Flora Quantified in the Human Feces
Before
10 g/d – 14 days 15 g/d – 14 days
Bacteroides (Log CFU/g) Clostridium perfringens (Log CFU/g) Lactobacilli (Log CFU/g)
8.543 ± 0.51 3.521 ± 1.65
8.958 ± 0.68 2.360 ± 1.53
7.2 ± 1.4
8.2 ± 1.2
45 g/d – 35 days
After
32
SCFAs (mg/caecum)
Fiber Ingredients: Food Applications and Health Benefits 70
(**): P < 0.01
60
(***): P < 0.005
*** **
50 40 30 20 10 0 Control
2.5% 5% 10% NUTRIOSE 06 NUTRIOSE 06 NUTRIOSE 06
®
®
®
Figure 3.6 Total amount of SCFAs in rat’s ceca after a 14-day administration of NUTRIOSE® 06 in feed.
performed at the end of the administration period. We noticed a significant decrease of the fecal pH following either the short or the long period of indigestible dextrin consumption. In study 1, fecal pH was 6.67 before the intervention phase and 5.99 after a 14-day administration period of 20 g/d (p < 0.05). In the long-term study (study 2) [13), fecal pH decreased at a nearly dose-dependent rate with treatment duration in both treated groups (30 and 45 g/d) unlike what happened in the placebo group, with a significant difference for the pH at day 21 of the 45 g/d resistant dextrin group compared to the placebo group (p < 0.05). The food dextrin increases production of short-chain fatty acids (SCFAs) in rats. Animal models are described as the only way to study production of colonic SCFAs because they are likely absorbed by the gut mucosa essentially to produce energy after metabolism [25]. The resistant dextrin was administered during 36 days to Sprague-Dawley laboratory rats. The total amounts of cecal SCFAs (acetic, propionic, and butyric acids) after 14 days were 36.04, 38.63, 51.10, and 62.39 mg/cecum for respectively the control group, the rats treated with 2.5%, with 5%, and with 10% resistant dextrin in feed (Figure 3.6). In the 10% group, the 108% increase observed for the propionic acid was significant (p < 0.005). The resistant polysaccharide induces changes in fecal bacterial enzyme concentration. In study 1, administering the resistant dextrin to human volunteers promoted changes in fecal bacterial enzyme concentration. Specifically, fecal concentrations of β-glucosidase, an inducible enzyme, were respectively 12.9 for the control group, 24.4, 22.6, and 31.4 UI/min/g for the 10 g/d, 15 g/d, and 20 g/d groups after 15 days administration. The concentra-
33
Nutriose® Soluble Fiber 35
(*): p < 0.05
bglucosidase (U/min/g)
30 *
25
*
20 15 10 5 0
Control
10g
15g
20g
Figure 3.7 Fecal β-glucosidase production after a 14-day administration of NUTRIOSE® 06 in humans.
tion was significantly higher for the 10 and 15 g/d groups as compared with the placebo group (p < 0.05; Figure 3.7). In a previous short-term tolerance study in 20 humans [12], where the food dextrin was administered at daily levels of 10 and 15 g up to 60 and 80 g, a similar significant increase of β-glucosidase fecal concentration (p < 0.05) had been already observed in all dextrin groups (10 to 80 g/d) as compared with the placebo, even at the lowest dose of 10 g/d. This clearly indicates that significant changes of the gut microflora occur early after the beginning of resistant dextrin consumption. In study 2 [13], a significant increase of β-glucosidase production (p < 0.05) was observed at the first observation (21 days) and still maintained after a 35-day consumption of 30 and 45 g/d (p < 0.05), showing a modification and a stabilization of the colonic flora. Results presented above show the specific fermentation pattern of resistant glucose polymer in humans. It is related to the molecular structure of this dietary fiber and to its specific physicochemical characteristics. As a glucose polymer, it likely stimulates the proliferation of colonic bacteria able to adapt to non-digestible carbohydrates [26], among which is the genus Bacteroides. This is a well-known producer of glucosidases, which is seen through the production of β-glucosidase in the previously described experiments. This enzyme [26] clearly indicates that oral consumption of as little as 10 g/d induces deep changes in the metabolic activity of the colonic flora. Glucosidases can act in the gut on residual polysaccharides coming from diet and remaining undigested, as for example vegetable residues. As a result, end products as minerals and other micronutrients can become available for the colon and the body [14]. An increase in Lactobacilli was also observed. These are classified as desirable colonic bacteria. They contribute to maintaining a healthy colon.
34
Fiber Ingredients: Food Applications and Health Benefits
SCFAs production is difficult to monitor in human clinical studies mainly for technical reasons [25]. Animal models are usually used in this context for studying SCFAs production following dietary fiber consumption. In all animal studies conducted, an increase in SCFAs production was observed. SCFAs and gases were indicators of the fermentation processes occurring after resistant dextrin consumption. As a result of these colonic fermentations, a pH decrease of the colonic content is visible through the fall in the fecal pH. This point is very interesting in terms of colonic health as a weak decrease in gut pH, coupled with propionic acid production (powerfully inhibiting enterobacteria in acidic conditions) is associated with a decrease in potentially harmful gram-negative bacteria. This is the case with 15 g/d resistant dextrin consumption as displayed by a decrease of the species Clostridium perfringens. The results presented show that the consumption of 10 grams or more per day of the soluble fiber produces positive observable changes in the gut microflora [27]. Bacteria that may ferment the food dextrin are likely bacteria from the glucidolytic flora. These bacteria are thus increasing in number to the detriment of proteolytic species such as Clostridium perfringens because of the promotion of acidic conditions in the gut. The enzymes produced by the saccharolytic flora are enzymes that can play an ultimate role in the production of end products of interest in terms of colonic health, like vitamins, minerals, and antioxidants. Recently published results [28, 29] indicate that the gut microbiota may be a contributing factor to the physiopathology of obesity. Among the dominant bacterial division, Bacteroidetes are decreased in obese people by comparison with what occurs in lean people. Moreover, the soluble fiber is outstandingly well-tolerated, even at high dosages, which should be used in order to reach such a type of goal in obese people. According to all these observations, and based on the definition given above, the convergent changes observed in the colonic environment globally allow concluding that NUTRIOSE® 06 can be considered as a prebiotic fiber.
Caloric Value By application of the equation published by Roberfroid [30], the caloric value of the resistant dextrin is 1.7 kcal/g (commercial base). This value of 1.7 can be used for the foodstuffs energy content determination in Europe [31]. In the United States, where the FASEB equation [32] is much more recognized, the caloric value has been estimated at 2.1 kcal/g (dry substance). The caloric value of the resistant dextrin was determined in healthy young men [14]. The authors concluded that the net energy value of NUTRIOSE® is 2.0 kcal/g; this is fully in agreement with the consensual caloric value of soluble dietary fibers [33]. It should be kept in mind that soluble dietary fibers may have a positive impact on the total daily energy expenditures through the colonic fermenta-
Nutriose® Soluble Fiber
35
tions and the rheological modifications of the gut contents. The impact of low-digestible carbohydrates consumption on the energy expenditures of healthy volunteers was studied [34]. The positive impact was explained by the increase of the gastrointestinal tract motility, the increase of the digestive tissue weight, and a lower energetic efficiency of short-chain fatty acids utilization compared with glucose. All these parameters were positively altered in animals fed with the resistant dextrin [13, 14, 35].
Technical and Physicochemical Properties Allowing Various Food Applications Thanks to stability towards industrial processing, neutral taste, and ease of use, the indigestible dextrin can be added or incorporated for nutritional or technological objectives in a very wide range of food and beverage processing, while preserving organoleptic characteristics and consumers’ pleasure. Powder’s Properties Thanks to its particle size and molecular configuration, dry NUTRIOSE® products are free flowing, easy to disperse, rapid to dissolve, and soluble. They can be used in dry mixes as well as alone, or used as carriers for tabletop sweeteners or flavors. Their theoretically unlimited solubility added to their low viscosity in solution allow their use at very high dosages during processing and in finished products. In products like reduced-sugar beverages or fruit fillings, reduced-sugar or low-fat biscuits, bars, and toppings, they will allow balancing the dry matter, and also enhance texture. Among fibers launched under powdered forms, this soluble fiber is one of the lowest in hygroscopy: It can resist up to 80% relative humidity (24h, 20°C) before clumping occurs. This characteristic is highly important on production lines, in warehouses, and for use in tropical countries. As it does not provide cloudiness in solution, it is dedicated for applications like beverages, some confectioneries, bouillons, and flavorings. It can be used as binder for granulation and has an excellent ability for compression, which allows its use in tablets both in food and pharmaceutical areas. Resistance to Various Industrial Processing The resistant dextrin’s product range is stable in high-temperature processing conditions, including sterilization, UHT treatment, or baking. It remains stable in acidic conditions, such as fruit and vegetable juices. These properties have been validated through measurement of the change in molecu-
36
Fiber Ingredients: Food Applications and Health Benefits
lar weight distribution (expressed as a ratio Mw/initial Mw*100) over time. After 90 days’ storage at 20°C, the molecular weight of the resistant dextrin remains unchanged or almost unchanged at any pH during storage (93% at pH 2, 100% at the other pH, tested until 8), and this result is also valid for higher temperatures as no hydrolysis occurs. This point has also been demonstrated in finished products. For example, in bread cooked at 200°C for 10 minutes, the percentages of soluble fiber, respectively on the one hand calculated for incorporation in bread and on the other hand analyzed after fermentation and cooking, go from 2.5% to 2.8% in a control (conventional) bread and from 8.1% to 8.2% in a resistant dextrin enriched bread, demonstrating the good stability of the soluble fiber towards fermentation and cooking. Similar results have been found for hardboiled candies cooked in an open pan at 180°C, UHT beverages sterilized at 140°C for two seconds, fruit fillings pasteurized at 95°C for five minutes, and soups sterilized at 110°C for 50 minutes. The resistant dextrin even remains stable when finished products are fried, frozen, or produced by extrusion, like cereal flakes, for example. This stability is very interesting for product formulations and quality maintenance over time. Indeed, no additional dosage is needed to guarantee the fiber content of the finished product after processes with potential impact on stability. The resistant dextrin is not fermented by S. cerevisiae and is easily processable on traditional equipment. Even if some recipe adjustments may be needed at the highest rates of incorporation, it will not affect the process. Softness, taste, and appearance of end products will be preserved during shelf life. The resistant dextrin is not fermented by most dairy strains and can be used in all kinds of dairy products for fiber or other health benefits claims, thanks to its stability to heat and acidity. In milk, it will not provide viscosity but will contribute to mouthfeel. As an example, enrichment with the indigestible dextrin (15 g/l) will provide to skimmed milk the creamy and smooth texture of the half skimmed one, together with fat reduction and fiber enrichment.
Taste and Mouthfeel The resistant dextrin NUTRIOSE® has a very slightly sweet taste depending on the grade (from 0.1% to 0.2% compared to sucrose) and can be used both in sweet and salty goods. It will provide no specific taste to finished products
Nutriose® Soluble Fiber
37
while contributing to or enhancing a nice mouthfeel. This can be achieved thanks to its bulking agent, mainly in liquid foodstuffs (beverages, dairy) as described previously, but also in semisolid goods. For example, the resistant dextrin can impact positively the chewiness of chewy sweets or the softness of some reduced-fat baked goods. Results of experiments performed on heattreated soups point out a recovered mouthfeel in reduced-fat versions using resistant dextrin. Thanks to its sugar-free reference, the resistant dextrin can be used in sugar-free confectionery, beverages, and flavors.
Safety, Regulation, and Labeling The resistant dextrin has been recognized as a soluble dietary fiber by the French Food Safety Agency [36] and by the Italian Ministry of Health. Therefore the range is also recognized among proposed constituents of dietary fibers by ILSI’s experts in the recently updated ILSI Europe monograph [37]. Products of this range are defined as food ingredients labeled as dextrins. Depending on local regulations, the vegetable origin of the raw material has to be declared if wheat. NUTRIOSE® can be safely used with no limitations because of its harmlessness [38]. The resistant dextrin is prepared from conventional (non-GMO) maize or from wheat. On top of all nutritional benefits previously described, use of NUTRIOSE® 06 is compatible with sugar(s)-free claims or no-sugar(s)-added claims, while the whole range can be used for low-sugar or reduced-fat claims as well as for any claims on fibers.
Conclusion NUTRIOSE® 06, as a soluble dietary fiber, very easily incorporated in foodstuffs, has an outstanding tolerance. Therefore, it can be used without digestive side effects at the dosage that is recommended for reaching some nutritional goals, such as, for example, prebiotic-type effects or decreased glycemic responses. It is therefore a key ingredient and a very useful tool for the food industry in the context of epidemic obesity and type 2 diabetes, and in accordance with many of the WHO/FAO nutritional recommendations for less sugar, and more fiber.
38
Fiber Ingredients: Food Applications and Health Benefits
References
1. Burkitt, DP, and Spiller, GA. Dietary fiber: From early hunter-gatherers to the 1990s. In: Spiller GA, CRC Handbook of Dietary Fiber in Human Nutrition, 3rd ed., CRC Press, Boca Raton, FL, 1986, pp. 3–6. 2. Trowell, HC, Southgate, DA, Wolever, TM, Leeds, AR, Gassull, MA, and Jenkins, DJA. Letter: Dietary fiber redefined. Lancet, 1976, 1, p. 967. 3. Oakenfull, D. Physical chemistry of dietary fiber. In: Spiller, GA, CRC Handbook of Dietary Fiber in Human Nutrition, 3rd ed., CRC Press, Boca Raton, FL, 1986, pp. 33–44. 4. Schneemann, BO. Dietary fiber and gastrointestinal function. In: McCleary, BV, and Prosky, L, Advanced Dietary Fiber Technology, Blackwell Science, London, 2001, pp. 168–176. 5. Diet, Nutrition and the Prevention of Chronic Diseases. Report of a Joint WHO/FAO Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases. Geneva, 28 January–1 February 2002. 6. Tharanathan, RN. Starch-value addition by modification. Critical Reviews in Food Science Nutrition 2005, 45 (5), pp. 371–384. 7. Laurentin, A, Cardenas, M, Ruales, J, Perez, E, and Tovar, J. Preparation of indigestible pyrodextrins from different starch sources. Journal of Agricultural & Food Chemistry, 2003, 51 (18), pp. 5510–5515. 8. Kerr, RW, and Cleveland, FC. Chemistry of dextrinization. Stärke, 1953, 5, pp. 261–266. 9. Srivastava, HC, Parmar, RS, and Dave, GB. Studies on dextrinization. Stärke, 1970, 2, pp. 49–54. 10. Prosky, L, Asp, NG, DeVries, JW, Schweizer, TF, and Harland, BF. Determination of total dietary fiber in foods and food products: collaborative study. Journal Association of Official Analytical Chemists, 1985, 68(4), pp. 677–679. 11. Van Den Heuvel, EGHM, Wils, D, Pasman, WJ, Bakker, M, Saniez, MH, Kardinaal, AFM. Short-term digestive tolerance of different doses of NUTRIOSE® FB, a food dextrin, in adult men. European Journal of Clinical Nutrition, 2004, 58, pp. 1046–1055. 12. Gordon, DT, and Okuma, K. Determination of total dietary fiber in selected foods containing resistant maltodextrin by enzymatic-gravimetric method and liquid chromatography: collaborative study. Journal of AOAC International, 2002, 85(2), pp. 435–444. 13. Pasman, W, Wils, D, Saniez, MH, Kardinaal, A. Long-term gastrointestinal tolerance of NUTRIOSE® FB in healthy men. European Journal of Clinical Nutrition, 2006, 60(8), pp. 1024–134 Epub 2006 Feb 15. 14. Vermorel, M, Coudray, YC, Wils, D, Sinaud, S, Tressol, JC, Montaurier, C, Vernet, J, Brandolini, M, Bouteloup-Demange, C, and Rayssiguier, Y. Energy value of a low-digestible carbohydrate, NUTRIOSE® FB, and its impact on magnesium, calcium and zinc apparent absorption and retention in healthy young men. European Journal of Nutrition, 2004, 43, pp. 344–352. 15. Marteau, P, and Flourié, B. Tolerance of low-digestible carbohydrates: symptomatology and methods. British Journal of Nutrition, 2001, 85, Suppl. 1, S17–S21. 16. Dahlqvist, A. Method for assay of intestinal dissacharidases. Analytical Biochemistry, 1964, 7, pp. 18–25.
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17. Englyst, HN, Kingman, SM, and Cummings, JH. Classification and measurement of nutritionally important starch fractions. European Journal of Clinical Nutrition, 1992, 46 (Suppl. 2), pp. 533–550. 18. Minekus, M. Development and validation of a dynamic model of the gastrointestinal tract. Ph.D. thesis, 1998, Utrecht University Elinkwijk b.v, Utrecht, Netherlands. 19. Barr, WH, and Riegelman, S. Intestinal drug absorption and metabolism. I. Comparison of methods and models to study physiological factors of in vitro and in vivo intestinal absorption. Journal of Pharmaceutical Sciences, 1970, 59(2), pp. 154–163. 20. FAO/WHO carbohydrates in human nutrition. Report of a Joint FAO/WHO expert consultation FAO, Roma, 1998. 21. Lefranc-Millot, C, Wils, D, Henry, J, Lightower, H, and Saniez-Degrave, MH. NUTRIOSE®, a resistant dextrin and MALTISORB®, a sugar alcohol, two key ingredients for healthy diets and obesity management. Obesity Reviews, 2006, 7(suppl 2), p. 269. 22. Livesey, G. Low-glycaemic diets and health: implications for obesity. Proceedings of the Nutrition Society, 2005, 64, pp. 105–113. 23. Woods, MN, and Gorbach, SL Influences of fibers on the ecology of the intestinal flora. In: Spiller, GA. Handbook of dietary fiber in human nutrition, CRC, New York, USA, 2001, pp. 257–270. 24. Roberfroid, MB. Introducing inulin-type fructans. The British Journal of Nutrition, 2005, 93, Suppl 1, pp. S13–S25. 25. Roberfroid, M, and Slavin, J. Nondigestible oligosaccharides. Critical Reviews in Food Science and Nutrition, 2000, 40, pp. 461–480. 26. Marteau, P, Pochart, P, Flourie, B, Pellier, P, Santos, L, Desjeux, JF, and Ramboud, JC. Effect of chronic ingestion of a fermented dairy product containing Lactobacillus acidophilus and Bifidobacterium bifidum on metabolic activities of the colonic flora in humans. The American Journal of Clinical Nutrition, 1990, 52, pp. 685–688. 27. Lefranc-Millot, C, Wils, D, Neut, C, Saniez, MH. Effects of a soluble fiber with excellent tolerance, NUTRIOSE® 06, on the gut ecosystem: a review. Dietary Fibre 2006, Helsinki, Finland, 12–14 June. 28. Turnbaugh, PJ, Ley, RE, Mahowald, MA, Magrini, V, Mardis, ER, and Gordon, JI. An obesity-associated gut microbiome with increased capacity of energy harvest. Nature, 2006, 444 (7122), pp. 1027–1031. 29. Ley, RE, Turnbaugh, PJ, Klein, S, and Gordon, JI. Microbial ecology: human gut microbes associated with obesity. Nature, 2006, 444 (7122), pp. 1022–1023. 30. Roberfroid, MB. Caloric value of inulin and oligofructose. The Journal of Nutrition, 1999, 129, pp. 1436S–1437S. 31. Coussement, P. Regulatory issues relating to dietary fiber in the European context. In: McCleary and Prosky, Eds. Advanced Dietary Fiber Technology, Blackwell Science, New York, 2001, pp. 139–145. 32. FASEB/LSRO. The evaluation of the energy of certain sugar alcohols used as food ingredients. Life Sciences Research Office, Federation of American Societies for Experimental Biology, Bethesda, MD, 1994. 33. Livesey, G. The energy values of dietary fibres and sugar alcohols for man. Nutrition Research Review, 1992, 5, pp. 61–84.
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34. Sinaud, S, Montaurier, C, Wils, D, Vernet, J, Brandolini, M, Bouteloup-Demange, C, and Vermorel, M. Net energy value of two low-digestible carbohydrates, Lycasin HBC and the hydrogenated polysaccharide fraction of Lycasin HBC in healthy human subjects and their impact on nutrient digestive utilization. The British Journal of Nutrition, 2002, 87(2), pp. 131–139. 35. Van den Heuvel, EGHM, Wils, D, Pasman, WJ, Saniez, MH, and Kardinaal, AF. Dietary supplementation of different doses of NUTRIOSE® FB, a fermentable dextrin, alters the activity of faecal enzymes in healthy men. European Journal of Nutrition, 2005, 44, pp. 445–451. 36. Saisine n0 = 2005 —SA— 0283 Aois de l'Agence Frangaise de securite sanitaire des aliments relatif à l’évaluation de la qualification comme fibre alimentaire soluble dúne dextrine et des justificatifs des allegations nutritionnelles qui lui sont anocies. Published the 30/07/2007. 37. Gray, J. Dietary fiber: Definition, analysis, physiology and health, 2006. In: ILSI Europe Concise Monograph Series. ILSI EUROPE Eds. 38. Wils, D, Scheuplein, RJ, Deremaux, L, and Looten, P. Oral sub-chronic 90-day study of NUTRIOSE® (a food dextrin) (submitted to Regulatory Toxicology and Pharmacology).
4 Inulin Anne Franck and Douwina Bosscher
Contents Introduction............................................................................................................ 41 Chemical Structure................................................................................................42 Natural Occurrence...............................................................................................42 Quantitative Determination of Inulin in Food..................................................43 Production............................................................................................................... 45 Properties................................................................................................................ 45 Physical and Chemical Properties.............................................................. 45 Material Properties....................................................................................... 46 Nutritional Properties.................................................................................. 47 Non-Digestibility.............................................................................. 47 Caloric Value...................................................................................... 47 Improvement of Lipid Metabolism................................................. 47 Effects on Gut Function.................................................................... 48 Modulation of Gut Microflora......................................................... 49 Resistance to Infections and Inflammation.................................. 49 Suitable for Diabetics........................................................................ 50 Modulation of Appetite and Food Intake...................................... 51 Reduction of Cancer Risk................................................................. 52 Increase in Mineral Absorption...................................................... 52 Intestinal Acceptability.................................................................... 53 Food Applications..................................................................................................54 Outlook and Perspectives..................................................................................... 55 References............................................................................................................... 56
Introduction Inulin, a non-digestible carbohydrate, is a fructan that has been part of our daily diet for some centuries and naturally occurs in many plants as storage carbohydrate. It is present for example in leeks, onions, garlic, wheat, chicory, 41
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Fiber Ingredients: Food Applications and Health Benefits
artichokes, and bananas. On an industrial scale, it is obtained mainly from chicory roots and used as a functional food ingredient that offers a unique combination of nutritional properties and technological benefits. In food formulations, inulin improves the organoleptic characteristics, upgrading both taste and mouthfeel in a wide range of applications. In particular, this tastefree fructan increases the stability of foams and emulsions and shows an exceptional fat-like behavior when used under the form of a gel in water. Additionally, the nutritional properties of inulin offer a wide range of benefits on health and well-being. In certain fields, such as gut function and health, increase in mineral aborption, reduction of colonic cancer risk, and modulation of appetite, data on the effects of inulin are well documented. Others, such as modulation of lipid and sugar metabolism and the effects on immunity, show promising data, and more evidence on the beneficial effects of inulin in these areas is expected. So, inulin as a functional food ingredient offers opportunities for fat and carbohydrate replacement without compromising on taste and texture, while delivering nutritional benefits to the final product. Inulin, therefore, represents a key ingredient offering new opportunities to the food industry looking for healthy and well-balanced, and yet better tasting, products for the future.
Chemical Structure Inulin is a polydisperse carbohydrate material consisting mainly, if not exclusively, of β(2-1)-fructosyl-fructose links [1]. A starting glucose moiety can be present but is not necessary. Fructan is a more general name, used for any compound in which one or more fructosyl-fructose links constitute the majority of linkages (i.e., covering both inulin and levan). Referring to the definition of inulin, both GFn and Fm compounds are considered to be included under that same nomenclature. In chicory inulin, n, the number of fructose units linked to a terminal glucose, can vary from 2 to more than 60 units [2]. This means that inulin is a mixture of oligomers and polymers. The molecular structure of inulin compounds is shown in Figure 4.1. Native chicory inulin also contains glucose, fructose, sucrose, and oligosaccharides. Native refers to inulin that prior to its analysis is extracted from fresh roots, taking precautions to inhibit the plant’s own inulinase activity as well as acid hydrolysis [3].
Natural Occurrence After starch, fructans are the most abundant non-structural polysaccharides found in nature. They are present in a wide variety of plants. Fructan-producing
43
Inulin HOCH2
O
OH HO HOCH2
HO O
O
O HO
(GFn)
O O
HO
CH2
HOCH2
OH HOCH2
O
HO
HO
HO
HO
O OH HO CH2
n–1
HO
CH2
HOCH2
O
HO
CH2OH HO
O
m–2
CH2OH
(Fm)
Figure 4.1 Chemical structure of inulin.
plants are commonly present among the grasses (1200 species), whereas 15% of the flowering plants produce them in significant amounts. They are widely spread within the Liliaceae (3500 species) and most frequently among the Compositae (25,000 species) [4]. Strictly β(2–1) defined inulin is typical for the Compositae. Inulin-containing plants that are commonly used for human nutrition belong mainly to either the Liliacea (e.g., leek, onion, garlic, and asparagus), or the Compositae (e.g., Jerusalem artichoke, dahlia, chicory, and yacon).
Quantitative Determination of Inulin in Food The AOAC method 997.08 [5] was developed because inulin and oligofructose are classified as dietary fibers but cannot be measured by the classical AOAC fiber method. An overview of the method is given in Figure 4.2. If inulin is the only compound present in the sample, the method consists only of steps 1 and 3. The inulin is extracted from a substrate at 85°C for 10 min; part of the extract is put apart for determination of free fructose, glucose, and sucrose by any reliable chromatographic method available (HPLC, HGC, or HPAEC-PAD); the other part is submitted to an enzymatic hydrolysis. After the hydrolysis step, resulting fructose and glucose are determined again by chromatography. By subtracting the initial glucose, fructose, and sucrose contents from the final ones, the following formula can be applied: Inu = k (Ginu + Finu), where k (<1) depends on the degree of polymerization (DP) of the inulin analyzed and corrects for the water gain after hydrolysis. Ginu and Finu are respectively glucose and fructose strictly originating from inulin.
44
Fiber Ingredients: Food Applications and Health Benefits Flow diagram of the enzymatic fructan method
Sample + 1 g fructan – Extraction Dissolution boiling water; pH 6.5–8.0 10 min. 85°C 100 g Sugar analysis 1
AG Hydrolysis 15 g extract and 15 g buffer; pH 4.5 Amyloglucosidase 30 min. 60°C Sugar analysis 2
Inulinase Hydrolysis Fructozyme (NOVO) 30 min. 60°C Sugar analysis 3 Figure 4.2 Flow diagram of the enzymatic fructan method.
If a complex sample needs to be analyzed, as is often the case dealing with food products, an amyloglucosidase treatment must be included before step 3 and an extra sugar analysis performed to avoid overestimation of the glucose originating from the starch or maltodextrins present. Although the AOAC method 997.08 is very reliable, it is very labor intensive and requires the use of chromatographic equipment. The AOAC method 999.03 [6], completely based on the use of enzymes as well for the hydrolysis as for the sugar determinations, requires only a spectrophotometer and some other standard lab equipment. This method is reliable for the determination of inulin but cannot be used for the determination of oligosaccharides obtained by hydrolysis of inulin, or any form of oligofructose that contains Fm-type compounds as these are significantly underestimated.
Inulin
45
Production Given their high inulin content (>10%), dahlia, Jerusalem artichoke (Helianthus tuberosus), and chicory (Cichorium intybus) could be considered good candidates for industrial production in temperate regions. However, most inulin produced for commercial applications is derived from chicory. Chicory is a biennial plant. During the first season, the chicory plants remain in the vegetative phase and make only leaves, taproots, and fibrous roots. The roots look like small oblong sugar beets. Their inulin content is high and fairly constant from year to year for a given region (between 16.0% to 17.6%). The production of inulin goes through two phases. The first step includes the extraction and a primary purification and results in a raw syrup; the second step is the refining phase which results in a commercial product that is more than 99.5% pure. The resulting inulin (Orafti® inulin) has a degree of polymerization (DP) that reflects the original DP present in chicory, varying between 3 and 60. A special-grade long-chain inulin (Orafti® HP) with DP > 23 is also available. It is made by physical elimination of the small DP fraction [7]. By partial enzymatic hydrolysis of inulin, oligofructose (Orafti® oligofructose) is obtained. A purified endo-inulinase is used since the aim is to produce inulin oligomers with the least possible formation of mono- and disaccharides. Oligofructose contains smaller inulin fractions with DP varying between 3 and 8. More recently a patented combination of carefully selected chain lengths of oligofructose and long-chain inulin (Orafti® Synergy1) has been developed with enhanced nutritional properties (see further).
Properties Inulin offers technological properties for a wide scope of food applications as well as important nutritional benefits, which makes it a unique food ingredient. Physical and Chemical Properties Chicory inulin is available as white and odorless powders. The taste is neutral, without any off-flavor or aftertaste. Native inulin is slightly sweet (10% sweetness compared to sugar), whereas long-chain inulin has no sweetness [8]. It behaves like a bulk ingredient, contributes to body and mouthfeel, provides a better-sustained flavor with reduced aftertaste (e.g., in combination with high-potency sweeteners), and improves stability. Inulin is moderately soluble in water (maximum 10% at room temperature), which allows its incorporation into watery systems where the precipitation
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Fiber Ingredients: Food Applications and Health Benefits
of other fibers often leads to problems. The viscosity of inulin solutions is rather low (e.g., 1.65 mPa.s at 10°C for a 5% dry matter (d.m.) solution and 100 mPa.s for a 30% d.m. solution) [3]. In very acidic conditions, the β(2–1) bonds between the fructose units in inulin can be (partially) hydrolyzed. Fructose is formed in this process, which is more pronounced under low pH, high-temperature, and low drysubstance conditions. Inulin is stable in applications with a pH higher than 4. Even at lower pH values, the hydrolysis of inulin can be limited to less than 10% if the products have high dry-matter content (>70%), are stored at a low temperature (<10°C), or have a short shelf life. At high concentrations (>25% in water for native inulin and >15% for longchain inulin), inulin has gelling properties and forms a particle gel network after shearing. When inulin is thoroughly mixed with water, or another aqueous liquid, a white creamy structure results that can easily be incorporated in foods to replace fat [8]. Inulin also improves the stability of foams and emulsions, such as aerated dairy desserts, ice creams, table spreads, and sauces. It can, therefore, replace other stabilizers in different food products. Material Properties Inulin products are available as powders with different particle size distribution and density. The content of the different chain length components also differs depending on the target application and desired nutritional effect. The longer chains behave more like polysaccharides and exhibit fatTable 4.1 Physicochemical Properties of Chicory Inulin Inulin Chemistry DPav Inulin content (% dry matter) Dry matter (%) Sugars (% dry matter) pH (10% in H2O) Ash (% dry matter) Heavy metals(% dry matter) Color Taste Sweetness vs. sucrose (%) Water solubility (% at 25°C) Water viscosity (5% at 10°C)
GpyFn DP 3-60 12 92 95 8 5-7 <0.2 <0.2 White Neutral 10% 12 1.6 mPa
Inulin HP GpyFn DP 10-60 25 99.5 95 <0.5 5-7 <0.2 <0.2 White Neutral None 2.5 2.4 mPa
Source: Adapted from Franck, A., Technological functionality of inulin and oligofructose, Br. J. Nutr., 87 (suppl. 2), S287–S291, 2002.
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47
replacing and stabilizing properties. They have a slower and more sustained fermentation along the large intestine. The shorter chains show technological properties close to those of sucrose and glucose syrups. They are more rapidly fermented with a subsequent higher increase in short-chain fatty acids in the proximal part of the large bowel. Nutritional Properties Inulin has been shown to provide several interesting nutritional properties to animal and human volunteers. Non-Digestibility Due to its chemical structure (β (2-1) bonds), which human digestive enzymes cannot hydrolyze, inulin passes through the mouth, the stomach, and the small intestine unaltered. This has been confirmed in ileostomized volunteers [9]. Inulin, therefore, enters the colon almost quantitatively (>90%) and is completely metabolized by the intestinal bacteria [10]. Even at high intake doses, no significant amounts of inulin have been detected in feces. Caloric Value The non-digestibility of inulin is the reason for its low caloric value in comparison with its component monosaccharide moieties. Inulin is completely converted, mainly into short-chain fatty acids (SCFA: acetate, propionate, and butyrate), lactate, bacterial biomass, and gases. Only SCFA and lactate can contribute to the host’s energy metabolism. SCFA and lactate are, in part, used by the bacteria themselves and are partly taken up by the host. Also, SCFA and lactate are less effective energy substrates than sugars. These factors together explain the reduced caloric value of inulin. Based on 14C studies in humans, the caloric value of fructooligosaccharides was calculated to be 1.5 kcal/g [11]. Experiments in vitro (fermentation) and in vivo (rat experiments) allowed Roberfroid et al. to calculate the caloric value of inulin and oligofructose to be about 1.5 kcal/g, according to basic biochemical principles [12]. Other scientific observations have even suggested lower caloric values [9, 13, 14]. Consequently, a caloric value between 1 and 1.5 kcal/g is currently being used for food labeling of inulin. Improvement of Lipid Metabolism In rats, distinct effects on lipid metabolism have been observed. Mainly, the serum triglycerides are affected. The observed metabolic changes originate at the level of the liver [15–19]. Biochemical studies with isolated hepatocytes have demonstrated that inulin and oligofructose consumption reduces the activity of key hepatic enzymes related to lipogenesis (de novo synthesis of fatty acids or assembling
48
Fiber Ingredients: Food Applications and Health Benefits
of triglycerides from acyl groups and glycerol) [20, 21]. Further research revealed that altered gene expression is at the basis of the down-regulation. Additionally, it is demonstrated that inulin and oligofructose, or their bacterial fermentation metabolites, affect the hormone status (insulin and/or glucose-dependent insulinotropic polypeptide or glucagon-like peptide-1) of the rats [22]. Also, a dose-effect study in golden Syrian hamsters showed a significant decrease in serum triglycerides and cholesterol (VLDL-C) [23]. In humans, inulin has a modulating effect on lipid metabolism. Indeed, it has been reported that the consumption of fructans reduces serum triglycerides and sometimes also cholesterol (mostly LDL cholesterol) in healthy volunteers who are (slightly) hyperlipidemic. The optimal lipid parameters of healthy normolipidemic young adults, on the contrary, are usually not affected. Studies also indicate that the triglyceride-lowering effect might take some time to establish (about eight weeks) [24–28]. Another line of thought is the impact of inulin on an unbalanced diet in normolipidemic subjects, a chronic problem in Western society. Experiments in rats demonstrated that the addition of 10% inulin (or oligofructose) to a fatrich diet reduced postprandial serum triglyceride contents, as well as serum cholesterol, by more than 50% compared with controls. Enhanced triglyceride-rich lipoprotein catabolism seems to be at the basis of this observation [22]. Moreover, rats on a high-fat diet fed fructans developed significantly less adipose tissue [29]. Inulin and oligofructose also impact glucose and insulin metabolism in rats as well as satiety [30–33]. Further studies in genetically obese (fa/fa Zucker) rats showed a similar tendency, with significantly lower body weight, fat mass, and steatosis when inulin (and oligofructose) was added (10%) to the diet as compared to the controls [34, 35]. These effects were, however, not seen with other (non-fermentable) dietary fibers (e.g., cellulose). The effects of inulin on lipid metabolism also have consequences on the development of atherosclerosis since high cholesterol levels and hyperlipemia are involved in the disease development. This has been demonstrated in mice (ApoE-deficient) in which inulin (10%) significantly inhibited atherosclerotic plaque formation (in aorta) compared to the controls [36]. Effects on Gut Function Inulin is a soluble dietary fiber [10, 37]. It is not hydrolyzed by the human digestive enzymes and it induces typical fiber-like effects on the functioning of the gut, such as a reduction of the intestinal pH, relief of constipation, and an increase in stool weight and frequency (also called bulking effect). Its fecal bulking is similar to that of other soluble fibers like pectin and guar gum [38]. Each gram of ingested inulin increases fecal wet weight by 1.5 to 2 grams. This is also reflected by an increased fecal dry weight excretion. The latter is mainly caused by an increased excretion of bacterial biomass [14, 39].
Inulin
49
The stimulation of the gut function also results in increased stool frequency. The increase is higher in volunteers with a low initial stool frequency. Relief of constipation has been reported in different studies with inulin [39–41]. The effects on the intestinal transit time are inconsistent, as only some researchers observed a decreased transit time. Modulation of Gut Microflora The large intestine harbours over 400 different types of bacteria that represent over 50% of the dry solids content in the colon. This microbial ecosystem in the large intestine is important for maintaining good health, and imbalances are thought to be a basis for the ethiology of various diseases. Inulin selectively promotes the growth and/or metabolic activity of a limited number of bacteria in the colon, especially Bifidobacteria and Lactobacilli, and thereby contributes to the health of the host. This is called the prebiotic or bifidogenic effect [42]. The bifidogenicity of inulin (and oligofructose) has been demonstrated in vitro [43, 44], in animal models and in humans [39–47]. The increase in the numbers of Bifidobacteria is inversely correlated with their counts at the start of the studies. A daily intake of about 5 grams of inulin is sufficient to significantly and selectively enhance Bifidobacteria [45]. In vitro experiments have demonstrated that the length of the inulin chain determines the rate of fermentation in the colon. Long-chain inulin fractions are fermented twice as slowly as the low-DP fraction (DP<10). So, the longchain inulin fraction has an interesting potential for the stimulation of the metabolic activity in the distal part of the colon [45]. Subjects who underwent endoscopic biopsies and were supplemented with oligofructose (7.5 g/day) and long-chain inulin (7.5 g/day) had indeed significantly higher numbers of (mucosal) Bifidobacteria and Lactocabilli in both the proximal and distal parts of their colon when compared to the controls [48]. This concept has led to the development of a second generation of prebiotics. By combining the bifidogenic properties of oligofructose and long-chain inulin, an oligofructose-enriched inulin (Orafti® Synergy1) was developed. The shorter inulin fraction (oligofructose) in Synergy1 has a bifidogenic effect in the proximal part of the colon, whereas the long-chain fraction maintains the beneficial metabolic activity toward the more distal parts of the large intestine. This generates a bifidogenic effect along the whole colon [49]. Resistance to Infections and Inflammation During the last decade, many beneficial effects have been attributed to Bifidobacteria. Objective observations support their potential as health-promoting bacteria. As Bifidobacteria counts increase after ingestion of inulin, a concomitant decrease in (potentially) pathogenic populations is often observed in vitro, in animal and human studies (e.g., Clostridia, E. coli, Salmonella, Veillonella, Shigella, and Listeria) [43, 44]. In experiments with gnotobiotic quails inoculated with a flora from a baby with necrotizing enterocolitis (comprising
50
Fiber Ingredients: Food Applications and Health Benefits
Clostridium butyricum) most of the quails died. However, quails that were given Bifidobacteria made a complete recovery. This was one of the first studies demonstrating the health effects of Bifidobacteria in living beings [50]. Also, in vitro, the antagonistic (antibacterial) activity of lactic-acid-producing bacteria (e.g., Bifidobacteria and Lactobacilli) against pathogens has been described, which in part is due to the production of organic acids, which are the end-products of inulin and oligofructose fermentation [51]. In addition, studies with epithelial layers have shown that inulin and oligofructose inhibit pathogen colonization and that end-products of their fermentation have the ability to support barrier function [52]. Furthermore, studies in various animal models have shown that inulin and oligofructose accelerate the recovery of beneficial bacteria, slow down pathogen growth, decrease pathogen colonization and systemic translocation [53]. Indeed, mice challenged by Candida albicans and fed inulin had significantly lower yeast densities in their intestinal contents as compared to control mice [54]. Also against systemic invaders inulin was shown to play a role, as demonstrated by the significantly higher survival rate of mice after intraperitoneal infection with Listeria monocytogenes and Salmonella typhimurium as compared to the control animals [54]. Finally, data from clinical trials in patients with intestinal disorders or disease, or prone to critical illness, found that inulin and oligofructose restore the balance when the gut microbial community is altered, inhibit the progression of disease, or prevent it from relapsing [55, 56]. In patients with C. difficile-associated diarrhea, triggered by antibiotic therapy, the administration of oligofructose significantly increased the numbers of Bifidobacteria and lowered relapse episodes of diarrhea compared to the controls [57]. Also in chronic gastrointestinal diseases such as inflammatory bowel diseases (ulcerative colitis and Crohn’s disease) and pouchitis the composition of the colonic microbial community and its activities are expected to play a role. Studies in patients with ulcerative colitis have revealed that bifidobacterial populations in their colons are about 30-fold lower compared to that of healthy individuals [58]. Supplementation of the diet with Synergy1 (and a probiotic) in patients with ulcerative colitis was able to restore bacterial levels and resulted in a 42-fold increase in bifidobacterial colonization in mucosal biopsies compared to the control group [58]. This resulted in a lower level of inflammation, better regeneration of the epithelial tissue, and improved clinical appearance of the chronic inflammation [59]. Decreased severity of the disease and improved recovery and/or remission were also observed after inulin therapy in patients with Crohn’s disease [60]. Reduced inflammation and associated factors were further observed in patients with pouchitis after inulin therapy [61]. Suitable for Diabetics As inulin is not hydrolyzed during passage through the mouth, stomach, and small intestine, it has no direct influence on the blood glucose and insu-
Inulin
51
lin levels when ingested. This has been confirmed by many scientists (e.g., in humans by Beringer and Wenger) [62]. The use of inulin as a food ingredient for diabetics has been known since the beginning of the 20th century. Lewis [63] referring to Persia [64] recommended inulin to diabetics and stated that the product is well digested and assimilated by those people in large doses and over long periods of time. Strauss [65] reported the feeding of inulin to be beneficial for the patient. This was also confirmed by Wise and Heyl [66]. Since then, many more applications for diabetics have been described in the literature (e.g., inulin-based diabetic bread and pastry [62] and inulin-based diabetic jam) [67]. Modulation of Appetite and Food Intake The mechanisms of appetite regulation are complex and involve the interaction of many orexigenic and anorexigenic hormones that are released by the body (gastrointestinal tract and peripheral tissues) in response to the diet and which send messages to the brain (primarily the hypothalamus) sensing the feeling of hunger and/or being full. Higher blood levels of these appetitesuppressing peptides, such as cholecystokinin (CCK), PP-fold peptide (PYY), and glucagon-like peptide-1 (GLP-1), are associated with lower subjective hunger ratings and lower food intake. On the contrary, high circulating levels of the hormone ghrelin (during fasting) induce hunger and subsequently initiate food intake. Evidence is accumulating about the role of inulin (and oligofructose) to modulate blood levels of certain gut hormones influencing appetite. Upon inulin (and oligofructose) fermentation in the colon, SCFA are produced and evidence is emerging about their role in human metabolism (e.g., lipid metabolism). Additionally, higher levels of SCFA in the colonic lumen might increase the expression of GLP-1 in the mucosa (and consequently increase blood GLP-1 levels) and decrease the levels of the gastric-derived hormone ghrelin. This has been demonstrated in various animal models (e.g., rats on a normal or high-fat diet, obese and diabetic rats) and is consistently associated with a significantly lower energy (and food) intake, as well as lower body weight and adipose tissue deposition (coming from high-fat diets), factors leading otherwise to the development of obesity (and related diseases) [30, 31, 33, 35]. The GLP-1 peptide might constitute a link between the outcome of fermentation in the colon and the modulation of food intake. The role of GLP-1 has been tested in mice using a GLP-1 receptor antagonist (exendin, ex 9-39). Administration of the antagonist totally prevented the beneficial systemic effects of oligofructose (e.g., improved glucose tolerance, fasting blood glucose, glucose-stimulated insulin secretion, insulin-sensitive hepatic glucose production, and lower body weight gain) versus control mice. Also, GLP-1R-/- mice appeared to be totally insensitive to the systemic effects of oligofructose [32]. To further investigate the effects of oligofructose on appetite and food (energy) intake in humans, a placebo-controlled (single-blinded) interven-
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Fiber Ingredients: Food Applications and Health Benefits
tion study including 10 healthy volunteers (2*8 g/day of BeneoTM oligofructose) was conducted. Administration of oligofructose increased satiety, reduced hunger and prospective food consumption (by visual analogue scale). This led to a lower total energy intake during the day [33]. Also in other human studies the effects of oligofructose, either alone or in combination with other dietary fibers (pea fiber), on satiety and food intake have been documented [68]. Reduction of Cancer Risk The chemopreventive potential of inulin is extensively demonstrated in diverse animal models of cancer. Inulin has been shown to prevent to a significant extent the formation of chemically induced colonic precancerous lesions (aberrant crypt foci) and tumors in rats [68, 70]. It was furthermore demonstrated that inulin inhibits the development of cancer cells transplanted in the thigh and peritoneum of mice [71]. The preventive effect of oligofructose-enriched inulin (Synergy1), especially with respect to colon cancer, might be most effective since cancerous lesions occur more in the distal regions of the colon where the bifidogenic action of Synergy1 reaches due to its long-chain inulin component. A recent phase II anticancer study (randomized, double-blind, and placebo-controlled) in 80 patients with a history of colon cancer or polyps and supplemented with Synergy1 (and probiotics) for 12 weeks showed indeed a decrease in markers of the risk of colonic cancer. Levels of Bifidobacteria and Lactobacilli in the group receiving the synbiotic were significantly higher compared to controls. This was accompanied by a decrease in the numbers of pathogens (coliforms and Clostridium perfringens). It was hypothesized that these bacterial changes beneficially altered the metabolic activity in this organ. Indeed, decreased inflammation and exposure of the epithelium to damaging agents were observed. This is important since mucosal inflammation and high cytotoxicity and genotoxicity of the luminal contents are associated with an increased risk of colon cancer. Additionally, the observed decrease in colonic cell proliferation and improved mucosal structure demonstrate the protective effect of the synbiotic against colon cancer development [72]. Increase in Mineral Absorption First studies in growing rats have shown increased calcium and magnesium availability with the addition of inulin to the diet. Further studies indicated that inulin also stimulates the accumulation of bone mineral as well as the formation of bone and its trabecular network structure [73]. In ovariectomized rats (a model for postmenopausal women), inulin increased bone mineral content and impeded ovariectomy-induced loss of bone structure [74, 75]. Furthermore it was found that the combination of both short- and long-chain inulin fractions (Synergy1) was the most effective in increasing
Inulin
53
calcium absorption and improving calcium balance compared to either inulin or oligofructose taken alone [76, 77]. In a study with healthy adult volunteers who were given 40 g/day of inulin, a significant increase in calcium absorption was observed using the balance technique [78]. Based on the method of dual stable isotopes (46Ca/42Ca) an increase in true calcium absorption in adolescent boys was also observed after the intake of oligofructose (15 g/day) [79]. Further (multicenter) studies with oligofructose-enriched inulin (Synergy1) in adolescent girls (11 to 13 years old) confirmed the significant increase in true calcium absorption (by approximately 20%), at the lower dose of only 8 g/day of Synergy1 [80, 81]. More in-depth evaluation of the subjects revealed that those girls with lower calcium absorption during the placebo period showed the greatest increase in calcium absorption in response to Synergy1 [81]. Subsequently, a long-term (one-year) intervention trial with 8 g/day of Synergy1 was conducted in pubertal girls and boys (Tanner stage 2 and 3) to determine whether the increased true calcium absorption resulted in an additional net mineral accretion in bone. Calcium accretion is at its optimal stage during the pubertal ages and its level impacts bone health at later age. About 100 girls and boys (9 to 12 years old) with normal calcium intakes (900 to 1000 mg of calcium per day) participated in this one-year study. Boys and girls who received Synergy1 showed significantly higher calcium absorption already after eight weeks of supplementation and the higher absorption percentage was kept during the whole intervention. Correspondingly, Synergy1-supplemented subjects had a significantly higher change in whole body bone mineral content compared to controls. Under the assumption that the fraction of calcium in bone mineral is 32%, these values correspond to an additional net accretion of 30 ± 15 mg calcium per day with Synergy1. The change in whole body bone mineral density was also significantly greater in the Synergy1 group compared to the controls [82]. Intestinal Acceptability Intestinal acceptability of non-digestible components is mainly determined by two phenomena. First, by osmotic effects that lead to an increased presence of water in the colon. Smaller molecules exert a higher osmotic pressure and bring more water into the colon. This is probably the reason why sorbitol has a significantly higher laxative potential than inulin. Second, there are the side effects caused by the fermentation products, mainly short-chain fatty acids and gases. Slowly fermenting compounds appear to be easier to tolerate than their fast-fermenting analogues. This can explain why inulin is easier to tolerate than polyols and short-chain fructooligosaccharides. Flatulence is a well-known and often accepted side effect of the intake of vegetables. Dietary fibers, in general, are known for their properties of stool softening. Scientific research has shown that portions of 5 to 10 grams of inulin are well tolerated by most people and that daily doses of 10 to 20 grams
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Fiber Ingredients: Food Applications and Health Benefits
cause no significant discomfort. At higher doses, flatulence may cause some discomfort to sensitive people. Inulin rarely causes diarrhea [83].
Food Applications Inulin can be used for either its nutritional advantages or its technological properties, but it is often applied to offer a double benefit: an improved organoleptic quality and a better-balanced nutritional composition. The use of inulin as a fiber ingredient is easy and often leads to an improved taste and texture [84]. When used in bakery products and breakfast cereals, this presents a major advancement in comparison with other fibers. Inulin gives more crispiness and expansion to extruded snacks and cereals, and it increases their bowl-life. It also keeps breads and cakes moist and fresh for longer. Its solubility allows fiber incorporation in watery systems such as drinks, dairy products, and table spreads. Inulin more and more is used in functional foods, especially in a whole range of dairy products, as a prebiotic ingredient, which stimulates the growth of the beneficial intestinal bacteria. Thanks to its specific gelling characteristics, inulin allows the development of low-fat foods without compromising on taste and texture. This is particularly true in spreadable products. In table spreads, both fat and watercontinuous, inulin allows the replacement of significant amounts of fat and the stabilization of the emulsion, while providing a short spreadable texture. Long-chain inulin (from 2% to 10% depending on the recipe) gives excellent results in water-in-oil spreads, with a fat content ranging from 20% to 60%, as well as in water-continuous formulations containing 10% fat or less. It can also be applied in fat-reduced spreads containing dairy proteins, as well as in butter-like products and other dairy-based spreads. In low-fat dairy products, such as fresh cheese, cream cheese, or processed cheese, the addition of a few percents of inulin increases the body, gives a creamier mouthfeel, and imparts a better-balanced flavor. Inulin also is destined to be used as a fat replacer in frozen desserts, due to its ease in processing, a fatty mouthfeel, excellent melting properties, as well as freeze-thaw stability, without any unwanted off-flavor. Fat replacement can further be applied in meal replacers, meat products, sauces, and soups. Reduced-fat meat products can be obtained, such as sausages, pâtés, and other meat-based spreads, with a creamier and juicier mouthfeel and an improved stability due to water immobilization. The synergistic effect of inulin with other gelling agents constitutes an additional advantage in all these applications. In several products inulin, and especially its high-performance (or long-chain) version, can even (partially) replace gelatin, starch, maltodextrin, alginate, caseinate, and other
Inulin
55
stabilizers. This is of particular interest in dairy desserts, yogurts, cheese products, and table spreads. In the yogurt market, low-fat products are showing the strongest growth, in particular diet yogurts with fruit. The incorporation of inulin (1% to 3%) in the recipe, possibly through the fruit preparation, improves the mouthfeel, reduces syneresis, and offers a synergistic taste effect in combination with high-potency sweeteners such as aspartame, acesulfame K, and sucralose, without increasing significantly the caloric content. Inulin furthermore increases the stability of foams and mousses: Its incorporation at 1% to 5% into dairy-based aerated desserts (chocolate, fruit, yogurt, or fresh-cheesebased mousses) improves their processability and upgrades the quality. The resulting products retain their typical structure for a longer time and show a fat-like feeling even in the case of low-fat or fat-free formulations. Inulin has found an interesting application as a low-calorie bulk ingredient in chocolate without added sugar, not to reduce fat but to replace sugar, often in combination with a polyol. It is also used as a dietary fiber or sugar replacement in tablets. So, inulin has become a key ingredient offering new opportunities to the food industry looking for the well-balanced and yet better-tasting products of the future.
Outlook and Perspectives A steady increase in the number of publications related to inulin can be observed over the last two decades. The fundamental mechanisms by which inulin exerts its nutritional benefits will shed more light on its effects on health and well-being. The impact of inulin on the composition of the colonic microflora and more importantly the implication of such an altered bacterial ecosystem on the host’s health status will be better elucidated. Modulation of the immune response and protection against infectious diseases will be thoroughly assessed as potential effects of regular inulin consumption. Improving mineral absorption and bone health is certainly another topic that deserves continuous research. Special efforts will be made also to investigate in depth the role of inulin in the reduction of (colon) cancer risk and the prevention of obesity. Given the high burden of these diseases in Western societies, functional ingredients such as inulin can have a major impact on health and well-being of populations. The technological properties combined with the ease by which inulin can be incorporated into foods offer the advantage of reaching a major part of the population in preventive measures taken by governments to stop these chronic diseases.
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Fiber Ingredients: Food Applications and Health Benefits
References
1. Watherhouse, A.L. and Chatterton, N.J., Glossary of fructan terms, in: Science and Technology of Fructans, Suzuki, M., Chatteron, N.J., Eds., CRC Press, Florida, 2, 1993. 2. De Leenheer, L. and Hoebregs, H., Progress in the elucidation of the composition of Chicory inulin, Starch, 46(5), 193, 1994. 3. De Leenheer, L., Production and use of inulin: Industrial reality with a promising future, in: Carbohydrates as Organic Raw Materials III, Van Bekkum, H., Röper, H., Voragen, F., Eds., VCH Publ. Inc., New York, 67, 1996. 4. Hendry, G.A. and Wallace, R.K., The origin, distribution and evolutionary significancy of fructans, in: Science and Technology of Fructans, Suzuki, M., Chatteron, N.J., Eds., CRC Press, Florida, 119, 1993. 5. Hoebregs, H., Fructans in foods and food products, ion-exchange chromatographic method: Collaborative study, Journal of AOAC 5, 80, 102, 1997. 6. McCleary, B., Murphy, A., and Mugford, D., Measurement of total fructan in foods by enzymatic/spectrophotometric method: Collaborative study, Journal of AOAC, 83(2), 356, 2000. 7. Smits, G., Daenekindt, L., and Booten, K., Fractionated polydisperse composition, Patent Application EPO 679026B1, 1997. 8. Franck, A., Rafticreaming: The new process allowing to turn fat into dietary fibre, in: FIE 1992 Conference Proceedings, Expoconsult Publishers, Maarssen, 193, 1993. 9. Ellegård, L., Andersson H., and Bosaeus, I., Inulin and oligofructose do not influence the absorption of cholesterol, and the excretion of cholesterol, Fe, Ca, Mg, and bile acids but increase energy excretion in man. A blinded, controlled cross-over study in ileostomy subjects, European Journal of Clinical Nutrition 51, 1, 1997. 10. Roberfroid, M., Dietary fiber, inulin and oligofructose: A review comparing their physiological effects, Critical Reviews in Food Science and Nutrition, 33(2), 103, 1993. 11. Hosoya, N., Dhorranintra, B., and Hidaka, H., Utilisation of U-14C fructo-oligosaccharides in man as energy resources, Journal of Clinical Biochemistry and Nutrition, 5, 67, 1988. 12. Roberfroid, M., Gibson, G., and Delzenne, N., Biochemistry of oligofructose, a non-digestible fructooligosaccharide: An approach to estimate its caloric value, Nutrition Reviews, 51(5), 137, 1993. 13. Delzenne, N. et al., Effect of fermentable fructo-oligosaccharides on energy and nutrients absorption in the rat, Life Science, 57(17), 1579, 1995. 14. Castiglia-Delavaud, C. et al., Net energy value of non-starch polysaccharide isolates (sugarbeet fibre and commercial inulin) and their impact on nutrient digestive utilization in healthy human subjects, British Journal of Nutrition, 80, 343, 1998. 15. Bhattathiry, E.P.M., Effects of polysaccharides on the biosynthesis of lipids in adult rats, Far East Med. J., 7(6), 187, 1971. 16. Delzenne, N. et al., Dietary fructo-oligosaccharides modify lipid metabolism in rats, American Journal of Clinical Nutrition, 57, 820S, 1993.
Inulin
57
17. Delzenne, N. and Kok, N., Effect of non-digestible fermentable carbohydrates on the hepatic fatty acid metabolism, Biochemical Society Transactions, 26, 228, 1998. 18. Levrat, M.-A. et al., Role of dietary propionic acid and bile acid excretion in the hypocholesterolemic effects of oligosaccharides in rats, Journal of Nutrition, 124(4), 531, 1994. 19. Fiordaliso, M. et al., Dietary oligofructose lowers triglycerides, phospholipids and cholesterol in serum and very low density lipoproteins of rats, Lipids, 30(2), 163, 1995. 20. Kok, N., Roberfroid, M., and Delzenne, N., Dietary oligofructose modifies the impact of fructose on hepatic triacylglycerol metabolism, Metabolism, 45(12), 1547, 1996. 21. Kok, N., Taper, H.S., and Delzenne, N.M., Oligofructose modulates lipid metabolism alterations induced by a fat-rich diet in rats, Journal of Applied Toxicology, 18(1), 47, 1998. 22. Kok, N. et al., Insulin, glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide and insulin-like growth factor I as putative mediators of the hypolipidemic effect of oligofructose in rats, Journal of Nutrition, 128(7), 1099, 1998. 23. Trautwein, E.A., Rieckhoff, D., and Erbersdobler, H.F., Dietary inulin lowers plasma cholesterol and triacylglycerol and alters biliary bile acid profile in hamsters, Journal of Nutrition, 128, 1937, 1998. 24. Canzi, E. et al., Prolonged consumption of inulin in ready-to-eat breakfast: Effect on intestinal ecosystem, bowel habits and lipid metabolism, COST ’92 Workshop on Dietary Fibre and Fermentation, Helsinki, 1995. 25. Davidson, M. et al., Effects of dietary inulin on serum lipids in men and women with hypercholesterolemia, Nutrition Research, 18(3), 503, 1998. 26. Brighenti, F. et al., Effect of consumption of a ready-to-eat breakfast cereal containing inulin on the intestinal milieu and blood lipids in healthy male volunteers, European Journal of Clinical Nutrition, 53, 726, 1999. 27. Jackson, K. et al., The effect of the daily intake of inulin on fasting lipid, insulin and glucose concentrations in middle-aged men and women, British Journal of Nutrition, 82, 23, 1999. 28. Causey, J.L., et al., Effects of dietary inulin on serum lipids, blood glucose and the gastrointestinal environment in hypercholesterolemic men, Nutrition Research, 2, 191, 2000. 29. Cani, P.D. et al., Oligofructose promotes satiety in rats fed a high-fat diet: Involvement of glucagon-like peptide-1, Obesity Research, 13, 1000, 2005. 30. Cani, P.D. et al., Involvement of endogenous glucagon-like peptide-1(7-36) amide on glycaemia-lowering effect of oligofructose in streptozotocin-treated rats, Journal of Endocrinology, 185, 457, 2005. 31. Cani, P.D., Dewever, C., and Delzenne, N.M., Inulin-type fructans modulate gastrointestinal peptides involved in appetite regulation (glucagon-like peptide-1 and ghrelin) in rats, British Journal of Nutrition, 92, 521, 2004. 32. Cani, P.D. et al., Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon-like peptide 1 receptor, Diabetes, 55, 1484, 2006. 33. Cani, P.D. et al., Oligofructose prompts satiety in healthy human: A pilot study, European Journal of Clinical Nutrition, 0954, 2006.
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Fiber Ingredients: Food Applications and Health Benefits
34. Daubioul, C.A. et al., Dietary oligofructose lessens hepatic steatosis, but does not prevent hypertriglyceridemia in obese Zucker rats, Journal of Nutrition, 130, 1314, 2000. 35. Daubioul, C.A. et al., Dietary fructans, but not cellulose, decrease triglyceride accumulation in the liver of obese Zucker fa/fa rats, Journal of Nutrition, 132, 967, 2002. 36. Rault-Nania, M.H. et al., Inulin attenuates atherosclerosis in apolipoprotein E-deficient mice, British Journal of Nutrition, 96, 840, 2006. 37. Prosky, L., Inulin and oligofructose are part of the dietary fiber complex, Journal of AOAC International, 82(2), 223, 1999. 38. Roberfroid, M.B., Health benefits of non-digestible oligosaccharides, in: Dietary Fiber in Health and Disease, Kritchevsky and Bonefield, Eds., Plenum Press, New York, 211, 1997. 39. Gibson, G.R. et al., Selective stimulation of bifidobacteria in the human colon by oligofructose and inulin, Gastroenterology, 108, 975, 1995. 40. Kleessen, B., Sykura, B., and Zunft, H.J., Effect of inulin and lactose on fecal microflora, microbial activity, and bowel habit in elderly constipated persons, American Journal of Clinical Nutrition, 65, 1397, 1997. 41. Den Hond, E., Geypens, B., and Ghoos, Y., Effect of high performance chicory inulin on constipation, Nutrition Research, 20(5), 731, 2000. 42. Gibson, G.R. and Roberfroid, M.B., Dietary modulation of the human colonic microbiota: Introducing the concept of prebiotics, Journal of Nutrition, 125, 1401, 1995. 43. Wang, X. and Gibson, G.R., Effects of the in vitro fermentation of oligofructose and inulin by bacteria growing in the human large intestine, J. Appl. Bacteriology, 75, 373, 1993. 44. Gibson, G.R. and Wang, X., Bifidogenic properties of different types of fructooligosaccharides, Food Microbiology, 11, 491, 1994. 45. Roberfroid, M., Van Loo, J., and Gibson, G., The bifidogenic nature of chicory inulin and its hydrolysis products, Journal of Nutrition, 128(1), 11, 1998. 46. Rao, A., The prebiotic properties of oligofructose at low intake levels, Nutrition Research, 21, 843, 2001. 47. Tuohy, K.M. et al., A human volunteer study on the prebiotic effects of HP-inulin-faecal bacteria enumerated using fluorescent in situ hybridisation (FISH), Anaerobe, 7, 113, 2001. 48. Langlands, S.J. et al., Prebiotic carbohydrate modify the mucosa associated microflora of the human large bowel, Gut, 53, 1610, 2004. 49. Van Loo, J., The specificty of the interaction with intestinal bacterial fermentation by prebiotics determines their physiological efficacy, Nutrition Research Reviews, 17, 89, 2004. 50. Butel, M., et al., Clostridial pathogenicity in experimental necrotising enterocolitis in gnotobiotic quails and protective role of bifidobacteria, Journal of Medical Microbiology, 47, 391, 1998. 51. Makras, L. et al., In vitro kinetic analysis of oligofructose consumption by Bacterioides and Bifidobacterium spp. indicates different degradation mechanisms, Applied and Environmental Microbiology, 2, 1006, 2006. 52. Naughton, P.J., Mikkelsen, L.L., and Jensen, B.B., Effects of nondigestible oligosaccharides on Salmonella enterica serovar typhimurium and non-pathogenic Escherichia coli in the pig small intestine in vitro, American Society for Microbiology, 67, 3391, 2001.
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59
53. Bosscher, D., Van Loo, J., and Franck, A., Inulin and oligofructose as prebiotics in the prevention of intestinal infections and diseases, Nutrition Research Reviews, 19, 216, 2006. 54. Buddington, K.K., Donahoo, J.B., and Buddington, R.K., Dietary oligofructose and inulin protect mice from enteric and systemic pathogens and tumor inducers, Journal of Nutrition, 132, 472, 2002. 55. Jain, P.K. et al., Influence of symbiotic containing Lactobacillus acidophilus La5, Bifidobacterium lactis Bb 12, Streptococcus thermophilus, Lactobacillus bulgaricus and oligofructose on gut barrier function and sepsis in critically ill patients: A randomized controlled trial, Clinical Nutrition, 23, 467, 2004. 56. Anderson, A.D.G. et al., Randomised clinical trial of symbiotic therapy in elective surgical patients, Gut, 53, 241, 2004. 57. Lewis, S., Burmeister, S., and Brazier, J., Effect of the prebiotic oligofructose on relapse of Clostridium difficile-associated diarrhea: A randomized, controlled study, Clinical Gastroenterology and Hepathology, 3, 442, 2005. 58. Mcfarlaine, S. et al., Mucosal bacteria in ulcerative colitis, British Journal of Nutrition, 93, Suppl. 1, S67, 2005. 59. Furrie, E. et al., Synbiotic therapy (Bifidobacterium longum/Synergy1) initiates resolution of inflammation in patient with active ulcerative colitis: A randomised controlled pilot trial, Gut, 54, 242, 2005. 60. Lindsay, J.O. et al., Clinical, microbiological, and immunological effects of fructo-oligosaccharide in patients with Crohn’s disease, Gut, 55, 348, 2006. 61. Welters, C.F.M. et al., Effect of dietary inulin supplementation on inflammation of pouch mucosa in patients with an ileal pouch-anal anastomosis, Dis Colon Rectum, 45, 621, 2005. 62. Beringer, A. and Wenger, R., Inulin in der Ernährung des Diabetikers, Deutsch. Zeitschr. f. Verdauungs-u. Stoffwechselkrankh., 15, 268, 1955. 63. Lewis, H.B., The value of inulin as a foodstuff, J. Am. Med. Ass. 58, 176, 1912. 64. Persia, Reference of Lewis (1912), Nuova Revista Clin. Therapeut., 8, 1905. 65. Strauss, H., Zur Verwendung inulinreicher Gemüse bei Diabetikern, Therapie der Gegenwart III, 347, 1911. 66. Wise, E. and Heyl, F., Failure of a diabetic to utilize inulin, J. Am. Pharm. Soc., 20(1), 26, 1931. 67. Birch, G.G. and Soon, E.B.T., Composition and properties of diabetic jams, Confect. Prod., 39(2), 73, 1973. 68. Whelan, K. et al., Appetite during consumption of enteral formula as a sole source of nutrition: The effect of supplementing pea-fibre and fructo-oligosaccharides, British Journal of Nutrition, 96, 350, 2006. 69. Reddy, D.S., Hamid, R., and Rao, C.V., Effect of dietary oligofructose and inulin on colonic preneoplastic aberrant crypt foci inhibition, Carcinogenesis, 18(7), 1371, 1997. 70. Rowland, I.R. et al., Effects of Bifidobacterium longum and inulin on gut bacterial metabolism and carcinogen-induced aberrant crypt foci in rats, Carcinogenesis, 19(2), 281, 1998. 71. Taper, H., Delzenne, N., and Roberfroid, M.B., Growth inhibition of transplantable mouse tumors by non-digestible carbohydrates, Int. J. Cancer, 71, 1109, 1997. 72. Rafter, J. et al., Dietary synbiotics reduce cancer risk factors in polypectomized and colon cancer patients, American Journal of Clinical Nutrition, 85, 488, 2007.
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Fiber Ingredients: Food Applications and Health Benefits
73. Roberfroid, M.B., Cumps, J., and Devogelaer, J.P., Dietary chicory inulin increases whole-body bone mineral density in growing male rats, Journal of Nutrition, 132, 3599, 2002. 74. Scholz-Ahrens, K.E., Açil, Y., and Schrezenmeir, J., Effect of oligofructose or dietary calcium on repeated calcium and phosphorus balances, bone mineralization and trabecular structure in ovariectomized rats, British Journal of Nutrition, 88, 365, 2002. 75. Zafar, T.A. et al., Nondigestible oligosaccharides increase calcium absorption and suppress bone resorption in ovariectomized rats, Journal of Nutrition, 134, 399, 2004. 76. Coudray, C. et al., Effects of inulin-type fructans of different chain length and type of branching on intestinal absorption and balance of calcium and magnesium in rats, European Journal of Nutrition, 42, 91, 2003. 77. Bosscher, D., Van Loo, J., and Franck, A., Inulin and oligofructose—In the prevention of osteoporosis, Nutrafoods, 4, 69, 2005. 78. Coudray, C. et al., Effects of soluble or partly soluble dietary fibres supplementation on absorption and balance of calcium, magnesium, iron and zinc in healthy youg men, European Journal of Clinical Nutrition, 51(6), 375, 1997. 79. Van den Heuvel, E. et al., Oligofructose stimulates calcium absorption in adolescents, American Journal of Clinical Nutrition, 69, 544, 1999. 80. Griffin, I.J., Davila, P.M., and Abrams, S.A., Non-digestible oligosaccharides and calcium absorption in girls with adequate calcium intakes, British Journal of Nutrition, 87, Suppl. 2, S187, 2002. 81. Griffin, I.J. et al., Enriched chicory inulin increases calcium absorption mainly in girls with lower calcium absorption, Nutrition Research, 23, 901, 2003. 82. Abrams, S.A. et al., A combination of prebiotic short- and long-chain inulintype fructans enhances calcium absorption and bone mineralization in young adolescents, American Journal of Clinical Nutrition, 82, 471, 2005. 83. Absolonne, J. et al., Digestive acceptability of oligofructose, Proc. First ORAFTI Research Conference, Brussels, 151, 1995. 84. Franck, A. and Coussement, P., Multi-functional inulin, Food Ingredients and Analysis International, Oct., 8, 1997.
5 Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient Chieko Hashizume and Kazuhiro Okuma
Contents Introduction............................................................................................................ 61 What Is Resistant Maltodextrin?..........................................................................63 Physiological Effects of Resistant Maltodextrin................................................64 Gastrointestinal Functions..........................................................................64 Beneficial Effects on Bowel Movement..........................................65 Improvement in Intestinal Environments.....................................65 Attenuation of Postprandial Blood Glucose Levels................................. 69 Improvement in Sugar and Fat Metabolism by Repeated Ingestion—Decreases in Total Cholesterol and Triglyceride Levels............................................................................ 70 Decreases in Body Fat Ratio........................................................................ 71 Safety and Food Applications.............................................................................. 72 Safety ............................................................................................................. 72 Food Applications......................................................................................... 74 Measuring Method of Total Dietary Fiber in Foods Containing Resistant Maltodextrin................................................................................. 75 References...............................................................................................................77
Introduction Dietary fiber is considered an essential nutrient in Japan based on continued research showing the health benefits of daily consumption along with the essential amino acids, essential fatty acids, vitamins, and minerals. The functions of dietary fiber are essential and of equal importance to the benefits of other essential nutrients. The beneficial effects of diets rich in dietary fiber include decreased risk of coronary heart disease and improvement in 61
62
Fiber Ingredients: Food Applications and Health Benefits 40 35
Adequate Intake
25 20 15
+ 71
–7 0 51
–5 0 31
–1 8 14
9– 13
4– 8
0
1– 3
5
Actual Intake
–3 0
Actual I for males Actual I for females Adequate I for males Adequate I for females
10
19
DF Intake (g/day)
30
(Age, years old) Figure 5.1 Dietary fiber intake of U.S. population: the gap between the actual intake and the adequate intake (AI). : actual intake amount of dietary fiber for males, : actual intake amount of dietary fiber for females, : adequate intake amount of dietary fiber suggested for males, : adequate intake amount of dietary fiber suggested for females. (Adapted from Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients), Food and Nutrition Board, Institute of Medicine, National Academies, 2005.)
intestinal regularity. The research behind a possible relationship between fiber-rich diets and a lower risk of type 2 diabetes shows potential. Although the importance of dietary fiber is well recognized, the actual intake of dietary fiber is declining. The Dietary Guidelines for Americans (2005) attributes this decline in dietary fiber intake to a lower consumption of whole grain foods, fruits, and vegetables. The problem is compounded by the lack of many foods that contain whole grains. While the recommended dietary fiber intake for Americans is 14 grams per 1000 calories (approximately 38 and 25 grams per day for men and women respectively), the average dietary fiber intake among Americans is only about half these recommended amounts (Figure 5.1). Dietary fiber consumption among almost all industrialized countries is less than 20 grams per day. Changes in lifestyles, especially the increasing habit of eating processed foods or ready-to-eat meals, are also a contributing factor for the lower dietary fiber intake than the recommended intake. In order to increase the consumption of dietary fiber and fill the gap between the current intake and the recommended intake, it appears prudent to add more dietary fiber to processed foods. Japanese scientists have developed various types of low-molecular-weight soluble dietary fibers and oligosaccharides to fill the fiber gap. One outstanding fiber product is Fibersol®-2, a resistant maltodextrin product developed and registered by Matsutani Chemical Industry Co., Ltd., Itami, Hyogo,
Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient
63
Japan. The resistant maltodextrin has the following physiological properties associated with dietary fiber: (1) improvement of intestinal regularity; (2) moderation of postprandial blood glucose levels; and (3) the reduction of serum cholesterol and triglyceride levels.
What Is Resistant Maltodextrin? Fibersol®-2 is prepared from moistened Starch (corn, etc.) starch (corn, tapioca, etc.) by heating to 140ºC –160ºC with a trace amount of acid Dextrinization with acid at 140–160°C (Moistened powdery starch) (Figure 5.2). During this most characteristic stage in the production process, Hydrolysis with amylases both hydrolysis and transglucosidation of Removal of glucose by filtration starch occur (dextrinization process). The resulting dextrin solution is hydrolyzed Decolorization by active carbon by enzymes, before being refined by filDeionization by ion-exchange resin tration through activated carbon and an ion-exchange resin. After concentration, Concentration and spray-drying the non-digestible material is spray-dried. Weighing and packaging The final product is stable to any further hydrolysis by heat, acid, and/or enzymes, Resistant Maltodextrin Product including the conditions found in the human digestive system. These proper- Figure 5.2 ties greatly contribute to its functionality Manufacturing process of resistant and acceptance in food systems and food maltodextrins. products. The resistant maltodextrin consists of a small ratio of saccharides that have the degree of polymerization (DP) 1–9, and a large amount of polysaccharides with a DP 10 or more. It has a typical carbohydrate composition of ~10 DE maltodextrin, with the average molecular weight of 2000. In 1990, the Matsutani Company obtained a letter of compliance from the U.S. Food and Drug Administration confirming that Fibersol®-2 meets the requirements for the GRAS status set forth in 21 CFR 184.1444 Maltodextrin. Therefore, it is officially recognized as a maltodextrin under the U.S. regulation. The glucosidic linkages and the molecular structure model of the resistant maltodextrin are illustrated in Figure 5.3. The resistant maltodextrin has a higher amount of 1-6 linkage than conventional maltodextrin of the same DE. Resistant maltodextrin not only has 1-4 and 1-6 linkages that are found in starch, but also contains 1-2 and 1-3 linkages, which are formed during the dextrinization process. The properties described above contribute to allow resistant maltodextrin to be approximately 10% digested and absorbed in the small intestine. Approximately 50% is fermented in the large intestine and the remaining approximate
64
Fiber Ingredients: Food Applications and Health Benefits
O
HO
CH2OH O OH
CH2OH OH O OH O OH
O
HO
CH2OH O OH OCH2 O OH
HO
CH2 OH
O
OH CH2OH O OH OH
OH
O O
OH CH2OH O OH
CH2OH O OH OH CH2OH O OH
O OH CH2OH CH2OH O O O OH OH O O OH OH O
O
O
CH2OH O OH
CH2O
O
O OH CH2OH O O OH
OH
OH
®
Chemical structure model of Fibersol -2 Glucosidic linkage
1
4
1
6
1
2
1
3
Conventional maltodextrin -Enzymatic hydrolysis
94.7%
4.5%
0.0%
0.9%
-Acidic hydrolysis
91.6%
5.1%
1.2%
2.2%
58.5%
27.0%
3.2%
11.3%
®
Fibersol -2
Figure 5.3 Structural characteristics of resistant maltodextrin: comparison with conventional maltodextrins prepared by enzymatic or acid hydrolysis. (Adapted from Okuma, K. and Matsuda, I., J. Appl. Glycosci., 49, 479–485, 2002.)
40% is excreted into the feces [1]. Therefore, the maltodextrin is distinguished from conventional digestible maltodextrin and the scientific categorization as “digestion-resistant maltodextrin” or “indigestible dextrin.”
Physiological Effects of Resistant Maltodextrin Gastrointestinal Functions As 90% of the resistant maltodextrin reaches the large intestine and 50% is fermented, these findings support and contribute to its physiological effects in the large intestine. The beneficial effects of Fibersol®-2 as a typical soluble dietary fiber are summarized in the following.
Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient
65
Table 5.1 Improvement of Stool Conditions by Resistant Maltodextrin
Test Group (n = 8) Control (n = 8)
Stool Wet Weight (g)
Stool Dry Weight (g)
Moisture (%)
Defecation Frequencies (n)
778.2 ± 93.2*
180.5 ± 12.9*
76.8 ± 1.8
5.92 ± 0.40a
571.5 ± 58.7
137.9 ± 5.6
76.2 ± 1.7
4.76 ± 0.36
Note: Test group was administered a resistant maltodextrin product (dietary fiber content: 20 g per day). A crossover study. Eight healthy male subjects were administrated controlled meals through the 5-day study period with or without the resistant maltodextrin. Whole stools were collected between the first defecation of a red color indicator taken on the 1st day and the next defecation of the indicator taken on the 5th (last) day. a Significantly different at p <0.05. Source: Satouchi, M. et al., Effects of indigestible dextrine on bowel movements, Japanese J. Nutrition. 51, 31-37, 1993.
Beneficial Effects on Bowel Movement The effect of the resistant maltodextrin on bowel regularity was confirmed in a crossover ingestion study with eight male subjects [2]. During the fiveday study, the subjects were administrated standard meals with a resistant maltodextrin product (dietary fiber content: 20 grams per day) (FS-2 group) and their fecal weight and fecal frequencies were compared with the data obtained by consuming the same controlled meals without resistant maltodextrin (the control group). The FS-2 group had significantly more bowel movements compared to the control group (Table 5.1). The average total fecal weight for the period was significantly higher in the FS-2 group, 778.2 ± 93.2 g compared with 571.5 ± 58.7 g for the control group (p < 0.05); fecal moisture content was not changed in either group. From these results, it was confirmed that resistant maltodextrin is effective to improve bowel regularity, which is one of the important physiological properties consistent with dietary fiber. As suggested from the fecal moisture content, resistant maltodextrin did not cause diarrhea. Improvement in Intestinal Environments Prebiotic Effect: Improvement of Intestinal Microflora The in vitro fermentability of Fibersol®-2 was evaluated with stock strains of human intestinal bacteria (Table 5.2) [3]. It was well fermented by major strains of Bifidobacterium and Bacteroides. The degree of fermentation by Bacteroide organisms was comparable or slightly inferior to that of glucose. In an in vivo test with six healthy male subjects who ingested 10 grams of the resistant maltodextrin with every meal for four weeks, the changes in the
66
Fiber Ingredients: Food Applications and Health Benefits Table 5.2 Fermentability of the Resistant Maltodextrin by Various Intestinal Bacteria Strains Bacteroides B. vulgatus ATCC 848 B. thetaiotaomicron ATCC 12552 B. fragilis NCTC 9343 B. ovatus VPI 10649 B. distasonis VPI 4243 Eubacterium E. aerofaciens VPI 1003 E. biforme VPI 9218 Peptostreptococcus P. productus YIT 0192 Clostridium C. perfringens PB 6 K C. paraputrificum ATCC 25870 C. bifermentans NCTC 506 Staphlococcus S. aureus 209 P Enterobacteriaceae E. coli H-1 K. pneumoniae H-2 E. cloacae H-3 Streptococcus S. thermophilus YIT 2001 S. faecium YIT 2004 Lactobacillus L. gasseri YIT 0192 L. acidophilus YIT 0070 L. salivarius YIT 0089 L. fermentum YTT 0081 L. bulgaricus YTT 0098 L. helveticus YTT 0100 L. plantarum YTT 0101 L. casei YTT 9018 Bifidobacterium B. bifidum 4007 B. bifidum E 319 B. infantis S-12 B. breve YIT 4010 B. breve S-1 B. breve As-50 B. longum 194 b B. longum H-1 B. adolescentis 194 a B. adolescentis YJ-9 Fusobacterium F. varium ATCC 8501 Propionibacterium P. acnes ATCC 6919
Fermentability ± + + ++ ++ – – ++ – – – – – – – – ± – – – – – – – – – – – ± ± ± ± ± – ++ – –
Note: Acid production: +++, within 1 day; ++, 2 days; +, 3 days. ± ~ –: negative. Source: Adapted from Ohkuma, K. et al., Pyrolysis of Starch and Its Digestibility by Enzymes, Denpun Kagaku, 37, 104–114, 1990.
Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient
67
Table 5.3 Changes in the Ratios of Bifidobacterium and Bacteroides in Total Colon Bacteria (%) among Six Healthy Male Subjects Consuming 30 g of the Resistant Maltodextrin per Day (10 g per meal) for Four Weeks. Bacteria
Baseline
After 4 weeks
After 8 weeksa
Bacteroides Bifidobacterium Others
49.4 ± 6.0 10.5 ± 3.4 40.1 ± 4.2
43.2 ± 2.5 17.9 ± 2.7 38.9 ± 2.5
49.8 ± 3.9 13.7 ± 1.9 36.5 ± 2.9
a
Second measurement made four weeks after consumption of resistant maltodextrin was stopped.
intestinal microflora counts (log number of colony-forming unit per gram of feces) were examined, and the ratios of Bacteroides and Bifidobacterium in percentages are reported in Table 5.3. Although the number of subjects in this study was rather small, a significant change in the intestinal microflora was observed after one month of consuming the resistant maltodextrin on a daily basis. While the population of Bifidobacterium organisms increased, the level of Bacteroides organisms and other non-specified organisms decreased. Production of Short-Chain Fatty Acids Saccharides that are resistant to digestion and reach the large intestine are fermented by intestinal bacteria, producing short-chain fatty acids (SCFA) and gases. The SCFA are considered to have the following properties in the large intestine: anti-inflammatory; a specific energy source for intestinal mucosal cell to promote cell growth, primarily butyric acid; aiding in water movement across the large intestine; and interfering with bile acid reabsorption thus lowering blood cholesterol levels. An in vitro experiment using human feces to ferment resistant maltodextrin was used to illustrate the potential changes in SCFA and pH values in the colon (Figure 5.4) [4]. Three sources of dietary fiber were incubated under anaerobic conditions with fecal samples taken just after defecation. The formation of SCFA and changes in pH were observed over a 24-hour period. Fructooligosaccharide is known to be completely fermented. The fermentation of resistant maltodextrin and FOS, as measured by the production of SCFA, was similar over the first 1.5 hours. After 6 hours, the fermentation of FOS was basically complete, but the fermentation of resistant maltodextrin was only 56% of that observed for FOS. While it took the complete 24 hours to ferment the gum arabic to achieve SCFA levels equivalent to that observed with FOS, the amount of SCFA resulting from the fermentation of resistant maltodextrin was only approximately 75%. This lower level of SCFA production of resistant maltodextrin compared to the fermentation of equal amounts of FOS and gum arabic attribute to the fact that not all resistant maltodextrin is fermented in the large intestine after ingestion (Figure 5.4). This in vitro experiment helps support the concept that resistant maltodex-
68
Fiber Ingredients: Food Applications and Health Benefits
FOS: Fructo Oligo Saccharide MD: Fibersol-2 GA: Gum Arabic SCFA Production
7.0
pH
Time (hr) 1.5 6 11 24
Total SCFA (mmol/g) FOS MD GA 1.08 1.02 0.06 7.12 3.20 0.30 7.26 4.08 1.42 7.66 6.01 8.08
FOS RMD GA
6.5 6.0 5.5
0
6
12
18
24
Time (hr) pH Value Changes
Figure 5.4 Total short-chain fatty acids accumulation and changes in pH values by in vitro fermentation with human feces. 1 ml of diluted human feces (1:10 wt/v) was incubated with 75 mg of each substrate in 9 ml of buffer. FOS (): fructooligosaccharides, MD (): resistant maltodextrin, GA (): gum arabic. (Adapted from Flickinger, E. A., Wolf, B. W., Garleb, K. A., Chow, J., Leyer, G., J., John, P. W., and Fahey, G. C., J. Nutr. 130, 1267–1273, 2000.)
trin is both effective in aiding laxation and serves as an energy source for intestinal bacteria, a prebiotic. The rapid fermentation of resistant maltodextrin observed at the start of the incubation indicates that the low-molecularweight fraction of resistant maltodextrin can be easily utilized by a variety of bacteria in the large intestine. Maintenance of Digestive Tract Functions When a non-residual, completely digested and absorbed enteral feeding system is administrated for a long period of time, the patient can suffer from gastrointestinal malfunctions such as diarrhea, constipation, or abdominal distention, all caused by lack of dietary fiber. During these extended periods of non-residual enteral nutrition, the intestine will lose its normal physiological functions and significantly reduce its absorptive surface area, mainly the reduction in size of the intestinal villi. The intestine will begin to atrophy. The favorable effect of the resistant maltodextrin when added to a non-residual enteral formula was evaluated in a two-week feeding study in rats. An enteral nutrition formula was fortified with or without 1.4% Fibersol®-2, while stock diet was fed to a third group of rats as the control. Distinct morphological changes were observed in jejunal mucosal microvilli with the microscope. More regularly spaced and orientated microvilli were observed in the jejunal sections of rats’ intestines fed the stock diet and enteral formula with resistant maltodextrin compared to that fed the non-residual enteral formula without resistant maltodextrin (Figure 5.5). Although not evaluated in this study, the production of SCFA through the fermentation of fermentable carbohydrates is considered to help maintain the structure and physiological functions of small intestinal mucosa [5]. These are examples of
Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient
Control (Stock Diet)
Enteral Formula (no fiber)
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Enteral Formula with 1.4% Fibersol -2
®
Figure 5.5 Micrograph of jejunal mucosal microvilli of rats fed on each diet for two weeks. (From Ohkuma, K., and Wakabayashi, S., Fibersol-2: a soluble, non-digestible, starch-derived dietary fibre, Advanced Dietary Fibre Technology, McCleary, B.V., and Prosky, L., Eds., Blackwell Science, Oxford, UK, 509–523, 2001.)
events occurring in the intestine that help maintain it by impacting primary and secondary nutritional aspects. Attenuation of Postprandial Blood Glucose Levels In a rat study in which these animals were fed digestible disaccharides and larger (DP≥2), the addition of Fibersol®-2 to their diet suppressed the postprandial rise in blood glucose and insulin levels. However, the resistant maltodextrin was not effective to attenuate postprandial blood glucose and insulin levels when rats were fed glucose or fructose, such as monosaccharides [6]. The effects of feeding a single meal with Fibersol®-2 are reported by Tokunaga and Matsuoka as illustrated in Figure 5.6 [7]. The subjects consumed a meal of wheat noodles and steamed rice with a tea beverage containing 5 g of Fibersol®-2 and were monitored for postprandial blood glucose levels. In Figure 5.6a, which shows the average of all subjects, the peak blood glucose levels (at 30 and 60 min) were significantly lower among subjects consuming the resistant maltodextrin compared to subjects not consuming resistant maltodextrin with their meal. The subjects were further classified into two groups based on the magnitude of the postprandial blood glucose responses. One group of subjects having the higher (Figure 5.6b) postprandial peak blood glucose levels than the average was compared to subjects having the lower postprandial peak blood glucose levels than the average (Figure 5.6c). In the group of subjects having high postprandial blood glucose levels, their attenuation in postprandial blood glucose levels was significantly (p<0.01) more pronounced and therefore more beneficial with consumption of resistant maltodextrin (Figure 5.6b), compared to the attenuation observed in the subjects with lower postprandial blood glucose levels (Figure 5.6c). Consumption of 5 grams of resistant maltodextrin alone to fasting individuals caused no change in their postprandial blood glucose levels (Figure 5.6d),
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Fiber Ingredients: Food Applications and Health Benefits
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Time (hour) Figure 5.6 Effects of tea beverage containing the resistant maltodextrin on postprandial blood glucose (BG) levels when loaded a standard-meal (mean value). : standard meal + 340 g green tea (control), : standard meal + test drink (340 g tea beverage containing Fibersol®-2). a: Mean BG curve of 40 subjects, b: Mean BG curve of 18 in 40 subjects whose peak BG levels were higher than the mean value (172 mg/dl) with standard meal + green tea loading, c: Mean BG curve of 22 in 40 subjects whose peak BG levels were <172 mg/dl, d: Mean BG curve of 6 subjects with 340 g test drink alone loading. *: p<0.05, **: p<0.01. (Tokunaga, K., and Matsuoka, J. Japan Diabetes Society, 42, 61–65, 1999.)
indicating that the resistant maltodextrin has no contribution to hypoglycemia or hyperglycemia. The attenuation of postprandial blood glucose achieved with the consumption of resistant maltodextrin has been verified in other meal-loading experiments [8–11]; as part of the evidential studies for approving the Japanese Foods for Specified Health Use (FOSHU) products, more than 30 clinical studies have been reported on the meal-loading effect of Fibersol®-2 on blood glucose attenuations. Improvement in Sugar and Fat Metabolism by Repeated Ingestion— Decreases in Total Cholesterol and Triglyceride Levels Long-term feeding studies in rats and humans fed Fibersol®-2 have demonstrated decreases in total cholesterol and triglyceride levels [12–14]. In rat studies, these animals were fed diets high in sucrose without cholesterol and their serum lipids were monitored. Total serum cholesterol and triglyceride levels were found to be significantly decreased with the administration of resistant maltodextrin [13–14]. Five patients having non-insulin-dependent diabetes mellitus (NIDDM) accompanied with hyperlipidemia were given 20 grams of Fibersol®-2 per meal for three months. Changes in blood parameters over the 12-week period among these individuals are reported in Table 5.4. At the start of the experiment, fasting blood glucose levels, total cholesterol levels, and triglyceride levels were above normal ranges. However, after 12 weeks, significant reduc-
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Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient Table 5.4 Effects of Resistant Maltodextrin (20 g per meal) on Serum Lipid and Plasma Glucose Levels, Erythrocyte counts, and Liver Function in NIDDM Patients (n = 5) with Hyperlipidemia. Time (week) FPG (mg/dl) Cholesterol (mg/dl) HDL-Cholesterol (mg/dl) Triglyceride (mg/dl) Ca (meq/l) Mg (mg/dl) P (mg/dl) Fe (μg/dl) RBC (×104/mm3) GOT (IU/l) GPT (IU/l) γ-GTP (IU/l) LDH (IU/l)
0
2
4
8
12
147 ± 17 265 ± 10 49 ± 2 243 ± 34 4.5 ± 0.3 2.0 ± 0.2 3.0 ± 0.2 96 ± 43 488 ± 31 22 ± 10 22 ± 5 69 ± 38 293 ± 36
112 ± 25 211 ± 29 45 ± 1 163 ± 33 4.3 ± 0.3 2.0 ± 0.2 3.3 ± 0.4 98 ± 29 — — — — —
107 ± 7 209 ± 22a 47 ± 3 134 ± 24a 4.5 ± 0.2 2.0 ± 0.2 3.3 ± 0.5 99 ± 18 — — — — —
147 ± 21 205 ± 10b 49 ± 3 148 ± 11a 4.5 ± 0.2 2.0 ± 0.2 3.2 ± 0.4 97 ± 16 — — — — —
103 ± 7a 209 ± 9b 40 ± 3b 176 ± 42 4.5 ± 0.2 2.0 ± 0.1 3.4 ± 0.3 88 ± 14 488 ± 14 19 ± 4 19 ± 4 63 ± 54 311 ± 95
Note: FPG: fasting plasma glucose, RBC: Erythrocyte count. Mean±SD, statistical significance: a p<0.05, b p<0.01 compared with data at 0 week. Source: Nomura, M., Nakajima, Y., and Abe, H., J. Jpn. Soc. Nutr. Food Sci., 45, 21-25, 1992.
tions in blood glucose and cholesterol levels were observed (Table 5.4). Blood triglyceride levels decreased by 28%, but this decrease was not significant [15]. In another placebo-controlled double-blind study, subjects were given a tea beverage with 5 grams of the resistant maltodextrin or a placebo (without resistant maltodextrin) three times a day for four weeks. Triglyceride levels were significantly reduced (p<0.05) after consumption of the tea containing resistant maltodextrin (Figure 5.7) [16]. Triglyceride levels generally returned to starting levels after subjects stopped consuming the resistant maltodextrin. It can be assumed that the long-term regulation or attenuation in postprandial blood glucose and insulin levels by consuming the resistant maltodextrin with every meal affects these chronic triglyceride and total cholesterol levels. Decreases in Body Fat Ratio It has been reported that the intake of a tea beverage containing 5 grams resistant maltodextrin with every meal for four weeks significantly lowered body weight, BMI, body fat ratio, and waist/hip ratio [16]. Similar results were observed in a study among 12 adult male subjects. They consumed 10 grams of resistant maltodextrin per meal for three months. At the start and upon termination of the three-month test period, glucose tolerance tests
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Fiber Ingredients: Food Applications and Health Benefits 60
∆ Triglyceride (mg/dl)
40
Test group Placebo group
20 0
*
–20 –40 –60 –80
** Administration Period Before Before Pre-administration Administration
*p < 0.026 (t-test) **p < 0.003 (paired t-test)
After After Administration Post-administration
Figure 5.7 Changes in serum triglyceride levels by four-week ingestion of the resistant maltodextrin. : test group, 250 ml of tea beverage containing 5 g Fibersol®-2, : placebo group, 250 ml of placebo tea beverage. Three times (every meal) per day ingestion for four weeks. Mean±SEM. (From Kajimoto, O. et al., J. Nutritional Food, 3 (3), 47–58, 2000.)
were assessed and blood chemical parameters were measured. Body fat was also measured by impedance, and the area for visceral fat and subcutaneous fat were measured by computed tomography (CT) scans [17]. Results of this experiment are reported in Figure 5.8. Glucose tolerance, body fat ratios, and visceral fat areas were significantly decreased by the ingestion of the resistant maltodextrin. Two indices of insulin resistance, total immunoreactive insulin (Σ IRI) and homeostasis model assessment insulin resistance index (HOMA-IR), were also decreased after consumption of resistant maltodextrin. It is assumed that resistant maltodextrin prevents the accumulation of fat (obesity) by moderating the postprandial rise in blood glucose and insulin levels, which would be a similar, but still unexplained mechanism(s) to decrease serum total cholesterol and triglyceride levels.
Safety and Food Applications Safety Fibersol®-2 has been approved as a Generally Recognized As Safe (GRAS) material, manufactured by enzymatic hydrolysis of pyrodextrin. Its safety was reviewed and authorized by the FDA in 1990 and it is classified as a
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Physiological Examination Before Intake (start) 3-Month Intake Age (years old) 46.1 ± 3.0 Height (cm) 168.8 ± 1.3 73.0 ± 3.3 Body Weight (kg) 73.7 ± 3.4 25.6 ± 0.9 BMI 25.8 ± 0.9 25.9 ± 1.0* 27.7 ± 0.9 Body Fat (%) 89.5 ± 2.3 90.8 ± 2.4 Waist (cm) 98.3 ± 2.1 98.8 ± 2.1 Hip (cm) 0.91 ± 0.01 0.91 ± 0.01 W/H 101.9 ± 11 .6 108.0 ± 13.7 V: Area for Visceral Fat (cm2) 163.9 ± 19.9 175.2 ± 25.2 S: Area for Subcutaneous Fat (cm2) 0.64 ± 0.07 0.70 ± 0.1 V/S “n = 12, average ± SEM” “n = 9, only for V, S, V/S values” *: Pair-matching t-test, significantly different from initial values at p < 0.05.
Glucose Tolerance Blood glucose levels
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“n = 10, average ± SEM” *: Pair-matching t-test, significantly different from initial values at p < 0.05. **: Significantly different from initial values at p < 0.01. Figure 5.8 Changes in physical examination and glucose tolerance by three-month ingestion of the resistant maltodextrin. 10 grams, 3 times (every meal) per day (= 30 grams) of resistant maltodextrin was administrated for 3 months. Graphs of glucose tolerance test. Left: blood glucose levels, right: insulin levels. : glucose or insulin response at the start time, : glucose or insulin response after three-month administration of resistant maltodextrin. (From Kishimoto, Y., Wakabayashi, S., and Tokunaga, K., J. Jpn. Assoc. Dietary Fiber Res., 4 (2), 59–65, 2000.)
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maltodextrin (21 CFR §184.1444). Safety studies have been accomplished on the potential consumption of high levels of the resistant maltodextrin. The lethal dose (LD50) determined in a rat feeding experiment was over 40 g/kg body weight, the maximum dosage in the acute toxicity study. There is no evidence of any mutagenicity caused by the consumption of the resistant maltodextrin [18]. Dietary fiber has been reported to inhibit the absorption of essential microelements. However, resistant maltodextrin was found to have no binding capacity for mineral ions when evaluated in an in vitro experiment [19]. A study in which rats were fed water containing 10% resistant maltodextrin for five weeks, showed no harmful effects on internal organs such as the pancreas, kidneys, and liver, including functional indices [13]. The effects of large intakes of resistant maltodextrin on gastrointestinal responses and fecal parameters were evaluated in a study that used 74 healthy adult subjects. Subjects were given a single dose of the resistant maltodextrin ranging from 10 to 60 grams. This particular resistant maltodextrin product contained 58% dietary fiber. Feeding these varied amounts of resistant maltodextrin to these subjects did not cause any clinical or problematic gastrointestinal symptoms. The ED50 (effective dose 50, the amount of material required to produce a specified effect in 50% of an animal population) to cause diarrhea was estimated to be more than 110 grams of a product containing 58% total dietary fiber (63 grams for a 100% dietary fiber product) [20]. Resistant maltodextrin would have less tendency to cause diarrhea compared to sugar alcohols or other totally fermentable oligosaccharides because it has a higher molecular weight than these materials, and approximately 40% is passed to the feces after consumption. Food Applications Resistant maltodextrin is a very user-friendly dietary fiber because of its low viscosity and its tasteless and flavorless characteristics, in addition to high stability in heat and acid; it can be added easily into any type of foods in the same manner as sugar or salt. Before such user-friendly dietary fiber was developed, the fiber sources used to fortify processed food products would have been cereals, vegetable, fruits, etc. In place of such ingredients, resistant maltodextrin can be added to any processed foods as a source of dietary fiber to enable the producers to make dietary fiber fortification claims such as “Rich in fiber” or “Good source of dietary fiber” without compromising quality characteristics of the fortified products. The Japanese Ministry of Health, Labor and Welfare has an approval program called Tokuho, Food for Specified Health Use (FOSHU), in which the approved products are allowed authorized claims, such as “Improves intestinal regularity” or “Beneficial for those concerned about blood glucose
Fibersol®-2 Resistant Maltodextrin: Functional Dietary Fiber Ingredient
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levels.” Numerous FOSHU products with Fibersol®-2 as the effective key ingredient have been introduced into the marketplace. Resistant maltodextrin is also used in low-calorie foods. When added with high-intensive sweeteners such as aspartame, sucralose, stevia, or acesulfame K, resistant maltodextrin provides significant body and texture to achieve a highly desirable sweetness with no harsh aftertaste. The caloric value for Fibersol®-2 is considered ~1.0 kcal/g [1, 21, 22].
Measuring Method of Total Dietary Fiber in Foods Containing Resistant Maltodextrin Although resistant maltodextrin functions fully as dietary fiber, it is necessary to determine its actual dietary fiber content for the purpose of nutrition labeling. The total dietary fiber value of resistant maltodextrin is not accurately determined by AOAC Official Method 985.29, in which the soluble dietary fiber components are precipitated in 78% ethanol. Therefore, an analytical method was developed to accurately measure the total dietary fiber content in foods containing resistant maltodextrin (Figure 5.9). This method has been approved through AOAC collaborative study, and has received Final Action approval as AOAC Official Method 2001.03 [23]. This method is applicable for nutrition labeling. As the first step, insoluble and high-molecular-weight soluble dietary fiber components are measured by AOAC Official Method 985.29. The material is treated with enzymes, four volumes of ethanol, and the residue and the filtrate are separated. The salts and protein remaining in the filtrate after the AOAC Official Method 985.29 protocol employed are removed by ion-exchange resins. The deionized filtrate is analyzed by high-performance liquid chromatography analysis to determine the low-molecular-weight soluble dietary fiber that does not precipitate in 78% ethanol. The amount of total dietary fiber is calculated by summing the insoluble and high-molecular-weight soluble dietary fiber with the low-molecular-weight soluble dietary fiber.
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Fiber Ingredients: Food Applications and Health Benefits (Enzymatic-Gravimetric Method) 1.0 g Sample 0.08 M Phosphate buffer, pH 6.0 α-amylase 95°C, 30 min pH 7.5 ± 0.1
Protease 60°C, 30 min pH 4.5 ± 0.2
Amyloglucosidase 60°C, 30 min 4 vol. 95% EtOH Filtration Washing
78% EtOH×3 95%EtOH×2 Aceton×2
(LC determination) Filtrate
Residue Ash and Protein Correction IDF + HMWSDF
Evaporation
Washing out the concentrate inside the flask by using deionized water and pipetts several times Glycerol solution Desalting Evaporation Adjusting vol. HPLC LMW RMD
Figure 5.9 Flow diagram for analytical procedure of the AOAC Official Method 2001.03, dietary fiber in foods containing resistant maltodextrin, high MW RMD by 985.29 (IDF and SDF) and low MW RMD by liquid chromatography. (From Official Methods of Analysis, 18th ed., AOAC International, 2006.)
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References
1. Tsuji, K. and Gordon, D. T., Energy value of a mixed glycosidic linked dextrin determined in rats, J. Agr. Food Chem., 46, 2253–2259, 1998. 2. Satouchi, M. et al., Effects of indigestible dextrin on bowel movements, Japanese J. Nutrition, 51, 31–37, 1993 (in Japanese). 3. Ohkuma, K. et al., Pyrolysis of starch and its digestibility by enzymes, Denpun Kagaku, 37, 104–114, 1990 (in Japanese). 4. Flickinger, E. et al., Glucose-based oligosaccharides exhibit different in vitro fermentation patterns and affect in vivo apparent nutrient digestibility and microbial populations in dogs, J. Nutr., 130, 1267–1273, 2000. 5. Vahouny, G. V. and Cassidy, M. M., Dietary fiber and intestinal adaptation, in Dietary Fiber: Basic and Clinical Aspects, Vahouny, G. V. and Kritchevsky, D., Eds., Plenum Press, New York, 1986, pp. 181–209. 6. Wakabayashi, S., Ueda, Y., and Matsuoka, A., Effects of indigestible dextrin on blood glucose and insulin levels after various sugar loads in rats, J. Jpn. Soc. Nutr. Food Sci., 46, 131–137, 1993 (in Japanese). 7. Tokunaga, K. and Matsuoka, A., Effects of a Food for Specified Health Use (FOSHU) which contains indigestible dextrin as an effective ingredient on glucose and lipid metabolism. J. Japan Diabetes Society, 42, 61–65, 1999 (in Japanese). 8. Kishimoto, T., Wakabayashi, S., and Yuba, K., Effects of instant miso-soup containing indigestible dextrin on moderating the rise of postprandial blood glucose levels, and safety of long-term administration, J. Nutritional Food, 3(2), 19–27, 2000 (in Japanese). 9. Inoue, T. et al., Attenuation effect of bread containing indigestible dextrin on elevation of postprandial blood glucose level and its safety in long-term ingestion, J. Jpn. Clin. Nutr., 26(4), 281–286, 2005 (in Japanese). 10. Morita, H., et al., Effect of yogurt containing indigestible dextrin on blood glucose and other blood components, J. Jpn. Council for Advanced Food Ingredients Res., 8(1), 33–42, 2005 (in Japanese). 11. Moriguchi, S., et al., The suppressive effect of the intake of beverage containing indigestible dextrin on the rise of postprandial blood glucose level, J. Jpn. Council for Advanced Food Ingredients Res., 7 (1), 63–67, 2004 (in Japanese). 12. Kishimoto, Y., Wakabayashi, S., and Takeda, H., Hypocholesterolemic effect of dietary fiber: Relation to intestinal fermentation and bile acid excretion, J. Nutr. Sci. Vitaminol., 41, 151–161, 1995. 13. Wakabayashi, S. et al., Effect of indigestible dextrin on cholesterol metabolism in rat, J. Jpn. Soc. Nutr. Food Sci., 44, 471–478, 1991 (in Japanese). 14. Wakabayashi, S. and Kishimoto, Y., The effects of indigestible dextrin on glucose tolerance (part VI), effects of continuous administration in WBN/Kob rat, a model of spontaneous diabetes, J. Jpn. Assoc. Dietary Fiber Res., 5(1), 33–40, 2001 (in Japanese). 15. Nomura, M., Nakajima, Y., and Abe, H., Effects of long-term administration of indigestible dextrin as soluble dietary fiber on lipid and glucose metabolism, J. Jpn. Soc. Nutr. Food Sci., 45, 21–25, 1992 (in Japanese).
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16. Kajimoto, O. et al., Beneficial effects of a new indigestible dextrin-containing beverage on lipid metabolism and obesity-related parameters, J. Nutritional Food, 3(3), 47-58, 2000 (in Japanese). 17. Kishimoto, Y., Wakabayashi, S., and Tokunaga, K., Effects of long-term administration of indigestible dextrin on visceral fat accumulation, J. Jpn. Assoc. Dietary Fiber Res., 4(2), 59–65, 2000 (in Japanese). 18. Wakabayashi, S. et al., Acute toxicity and mutagenicity studies of indigestible dextrin, and its effect on bowel movement of the rat, J. Food Hyg. Soc. Japan, 33, 557–562, 1992 (in Japanese). 19. Nomura, M. et al., Effect of dietary fibers on the diffusion of glucose and metal ions through cellulose membrane, J. Jpn. Soc. Clin. Nutr., 13, 141–147, 1992 (in Japanese). 20. Satouchi, M. et al., Effects of indigestible dextrine on bowel movements, Jpn. J. Nutr., 51, 31–37, 1993 (in Japanese). 21. Goda, T. et al., Availability, fermentability, and energy value of resistant maltodextrin: Modeling of short-term indirect calorimetric measurements in healthy adults, Am. J. Clin. Nutr., 83, 1321–1330, 2006. 22. Nakamura, S. and Oku, T., Evaluation of available energy of several dietary fiber materials based on the fermentability from breath hydrogen excretion in healthy human subjects. J. Jpn. Assoc. Dietary Fiber Res., 9, 1, 34–45, 2005. 23. Okuma, K. and Gordon, D. T., Determination of total dietary fiber in selected foods containing resistant maltodextrin by enzymatic-gravimetric method and liquid chromatography: Collaborative study, J. AOAC Int., 85, 435–444, 2002.
6 Partially Hydrolyzed Guar Gum Dietary Fiber Mahendra P. Kapoor and Lekh R. Juneja
Contents Introduction............................................................................................................80 Dietary Gums................................................................................................80 Guar Gum...................................................................................................... 81 Partially Hydrolyzed Guar Gum (PHGG; SunFiber®)...................................... 82 Guar Gum Processing into PHGG.............................................................83 Physicochemical Properties and Food Grade Specifications of PHGG.............................................................................................85 Physiological and Metabolic Functions of PHGG.............................................85 Improvement in Acute Postprandial Glycemic Responses and Insulin Response............................................................................... 86 Impact on Blood Cholesterol Concentration............................................. 88 Effect of PHGG on Laxation Improvements.............................................90 Improvement in Intestinal Microflora Balance and Prebiotic Effects................................................................................................. 94 Effectiveness in Irritable Bowel Syndrome (IBS)...................................... 96 Improvement in Glycemic Index................................................................ 97 Preferential Influence on Weight Control and Satiety.......................... 100 Immunological Effects of PHGG.............................................................. 101 Improved Mineral Absorption................................................................. 102 PHGG: An Effective Beauty Supplementation....................................... 103 Safety Issues and Toxicological Behavior of PHGG........................................ 104 Some Possible Adverse Effects of Dietary Fiber.............................................. 107 Anticarcinogenic Properties of PHGG.............................................................. 108 History of Regulatory Status of PHGG............................................................. 108 PHGG as Food Additive: Commercial Applications...................................... 109 Summary............................................................................................................... 110 References............................................................................................................. 112
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Fiber Ingredients: Food Applications and Health Benefits
Introduction Dietary fiber is a vital component of a healthy diet. In recent years, the beneficial effects of dietary fibers have received considerable attention. Substantial health benefits are associated with dietary fibers and they have been shown through research to support heart health, gastrointestinal health, diabetes, weight management, and immune function. Dietary fibers are divided into categories of soluble and insoluble. Soluble indicates a fiber source that readily dissolves in water. Soluble fibers may play a role in lowering blood cholesterol and in regulating the body’s use of sugar [1]. The American Association of Cereal Chemists defines soluble fiber as fermentable fibers, which are the edible parts of plants or similar carbohydrates resistant to digestion and absorption in the human small intestine with complete or partial fermentation in the large intestine [2]. These fermentable fibers yield short-chain fatty acids that affect blood glucose and lipid levels, improve the colonic environment, and regulate immune responses [3]. The fermentable fibers have also been shown to interfere with the enzymatic hydrolysis of nutrients within the gastrointestinal tract, reduce enzyme function, and delay emptying of food from the stomach [4]. The term insoluble fiber refers to lack of solubility in water, but insoluble fiber has passive water-attracting properties that help to increase bulk, soften stools, and shorten transit time through the intestinal tract or gut. Dietary fibers, especially soluble fibers, have several biological functions. They help with slowing down the absorption of toxic materials in the intestines, appetite suppression, antidiarrhea nutrition support of colonocytes, colonic barrier function, and bulking on the colon [5–7]. Fibers also slow down the gut transit time while delaying digestion of macronutrients and the ability to prevent the atrophy of small intestinal villi generated by longterm supplementation of low-viscosity foods [8]. Although several dietary fibers are recognized for their physiologic actions and demonstrable health benefits with clinical data that support their effectiveness, the intent of this chapter is to summarize the physiologic data for partially hydrolyzed guar gum (PHGG) derived from dietary guar gum. Dietary Gums Gums are classified as dietary fiber. The key functions of gums in functional food and beverage applications are the same as traditional food applications, similar to how starches are used, including thickening, gelling, emulsification, suspending water-soluble carbohydrates, stabilization, and mouthfeel. Unlike gelatin products, gum products do not melt away at room temperature. Because of this unique property, many applications can be found within the food, pharmaceutical, cosmetics, mining, and oil industries. Gum acacia has been around for thousands of years. Gums were first used as glue by the ancient Egyptians to wrap mummies. In recent years, there
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has been an increased awareness and recognition of gum arabic products as fiber sources. Gums make excellent adhesives. Gum arabic is a high-quality adhesive that is still being used on the backs of postage stamps, and tragacanth gum is the glue used for cigar wrappers. In addition, gums have been used for many years as emulsifiers and as film-coating agents. They can be used in the artisan crafts, printing, and textile industries. They also appear in the ingredients of air freshener gels, and the like. Tragacanth gum and gum arabic are basically saps (exudates) that come from gum trees. Guar gum and locust (carob) bean gum, like wheat, are seed extracts. Being 85% soluble fiber on a dry weight basis, hydrocolloids such as gum acacia and guar gum are now being used when formulating foods with lower carbohydrate counts. Carrageen gum and alginates gum are seaweed extracts. Xanthan gum is a by-product of microbial fermentation and basically is a brewed product from natural ingredients. Recently, Dikeman et al. [9] have published that guar gums, psyllium gum, and xanthan gum have the highest viscosities of the several soluble and insoluble dietary fibers. A wide variety of gums also come from various botanical sources, including tree exudates, seeds, seaweeds, and beet/corn sugar. In food applications, a blend of gums often offers synergistic and complementary effects. Therefore, it is important to know the intended use and combination of ingredients being used with a gum, as well as the manufacturing conditions, in order to select the right gum for desired applications. In manufactured or processed foods, gums are called stabilizers. They bind and control moisture (water), stabilizing the product from drying out. In other words gums form a matrix, thereby preventing or at least slowing down the migration and evaporation of water moieties. Such a phenomenon plays a major role in stabilizing frozen foods, by binding the moisture within food. Gums, such as guar gum, locust bean gum, xanthan, and carrageenan, can be used as fat mimetics. The details of guar gum are summarized in the subsequent section of this chapter. Guar Gum Guar gum is a soluble dietary fiber from the seed of guar plants. Guar gum is also called guaran and is extracted from the seed of the leguminous shrub Cyamopsis tetragonoloba. The plant originated from India, West Pakistan, South Africa, Australia, and the United States. The guar or cluster bean is most grown in India, where the young beans are used as a vegetable (Figure 6.1). Guar gum is a white to yellowish-white powder and is nearly odorless. It is commonly used as a thickener and emulsifier in commercial food processing. Guar gum has almost eight times the thickening power as cornstarch, and is used in dressings, sauces, milk products, and baking mixes. It is also used in paper manufacturing, textiles, printing, cosmetics, and pharmaceuticals. Guar gum is a natural high-molecular-weight hydrocolloidal polysaccharide composed of galactose and mannan combined through glycosidic linkages,
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Fiber Ingredients: Food Applications and Health Benefits
Figure 6.1 Guar gum plant and guar seeds.
which may be described chemically as galactomannan. It can be dissolved in cold or hot water and forms a slime of high viscosity. Guar’s viscosity is a function of temperature, time, and concentration. Fine-finished guar gum powder is available in different viscosities and different granulometries depending on the desired viscosity development and application. Guar gum works as a bulk laxative. When ingested, it expands in the presence of water and tends to normalize bowel function. The bulk-forming properties of guar gum also cause a sense of fullness and decreased appetite. Guar gum has a beneficial impact on postprandial blood glucose [10] and insulin concentrations in humans [11–16]. Ellis et al. [12] investigated the influence of molecular weight on the ability of guar gum to attenuate postprandial glucose and insulin excursions. Additional research that bears on the effect of guar gum on blood glucose levels is also being conducted [17–23]. In other relevant contexts, guar gum has been shown to lower blood cholesterol levels in numerous animal and human studies. Hypothetical mechanisms of actions include impaired absorption of dietary cholesterol or bile acids due to the viscous nature of the polysaccharide and impaired absorption of bile acids through direct binding to the fiber. Gee et al. [24] showed the effect of guar gum on blood lipids is mainly attributable to its viscosity. On the other hand, Evans et al. [25] revealed that viscosity is not the whole answer to the question of plausible mechanisms of action in reducing blood cholesterol. It has also been suggested that gums such as guar gum are readily available for colonic fermentation, with the production of short-chain fatty acids, particularly propionate, which has been shown in animal and human studies to lower blood cholesterol through a suppression of hepatic cholesterol synthesis.
Partially Hydrolyzed Guar Gum (PHGG; SunFiber ®) Although guar gum has positive physiologic benefits, its high viscosity makes it difficult to incorporate into food products and enteral solutions. To
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overcome problems of guar gum with food formations, Taiyo Kagaku has developed partially hydrolyzed guar gum (PHGG), which has low viscosity while preserving various health benefits similar to intact guar gum. Thus, we will limit this review to the dietary effects of partially hydrolyzed guar gum (PHGG) also known under the trade name SunFiber®. Guar Gum Processing into PHGG Guar gum, derived from the Indian cluster bean Cyamopsis tetragonolobus, comprises approximately 70% to 80% galactomannan, a gel-forming polysaccharide with a molecular weight in the range of 200 to 300 kilodaltons (kDa). The recognized chemical name of galactomannan is d-galacto-dmannan, which is a straight backbone chain composed of (1,4)-linked-β-dmannopyranosyl residue with side-branching α-d-galactopyranosyl residue linked through the O-6 position of approximately every second mannopyranosyl residue of the backbone [26] (see Figure 6.2). A typical viscosity of a 1% solution of guar gum is about 2700 centipoises (cps) [27]. Guar gum meeting the specifications enumerated in the Food Chemicals Codex (FCC) is Generally Recognized As Safe (GRAS) for addition to foods. Partially hydrolyzed guar gum (PHGG) can be produced via controlled partial enzymatic hydrolysis of guar gum. Enzymatic partial hydrolysis produces shorter chains having molecular weights between 1 and 100 kDa, with OH OH
OH OH H H HO
H
O 1 OH α
H
H HO
H
1 OH α
H
H O
H
OH
4 O HO
H
H O H
H
1 β
HO 4
O
OH
H
H
1 β
O
O
OH
H O
HO
H
H H
H OH
OHOH
H
H O 6 4
H
H
H
O
1 β
H H
HO 4
H
O
OH
H
1 β
O
O
H OH
OH OH H
H HO H
H
O 1 OH α
H HO
H
H
H O
H
OH
4 O HO H H
H
H O H
1 β H
HO 4
H
H
O
OH H OH
O
O 1 OH α
H
H O 6 4 + 1 HO β OH HO
H
OH
H H
H O H
1 β H
HO 4
H H
H
O
OH H OH
Figure 6.2 Chemical structure of intact guar gum and partially hydrolyzed guar gum.
O
1 β
O
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Fiber Ingredients: Food Applications and Health Benefits
an average of 20 kDa [28]. This is approximately a 10-fold reduction in the degree of polymerization found in intact guar gum. The subunits of both intact guar gum and PHGG are d-mannose and d-galactose. The substance is purified to produce a substance that is at least 92% galactomannan. Greenberg and Sellman [28] estimated that only about 5% of the 1,4-d-mannopyranosyl glycosidic bonds in guar gum’s galactomannan are susceptible to enzymatic hydrolysis, thus avoiding the production of very low molecular weight hydrolysis products. Further, the enzymatic process does not affect the link with the pendant galactosyl residue, but hydrolyzes the main mannan chain and results in shorter chain galactomannans (MWavg = 20 kDA). The enzyme employed in the partial hydrolysis of guar gum was 1,4-β-dmannan mannanohydrolase, a hemicellulase endoenzyme derived from Aspergillus niger, which complies with Food Chemicals Codex specifications regarding activity, purity, and processing for food-grade enzymes. The enzyme 1,4-β-d-mannan mannanohydrolase is commercially available as a dark brown clear liquid prepared by purification and standardization of a culture broth and preserved by addition of potassium sorbate (0.07%) and sodium benzoate (0.14%). Daas et al. [29] were the first to use endo-β-mannanase from Aspergillus niger. Prior to use, they have purified endo-β-mannanase to remove any trace amounts of β-galactosidase activity, to degrade the galactomannan polymers from a variety of sources, including guar, cassia, locust bean, and tara. The degradation products were studied using high-performance anion-exchange chromatography to determine the distribution of the galactosyl residues on the d-mannose backbone. The overall mannose:galactose ratios range from over 8:1 in cassia to 1.5-2:1 in guar; the ratio is about 3.5:1 in locust bean and about 3:1 in tara. Daas et al. [29] have also classified galactose distributions as ordered if the galactose-substituted mannose units occurred every n units in the backbone; as random if such mannose units occurred regularly but with some variance in the number of mannose units between galactose substituted units; and as block-wise if the mannose backbone was characterized by long stretches of unsubstituted mannose units alternating with long stretches of galactose-substituted units. Of the galactomannans tested, those from guar exhibited by far the most ordered pattern of galactose substitution with relatively little random variation. McCleary and Neukom [30] suggested that the galactose substitution is not perfectly regular; that is, there exist occasions when neighboring mannose units are both substituted and occasions when neighboring mannose units are both unsubstituted. The mannose:galactose ratio is nearly 62:38. Therefore, enzymatic hydrolysis of guar gum cleaves the main mannan chain, leaving the pendant galactosyl groups intact. In a typical synthetic process, food-grade guar gum is dissolved in water and the pH is adjusted as needed with hydrochloric acid. The endo-β-dmannase is added and the concentration and reaction time are controlled to provide the desired degree of hydrolysis. The temperature is raised to inactivate the enzyme as well as halt the hydrolysis process. The solution is buffered with sodium hydroxide or potassium hydroxide as needed and then
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centrifuged to separate the larger insolubles. Activated charcoal is used to provide purification and decolorization. The solution is filtered and heated to reduce the moisture content, after which it is pasteurized and spray-dried, agglomerated as needed, and finally packaged. Physicochemical Properties and Food Grade Specifications of PHGG Partially hydrolyzed guar gum is almost tasteless, colorless, and odorless. It is slightly sweet in taste, highly soluble in water, but insoluble in ethanol. Its appearance is a fine white powder, and in solution is transparent and colorless. In dry form it absorbs less than 7.0% moisture, estimated by loss on drying. PHGG contains less than 1.0% proteins and less than 2.0% ash, while fiber content estimated by AOAC method is nearly 76%. Depending on the molecular weight, a 10% solution of PHGG in water has pH in the range of 4.5 to 7.0 and viscosity < 10 cps.
Physiological and Metabolic Functions of PHGG PHGG has postprandial blood glucose response, a lowering effect on blood cholesterol concentrations, and improved laxation. Figure 6.3 displays several other potential functional effects of PHGG on metabolism and physiological functions.
Acute Postprandial Blood Glucose and Insulin Response Blood Cholesterol Concentration Laxation Improvements
Partially Hydrolyzed Guar Gum (PHGG)
Intestinal Microflora Balance and Prebiotic Effects Irritable Bowel Syndrome (IBS) Glycemic Index Weight Control and Satiety Immunological Effects Mineral Absorption Effective Beauty Supplementation
Figure 6.3 Potential metabolic benefits of PHGG.
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Improvement in Acute Postprandial Glycemic Responses and Insulin Response Guar gum and pectin are reported effective in postprandial glycemia in diabetic patients, often coupled with a reduced need for insulin secretion [14]. However, an addition of soluble fiber to enrich liquid enteral formulas in physiologically effective concentrations often resulted in a substantial increase in viscosity, thus preventing easier oral consumption or gastronomy applications. Therefore, the use of PHGG helps to lower viscosity in comparison to intact guar gum and the resulting product is suitable for oral supplementation applications. Golay et al. [31] have reported a study wherein 20 g of PHGG in 500 mL of a fructose-containing enteral formula was administered to six patients with insulin-dependent diabetes (IDDM). The blood glucose and insulin concentrations were significantly reduced compared to fiber-free formulas containing only fructose or sucrose. Further, they have [32] tested postprandial glucose and insulin excursions in six male and female NIDDM patients (with type 2 diabetes) with a randomized double-blind crossover design method. It was revealed that enteral formula with 20 g/Lit PHGG and fructose or the same formula with fructose, considerably lowered postprandial (after two hours) plasma glucose levels, whereas plasma insulin level reduction was not significant. However, after four hours, the areas under the curve for blood glucose and insulin levels were considerably reduced. Interestingly, the substitution of fructose for glucose alone showed no effect on postprandial glucose fractions. In a separate protocol, Blanchet et al. [33] have performed a similar study on 24 NIDDM patients (12 male and 12 female) who were allowed to consume their choice of breakfast meals for one week. In the second week, the subjects were fed 6 g/day of PHGG along with the same breakfasts they had consumed in the previous week. The results revealed that addition of PHGG did not affect one-hour postprandial glucose levels, but the two-hour postprandial glucose levels were significantly lowered. A majority of the patients showed no side effects from PHGG addition whereas a few patients suffered minor diarrhea, skin rash, gas/bloating, or constipation. In a study by Tsuda et al., an effect of PHGG on elevation of blood glucose and on insulin secretion after sucrose intake was reported on humans. In a controlled experiment, 30 grams of sucrose was ingested and the peak of blood glucose and insulin level was monitored after 30 minutes of ingestion. When 5 grams of PHGG was ingested simultaneously with 30 grams sucrose, the blood glucose level after 60 minutes of ingestion was significantly lower than that of sucrose alone (control). Serum insulin level was also reduced. Reduction in postprandial glucose levels was also observed by Gu et al. [35] when individuals were fed a PHGG solution and a rice meal concurrently. In this protocol, 30 healthy individuals with an average BMI of 21.6 kg/m2 consumed 300 grams of rice immediately after a control or 2.5 grams PHGG solution. Blood sugar was measured before and periodically
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after intake. The results demonstrated that postprandial blood sugar levels were significantly lower in individuals who initially had greater levels of glucose in their blood (>140.5 mg/dL or 7.81 mmol/L) indicating that they were hyperglycemic and may be at risk of diabetes. The area under the curve was significantly reduced by PHGG intake combined up to 30 minutes. The group of individuals who initially had lower levels of glucose in their blood (<140.5 mg/dL) also showed a similar trend [35]. In another double-blind crossover study, Peters and Davidson [36] carried out a study with 12 NIDDM patients who were enterally given one each, of three different formulas: two containing PHGG and one control. The blood glucose level of patients was brought to 8.4 mmol/L after an overnight fast and considered as the blood glucose level at time 0. Thereafter, every 15 minutes up to four hours the patients ingested 30 mL of formula to a total of 480 mL and blood glucose was measured every 30 minutes. The two formulas containing PHGG were found to be not effective in attenuating the postprandial glucose excursion. Alam [37] have measured plasma concentrations of glucose and insulin along with arginine, total lipids, and short-chain fatty acids in 10 healthy men consuming enteral formulas with or without 42 to 63 g/day PHGG for one week. They did not observe any considerable differences in plasma concentrations of glucose and insulin. Similarly, Yamatoya et al. [38] fed 75 grams of glucose dissolved in 200 mL of water to five healthy individuals, with or without 15 grams of PHGG dissolved in 150 mL of water. Blood glucose and insulin levels were estimated from the aliquots taken after 30, 60, 90, 120, and 180 minutes. The results demonstrate that an addition of PHGG did not affect the glucose peak time, but reduced the blood glucose and insulin levels with statistical significance at 60 and 90 minutes. It is difficult to correlate the ineffectiveness of PHGG in aforementioned studies to the significant success of PHGG in improvement of acute postprandial plasma glucose and insulin response. However, it may be attributed to typical problems associated with the protocol design and evaluation of the statistical data with flawed or incomplete experimentations. Therefore, it can be proposed that PHGG lowers postprandial serum glucose level at least by three mechanisms. First, PHGG increases the viscosity of small intestine juice and hinders diffusion of glucose. Second, PHGG binds glucose and decreases the concentration of available glucose in the small intestine; and last, the PHGG retards α-amylase action through capsuling starch [37]. The combination of all these steps decreased the absorption rate of glucose and the concentration of postprandial serum glucose. These data revealed that the viscosity of the PHGG is greatly lower than that of intact guar gum, but the reduction effect on blood glucose level after sucrose intake remained constant. Therefore, an acute glucose lowering effect of guar gum is not solely explained by delayed gastric emptying in the delivery of viscous material from the stomach into the small bowel [38, 39].
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Impact on Blood Cholesterol Concentration High cholesterol and triglyceride levels are considered key risk factors for many chronic and lifestyle-related diseases, such as stroke and heart disease. Recently, dietary fibers have drawn considerable attention because of their ability to improve lipid metabolism, reducing the risk of chronic diseases. Kay [41] have demonstrated that water-soluble dietary fibers have lipid-lowering effects. The functional improvement of blood lipid status by PHGG has been explored in a number of animal and human studies. Takeno et al. [42] compared the effect of enzymatically partially hydrolyzed guar gum with an average molecular weight of 24 kDa, and viscous guar gum with an average molecular weight of 300 kDa. Rats were fed hypercholesterolemic diets containing either 5% PHGG or 5% intact guar gum for 21 days. Intact guar gum suppressed the elevation of total (plasma and liver) cholesterol and triacylglyceride levels, while PHGG suppressed only the plasma levels. This indicates that PHGG retained the ability to lower the plasma cholesterol despite its significant lower viscosity. In a study of Yamada et al. [43], Sprague-Dawley male rats were fed the diets with water-insoluble cellulose or various water-soluble fibers such as intact guar gum, PHGG, glucomannan, or highly methoxylated pectin to study the effects on serum lipids. Various soluble fibers reduced total cholesterol and triacylglyceride levels as much as guar gum, while only intact guar gum or glucomannan was able to show lowered phospholipid levels. Ide et al. [44] also compared the cholesterol lowering effects of intact guar gum and partially hydrolyzed guar gum. Four-week-old male Sprague-Dawley rats were given a basal diet supplemented (at expense of sucrose) with 8% intact guar gum, 8% PHGG, or 8% fructooligosaccharide for 24 days. Both intact guar gum and PHGG reduced hepatic cholesterol and triacylglycerides but not phospholipids. Guar gum greatly reduced serum lipid levels, while PHGG reduced blood lipids to a lesser degree, except that the reduction in triacylglycerides was the same. From these observations, it was suggested that the highly polymeric structure of guar gum is not a necessary factor in lowering serum lipids, and that PHGG is also effective in attenuating blood cholesterol concentrations. In a study with rats, Suzuki and Hara [45] studied hypertriglyceridemia associated with fructose feeding to obtain a dietary model of insulin resistance, which was ameliorated by supplementation with a guar gum hydrolysate. In a study by Favier et al. [46], Wistar rats were fed with either 8% intact guar gum or 10% PHGG. Results showed that the intact guar gum effectively lowered blood cholesterol concentrations, particularly in the triacylglyceride-rich lipoprotein fractions. It was demonstrated that PHGG also altered some parameters of the enterohepatic cycle of cholesterol and bile acids, thus having a significant cholesterol-lowering effect. PHGG also appears to influence human lipid profile in short-term trials. In a human volunteer study by Takahashi et al. [47], serum cholesterol was reduced in eight subjects after consumption of PHGG (36 g/day) in a beverage
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for four weeks. Fasting blood parameters were measured before and after supplementation. Serum cholesterol concentration decreased significantly and all subjects had a reduction in cholesterol levels along with a reduction in serum free fatty acid concentrations [48]. Similar results were observed in the study of Alam et al. [49], when six female volunteers took PHGG (15 g/day) for two weeks. Enterally fed adults with persistent diarrhea given 2% PHGG had reduced plasma cholesterol levels after four days of supplementation. Results were also monitored postprandially after consumption of PHGG with a test meal or product. A short-term study showed reduction of blood cholesterol levels four hours after consumption of a test meal and 15 g PHGG [38]. They gave 75 g of glucose dissolved in 200 mL of water to six healthy volunteers, either with or without 15 g of PHGG dissolved in 150 mL of water. Blood total cholesterol, triacylglycerides, LDL, very low-density lipoprotein (VLDL), and phospholipid levels were measured after 1, 2, 4, 6, and 8 hours. The addition of PHGG reduced the levels of all of these lipids at nearly all time points; the differences were statistically significant only for total cholesterol at 4 hours, VLDL at 6 and 8 hours, and phospholipids at 4 hours. The effect of PHGG on serum total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, and triacylglycerides was evaluated in a 12-week double-blind, placebo-controlled clinical trial in 62 postmenopausal hypercholesterolemic women consuming the American Heart Association (AHA) Step 1 diet [50]. It was found that in the PHGG-treated group (n = 33) as a whole, the HDL cholesterol concentrations were significantly decreased at nine weeks in those women with adherence rates of 80% or greater. In another randomized, double-blind crossover study of 20 individuals with moderately elevated plasma cholesterol performed by Blake et al. [51], participants received either control wheat bread or wheat bread supplemented with partially hydrolyzed guar gum having an average molecular weight of 1070 kDa. Study participants received each diet for three weeks with a four-week washout period. The PHGG-supplemented diet resulted in a significant reduction in plasma levels of total cholesterol, particularly in LDL. There were no significant differences in HDL or in triacylglyceride levels. There were no palatability issues and no serious side effects. Yamatoya et al. [48] prepared PHGG with a peak molecular weight of ~20 kDa by means of enzymatic hydrolysis. Healthy young females with serum cholesterol concentrations of 190 mg/dL or higher ingested either 5 or 15 g/ day of PHGG for two weeks. In the 5 g/day groups, the serum cholesterol was slightly reduced and free fatty acids decreased significantly; in the 15 g/ day groups, both cholesterol and free fatty acids were significantly reduced. However, no changes were seen in triacylglycerides or phospholipids. Kondo et al. [52] have conducted a randomized, single-blind placebocontrolled crossover design test, wherein 11 healthy adult males were given yogurt with or without 6 g/day of PHGG for one week, with no washout period between administrations of the test and control yogurts. There were no complaints of diarrhea or gastrointestinal discomfort and no change in body weight. PHGG caused suppression of peak levels of postprandial serum
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triacylglycerides and remnant-like lipoprotein particle cholesterol (RLP-C). The authors suggested that PHGG might have affected the rate of fat absorption. These studies suggest that levels of cholesterol and triglyceride in both serum and liver could decrease due to such dosings, thereby PHGG might be applied as a hypocholesterolemic agent. This can be supported by the fact that PHGG entraps the bile acids in the small intestine by interruption of the enterohepatic circulation of bile salts and increases their fecal excretion, which accelerates cholesterol oxidation to bile acids, and a spillover of the body cholesterol pool. Effect of PHGG on Laxation Improvements Gastrointestinal side effects, such as diarrhea, are generally recognized as one of the most common complications associated with tube feeding after clinical practice wherein diarrhea is attributed to infectious processes, antibiotic medication, protein energy malnutrition, patient-related causes such as stress and surgical procedures, and bacterial gut contamination [53]. Diarrhea is one of the main reasons that enteral nutrition is discontinued, as it disturbs fluid and electrolyte balance and worsens nutritional status. In humans, dietary fiber is mainly degraded in the large intestine by bacterial flora, in which short-chain fatty acids (SCFA) are produced. The SCFAs are absorbed by the colon, stimulating sodium transport in several species, including humans [54, 55]. This effect may be particularly important in acute diarrheal diseases in the colon and may cause colonic dysfunction [56]. SCFA levels in the colon may therefore influence the clinical course of acute diarrheal conditions. Fiber added to tube-feeding formulas may aid in reduction of diarrhea, but this is dependant on both the physical and chemical characteristics of the fiber. Rabbani et al. [57] have reported that children receiving either green plantain or pectin had significantly less stool output and duration of diarrhea. However, soluble fiber, such as guar gum, has limited use in tube-fed enteral formulas because its addition at physiologically effective concentrations results in liquid products with very high viscosity. Fiber is also an important constituent of the diet in the elderly but certain problems, such as poor dentition and food preferences, can limit the amount consumed. PHGG supplementation appears to reduce the amount of laxatives used in an elderly population because the PHGG can easily be incorporated into food and beverages. Improved laxation is a physiological benefit that has a variety of manifestations. Test endpoints related to improved laxation include changes in stool weight or consistency, beneficial modifications to frequency and regularity of bowel movements, changes in stool transit time, reduction in use of laxatives, reduction in constipation, and amelioration of diarrhea. Takeno et al. [42] compared the effect of PHGG (MW 24 kDa) and intact guar gum (MW 300 kDa) on fecal moisture and volume of stooling. Rats were fed hypercholesterolemic diets containing either 5% PHGG or 5% intact guar gum for three weeks. Both guar gum and PHGG increased fecal moisture and amount of feces excreted during an 18-hour period. However,
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PHGG retained the ability to affect laxation despite its lower viscosity. Alam [37] measured the effects of PHGG added to an enteral formula at 21 g/L on stool weight and consistency, fat excretion, and stool frequency in 10 healthy men consuming 2 to 3 L of the formula (42 to 63 g/day of PHGG) daily for one week. Consumption of the formula containing PHGG did not result in a statistically significant increase in stool weight, fat excretion, or frequency but did result in a significant decrease in the number of hard stools compared with the enteral formula without fiber. Nakao et al. [58] studied the effect on 20 elderly males and females who had been bedridden for long periods and were receiving enteral feeding. They were suffering from diarrhea or loose stools. They received 7 g/day of galactomannans during the first week and the dose was increased by 7 g/day each week until they received 28 g/day at the fourth week. Serum diamine oxidase activity as an indicator of morphologic change in small intestinal mucosa was significantly increased. The water content of the feces decreased, and the frequency of normal stools increased. The frequency of bowel movements, number of aerobic bacteria, and the pH of feces decreased, while fecal SCFA, especially acetic and propionic acids, increased. All effects reversed after termination of the galactomannan supplementation. There was no change in counts of total bacteria or anaerobes, nor in body weight, total serum protein, prealbumin, transferrin, retinol-binding protein, total cholesterol, triacylglycerides, iron, copper, or zinc. Meier et al. [59] reported that consumption by 12 healthy men of an enteral formula supplemented with nearly 42 g/day PHGG for seven days resulted in significantly increased colonic but not orocecal transit time compared with either a self-selected diet or the enteral formula without fiber. PHGG had no effect on stool consistency or frequency. Also, Mijan de la Torre and de Mateo Silleras [60] have reported that PHGG is almost completely fermented by colonic bacteria and fermentation of PHGG produces more butyrate and other SCFA (short-chain fatty acids) than did fermentation of other fibers. Butyrate, propionate, and acetate accounted for 85% of SCFA production. The authors suggested that butyrate is preferentially oxidized by the colon and is considered its preferred fuel. SCFA enhance sodium absorption, colonocyte proliferation, metabolic energy production, colonic blood flow, stimulation of the autonomous nervous system, and production of gastrointestinal hormones. Increased water and sodium absorption produce an antidiarrheal effect. Similarly, Lampe et al. [61] fed an enteral formula containing 15 g/day PHGG to 11 healthy men for 18 days. This resulted in significantly longer mean transit time compared with either a self-selected diet or a diet containing soy polysaccharide, but not when compared with the enteral formula without fiber addition. Fecal wet and dry weights, fecal moisture content, and stool frequency were slightly decreased, but these changes were minimal. The fecal pH also significantly decreased with the PHGG-containing enteral formula as compared with the self-selected diet, but did not differ significantly from the enteral formula without fiber. Stool weight and fecal consistency did not change significantly with any dietary treatment.
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Fiber Ingredients: Food Applications and Health Benefits 150
130.8 114.5
Weight
120 90
87.3
104.4
Moisture weight Dry weight
60 30 0
Before
After 2 weeks
Figure 6.4 Beneficial effect of partially hydrolyzed guar gum (9.7 g/day) on the weight and moisture of human feces.
Takahashi et al. [62] gave 11 g/day of PHGG in a beverage to 15 constipated young women for three consecutive weeks. It was observed that PHGG supplementation increased the defecation frequency by 40%, and also increased fecal moisture content, while reducing the fecal pH (Figure 6.4). However, the frequency of reported abdominal pain was unchanged from pretreatment while the reported sense of flatulence was found to increase at the beginning of treatment but decreased over the time of treatment. In another report, Yamatoya et al. [63] investigated laxative effects of PHGG in a beverage as given to 65 healthy young female adults aged 19 to 21 years. Subjects received either 5 or 15 g/day PHGG for two weeks, and finally the treatment was discontinued for another two weeks of observation. The frequency of defecation and fecal volume was increased and dose-dependence was observed during the PHGG period, but returned to initial-test levels after termination of the treatment. Particularly, no changes in diarrhea or abdominal pain were monitored. A randomized prospective double-blind trial [64] was employed with 100 patients receiving total or partial enteral feeding to compare a standard diet with the same diet supplemented with 20 g of PHGG per 1000 mL of formula. The patients were divided into two groups and the 30 patients received total enteral nutrition (average daily intake = 1200 mL/day of formula providing 24 g/day of PHGG) while 70 received enteral supplementation (average daily intake = 1000 mL/day providing 20 g/day of PHGG). Those receiving either total or supplemental enteral nutrition had reduced incidence and severity of diarrhea but increased flatulence. No bloating or cramping was noted during the treatment period. Increased colonic fermentation was indicated by increased H2 production. Four patients on the standard total enteral diet, but no patients receiving PHGG, had to be discontinued due to gastrointestinal side effects. Twenty-one residents who required daily laxatives for constipation (mean age 83 years) at two nursing homes were given 8 to 12 g/day of PHGG in
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four ounces of juice or water [65]. A three-week observational baseline and a five-week PHGG-supplementation phase were implemented. Sixteen residents completed the trial and showed a significant reduction in laxative use, an increase in flatulence, and no differences in number, consistency, or ease of bowel movements. The effect of supplementation of PHGG on the occurrence of constipation and use of laxative agents was recognized. Fussell et al. [66] studied the effects of PHGG on diarrhea in critically ill, tube-fed patients in a double-blind randomized study. The 57 adults in this trial were divided into five diagnostic categories such as abdominal surgery/ trauma, head/neck surgery, cerebral trauma, vascular surgery, and multiple fractures. Patients received either a fiber-free formula or the same formula with 14 g/L of PHGG for 5 to 14 days. The PHGG was generally very well tolerated. No significant effect on diarrhea was observed. Further, Homann et al. [67] executed a randomized controlled double-blind study to demonstrate the effect of PHGG on diarrhea in patients receiving enteral nutrition. Thirty patients were given total enteral nutrition following upper GI surgery and 70 patients were given supplemental enteral nutrition of 1000 mL/day, receiving either the standard enteral diet or the standard diet supplemented with 20 g/L of PHGG. The first group of patients receiving the total enteral nutrition supplemented with PHGG experienced significantly reduced diarrhea, but higher hydrogen exhalation and flatulence than those who received the control formula. No overall increase in reported gastrointestinal side effects was monitored. In another study, Rushdi et al. [68] performed a prospective, randomized, double-blind, controlled study wherein 20 patients on enteral nutrition with three or more liquid stools per day were randomly assigned to two groups called fiber-free control group or a test group that received 2% PHGG-enriched enteral foods. The intake of PHGG was about 22 to 37 g/day. The total duration of the study was four days. Supplementation with PHGG significantly reduced the number of liquid stools in the test group from Day 1 to Day 4, while the difference between the test and control groups was significant on Day 4. The PHGG was well tolerated with fewer adverse gastrointestinal symptoms. Although most of the studies in this field have dealt with patients reliant on enteral feeding, Spapen et al. [69] examined 25 patients with severe sepsis and septic shock, who received either enteral formula alone or enteral formula supplemented with 22 g/L PHGG for at least six days. The group receiving PHGG supplementation exhibited significantly reduced frequency of diarrhea and a reduction in the number of days with diarrhea. Moreover, there was not a significant effect on sepsis-related mortality (one death in the test group, four in the control) or duration of stay in the intensive care unit. The first two double-blind randomized controlled clinical trials in 150 young male children age 4-18 months with watery diarrhea was performed by Alam et al. [70] to evaluate the effects of PHGG on diarrhea in babies who had non-cholera diarrhea. Children received either the WHO Oral Rehydration Solution (ORS) or ORS supplemented with 20 g/L of PHGG until recovery. The average consumption of ORS was 429 mg/kg, providing approximately
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8.6 mg/kg of PHGG. No side effects were reported while significant reduction was observed in the duration of diarrhea and in stool output. The results of the aforementioned study were supported by further research. Alam et al. [49] carried out a second double-blind randomized controlled clinical trial with children having persistent diarrhea. The 116 male children age 5–24 months with watery diarrhea were randomized to a diet of comminuted chicken supplemented with PHGG or a control diet without PHGG. Participants received either a comminuted chicken-based diet or the same diet with 20 g/L of PHGG for seven days. There was a significant increase in the proportion of children whose diarrhea stopped within seven days and significant overall reductions in diarrhea duration and stool output in the group that received PHGG. These studies have consistently found statistically significant improvements in the participants’ laxation parameters as a result of PHGG supplementation. It is concluded that PHGG can be defined as a functional fiber based on its ability to provide beneficial physiological effects on a variety of laxation endpoints as well as gastrointestinal side effects. Improvement in Intestinal Microflora Balance and Prebiotic Effects Research has demonstrated that dietary fiber has beneficial effects on improving the intestinal environment. Studies of Salyers et al. [71] have consistently demonstrated that galactomannan is readily fermented by fecal microflora. This fermentation may result in lower intestinal pH and increased production of short-chain fatty acids (SCFA). A low pH may improve intestinal conditions by providing an ideal environment for the growth of beneficial bacteria and reducing formation of harmful bacterial metabolites [72, 73]. Research has demonstrated the beneficial effects of PHGG on the intestinal environment and their ability to alter the gut microflora is considered a prebiotic effect and may improve immunologic status. Male volunteers given a beverage supplemented with 21 g/l PHGG had increased levels of plasma SCFA [74]. Stool consistency was also improved. PHGG (36 g/day) given to eight healthy men for eight weeks resulted in increased frequency of defecation and increased fecal weight. SCFA content remained constant but fecal pH decreased in all four weeks of administration of PHGG [47]. Velazquez et al. [75] used fresh fecal inocula to compare the effects of glucose, soy oligosaccharide, fructooligosaccharide, inulin, hydrolyzed inulin, cellulose, powdered cellulose, methylcellulose, psyllium husk, and PHGG on production of SCFA. Inoculation with each of these carbohydrates resulted in the production of SCFA, with PHGG producing the highest levels of propionate and butyrate. Pylkas et al. [76] tested seven different fiber substrates and glucose control to assess SCFA production: psyllium husk, methylcellulose, indigestible dextrin, arabinogalactan, polydextrose, and PHGG using the same model as Velazquez et al. [75]. Fresh feces were collected from three healthy individuals; a homogeneous solution of the feces was used as the fermentation inoculums. Aliquots were removed
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Partially Hydrolyzed Guar Gum Dietary Fiber Bifidobacterium spp.
Bifidobacterium spp.
Others
Others 14.7%
31.7%* After 1 week
Bacteroidaceae
Bacteroidaceae
Figure 6.5 Effect of PHGG (10 g/day) on improvement of intestinal microflora in humans.
at 0, 2, 4, 8, 12, and 24 hours. PHGG showed the highest production of SCFA at all time points. The SCFA produced in the presence of PHGG were high in acetate and butyrate but low in propionate. It appears that PHGG may have a prebiotic effect, reflected in increased proliferation of lactic-acid bacteria and production of SCFA, but this effect is not as clearly elucidated as the effects of other well-studied prebiotic carbohydrates such as fructooligosaccharide and galactooligosaccharide. Fecal pH was also reduced in 15 women who were supplemented with 11 g/day of PHGG for three weeks [62]. The frequency of Lactobacillus spp. occurrence in the feces increased, but the average cell number of Lactobacillus spp. remained virtually unchanged (Figure 6.5). An in vitro study that found PHGG moderately enhanced the growth of several bacterial strains was performed by Okubo et al. [77]. Also, the human volunteers taking PHGG in a functional food had significantly increased numbers of Bifidobacteria. Tuohy et al. [78] studied the prebiotic effects of PHGG and fructooligosaccharide in a double-blind randomized placebo-controlled crossover study. Thirty-one people took three placebo biscuits or three biscuits containing 3.4 g PHGG and 6.6 g fructooligosaccharides daily for two 21-day crossover periods. There was a correlation between subjects who had lower Bifidobacteria values at the beginning of the trial and the degree of increase after ingestion of the biscuits. Therefore, prebiotic biscuits may prove efficacious for increasing Bifidobacteria numbers in the gut. The effect of PHGG intake (21 g/day) on fecal microflora, pH, and SCFA were investigated in nine healthy males, ages 22 to 39, for two weeks (three 7 g doses of PHGG as a 7% (w/v) solution in water). Feces were collected on Days 12 and 14. Bifidobacterium spp. and Lactobacillus spp. were significantly increased by PHGG intake. No significant changes in volatile fatty acid levels were found but the pH was reduced during the second week of PHGG supplementation [77]. Also, Takahashi et al. [79] studied the effect of liquid diets with or without PHGG on intestinal microbial flora and function of
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rats. PHGG increases the beneficial bacteria in the gut but may also have a preventative effect on harmful bacterial colonization. Recently, Rastall and Gibson [80] represented one means of encouraging the proliferation of these lactic acid bacteria by ingesting fermentable carbohydrates that provide a substrate upon which these bacteria can grow. Several in vitro studies have explored the ability of PHGG to encourage proliferation of lactic acid bacteria, either by direct measurement of microbial prevalence or by evaluation of bacterial production of SCFA. Miller-Fosmore et al. [81] screened 13 bacterial species for growth on several oligosaccharide preparations and PHGG. Little growth was shown of any species on PHGG, although Bifidobacteria grew on the oligosaccharides. Herein, the discussion of the benefits of a well-balanced colonic microbiota is very important because maintaining healthy populations of certain bacteria—especially Bifidobacteria and Lactobacilli—is increasingly regarded as beneficial [82]. Effectiveness in Irritable Bowel Syndrome (IBS) Irritable bowel syndrome (IBS) is the most common disease diagnosed by gastroenterologists and presents symptoms of abdominal pain, bloating, and defecation irregularity. IBS alters physiological function and consequently it is very difficult to diagnose by a specific abnormality. Giannini et al. [83] reported that the prevalence of irritable bowel syndrome (IBS) in the U.S. and Europe is about 10% to 20%, with women being predominant. They further estimated that up to 70% of adults with symptoms do not present for medical evaluation. IBS is not at all life-threatening; however, it lowers the quality of life (QOL). Usually, the therapy in general is symptomatic: directed at reduction of constipation, diarrhea, and pain. Fiber supplementation [84] is generally recommended, especially for constipation-predominant IBS, because it decreases whole-gut transit time, which decreases intracolonic pressure and reduces pain. The different types of fiber usually have different effects. Soluble fiber is widely metabolized in the large bowel, producing short-chain fatty acids and selective stimulation of microbial growth, eventually increasing the water-holding capacity of the colonic content, while insoluble fiber is minimally modified during intestinal transit and mechanically increases fecal mass by retaining water, thus decreasing transit time and improving defecation. Patients with IBS are often recommended to consume 20 to 30 grams of fiber per day but compliance is often a problem. In a study by Giaccari et al. [85], 134 patients with IBS were divided on the basis of body-mass index into obese and normal categories, and were given 5 grams per day of PHGG in their diet for 24 weeks. Both obese and normal patients showed an increase in the frequency of bowel movements and decreases in the frequency of such IBS symptoms as flatulence, abdominal tension, and abdominal spasm. While no change in plasma electrolytes was observed, there was a higher incidence of normal levels of blood cholesterol, lipids, triacylglycerides, and glucose than prior to treatment. In a regular study, the subjects (49 men and 139 women) with IBS took the prescribed
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supplement for 12 weeks. The study was an open trial and the subjects could switch treatment groups after four weeks based on their perception of treatment. Of the patients who decided to switch, 82.1% moved to the PHGG group and only 17.9% of patients switched out of the PHGG group. PHGG was better tolerated and preferred by the study subjects [75]. PHGG also reduced symptoms of IBS, such as flatulence, abdominal tension, and abdominal spasm after three weeks of consumption in normal and obese patients. In another study, Parisi et al. [86] randomly assigned 188 male and female IBS patients to receive diets with either 30 g/day of wheat bran or 5 g/day of PHGG for four consecutive weeks, after which they were permitted to choose either diet for the remaining eight weeks. Both treatments improved bowel habits and pain, but were not significantly different. More patients receiving bran chose to switch to PHGG after four weeks and patients receiving PHGG were more satisfied and reported greater subjective improvement. In this continuation, Parisi et al. [87] performed another study wherein 86 male and female IBS patients were randomly assigned to receive either 5 or 10 g/day of PHGG for 12 weeks. Both treatments significantly improved all dimensions of a quality of life scale and an anxiety and depression scale, with no significant difference between doses. Scores were returning toward baseline, though still above it, three months after treatment. Forty patients suffering from constipation-predominant IBS and noncomplicated diverticulosis were randomized into groups that supplemented their diets with 100 g/day of brown bread or 10 g/day of PHGG dissolved in water for 60 days [84]. In the PHGG only group, the number of evacuations per week increased significantly. Both groups significantly improved in symptoms such as meteorism, abdominal pain, and incomplete evacuation, but the PHGG group had greater reduction in bloating. The diet supplementation with PHGG was well tolerated. It is unclear if PHGG supplementation has a significant beneficial effect in amelioration of the symptoms of IBS other than those resulting from improved laxation. These studies indicate that PHGG can provide beneficial results in improving IBS symptoms and psychological aspects related to IBS, and that it is well tolerated by patients. Further research in this area is likely to elucidate what role PHGG may play in the clinical management of IBS. Improvement in Glycemic Index The glycemic index (GI) indicates how rapidly carbohydrate food is metabolized (digested) into glucose and how much it causes the blood glucose (sugar) to rise. The glycemic index describes this difference by ranking carbohydrates according to their effect on our blood glucose levels. Scientifically, the glycemic index is defined as the incremental area under the blood glucose response curve of a 50 g carbohydrate portion of a test food expressed as a percent of the response to the same amount of carbohydrate from a standard food taken by the same individual. Not all carbohydrate foods are created equal; in fact they behave quite differently in our bodies.
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The World Health Organization (WHO) claims the glycemic index is considered a valid index of the biological value of dietary carbohydrates. Insulin users first discovered the phenomenon of the glycemic index in the 1960s. Choosing low glycemic index foods that produce only small fluctuations in our blood glucose and insulin levels is the total secret to long-term health, reducing the risk of heart disease and diabetes, and is the key to sustainable weight loss. On the other hand, eating a lot of high glycemic index foods can be detrimental to health because it pushes the body to extremes, especially for overweight and sedentary individuals. Eating mainly low glycemic index foods that slowly trickle glucose into the bloodstream keeps the energy levels balanced and helps us to feel fuller for longer between meals. In addition, the low glycemic index foods help people control their body weight, improve the body’s sensitivity to insulin, help to control diabetes, reduce the risk of heart disease, reduce blood cholesterol levels, reduce hunger and increase satiety, prolong physical endurance, and help refuel carbohydrate stores after exercise [2]. Low glycemic index foods (less than 55) produce a gradual rise in blood sugar that is easy on the body. Foods having a glycemic index rating of between 55 and 70 are intermediate glycemic index foods. Foods with high glycemic index numbers (> 70) make blood sugar as well as insulin levels spike fast. That can be realized as a health threat. The dietary fiber partially hydrolyzed guar gum (PHGG) has been shown to flatten the blood glucose tolerance tests [4]. They also decrease the rate of gastric emptying [1, 80]. The physical and chemical properties of dietary fibers play an important role in the release and absorption of nutrients in the gastrointestinal tract. There have been human studies on adding fiber to foods with a high glycemic index rating to see if the fiber will slow the absorption of glucose and therefore lower the glycemic index number. PHGG, a soluble fiber, binds with bile acids that surround fat molecules in order to carry them out of the body. This results in decreased absorption of cholesterol and lipids as well as an increase in fat excretion. Yamatoya et al. [38] has declared the effects of partially hydrolyzed guar gum (PHGG) on postprandial plasma glucose and lipid levels in humans. Moreover, as PHGG passes through the stomach, it slows the rate of emptying, therefore providing a feeling of fullness. Rose et al. [89] and Aro et al. [11] showed that another benefit of PHGG is that it lowers the glycemic index by slowing the rate of glucose absorption. Actually, PHGG is not digested in the small intestine but is fermented/hydrolyzed in the colon and produces short-chain fatty acids such as propionate, butyrate, and acetate. For PHGG to work this way, it has to form a gel-like colloidal state in the small intestine. In another report by Trinidad et al. [90], the glycemic index of PHGG in normal and diabetic individuals has been discussed. The report presented a dose response study on the glycemic index of normal and diabetic individuals and reported on the effect of PHGG intake in white bread and rice, as well as PHGG taken as a drink with white bread. The white bread contained mostly carbohydrates (53.5%) and dietary fiber content was estimated at nearly 2.3%. Rice used in the study contained 80.3% carbohydrates with-
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Glycemic Index
120 100
a
a b
80
b
60
b
b
b
b
c
c
40 20 0
White Bread
WB+3g
WB+5g
Diabetic subjects n=9
WB+10g
WB+15g
Control subjects n = 11
Figure 6.6 Glycemic index of normal and diabetic individuals consuming white bread (WB) doped with varied amounts of PHGG during baking (letters denote significant differences at a level of p<0.05).
out any dietary fibers. The PHGGs of varied viscosity used for the doping contained nearly 87% of dietary fibers and less than 6.5% carbohydrates. The glycemic index of white bread was significantly reduced when doped with increasing levels of PHGG in both normal and diabetic individuals. Figure 6.6 shows the significant decrease (nearly 55%) in the glycemic index when doped with 15 g of PHGG. Interestingly the effect was more pronounced with diabetic individuals when higher dosing of PHGG was used. Increasing amounts of PHGG did not result in considerably lower glycemic indexes in normal individuals (r = –0.72 NS; P<0.01), but resulted in much lower glycemic indexes in diabetic individuals (r = –0.91 NS; p<0.01). A similar effect was observed with the white bread when PHGG with higher viscosity (800 kDA) was used, which showed much lower glycemic index (55 ± 4) compared to the low viscosity PHGG (68 ± 5) having identical (5 g) leadings. Otherwise, it is necessary to mention that not much difference was observed in the glycemic response between normal and diabetic individuals. A lower glycemic response produces a lower insulin response, which is beneficial for long-term glucose control. Therefore, obtaining a low glycemic response is ideal for individuals with blood glucose management problems such as diabetes [90]. PHGG is one fiber that has been extensively studied in diabetic humans and it has been proven to significantly reduce the absorption of glucose from any food that it is mixed with. But it also slows mineral absorption, vitamin absorption, and essential amino acids absorption. The key word here is slow. As the food with guar gum makes its way along the small intestine, it will eventually come in contact with bacteria that will start to break it down and decrease the viscosity, which will then result in a normal rate of absorption for the essential nutrients in food. Hence, PHGG is an excellent fiber supplement for humans because it produces less gas than some other kinds of fiber would.
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PHGG has significant water-holding ability, but produces very low viscosity, contributing to a low glycemic index. In contrast, Citracel, hydroxycellulose, has good water-holding capacity but no viscosity capability. Metamucil (psyllium) has even better water-holding ability compared to Citracel but it does not increase viscosity that much. Gelatin and PHGG are both approved food additives that are used to stabilize and thicken food. Gelatin cannot form a viscous mix in the human gut because it is partially degraded by human digestive enzymes (starting in the stomach). PHGG, on the other hand, can be handled by bacteria only in the human gut so in the upper end of the small intestine, where the food comes out of the stomach, one can have an extremely viscous mix that stays intact for a long way through the small intestine if there is a sufficient amount of PHGG in the intake foods. Preferential Influence on Weight Control and Satiety The research regarding the effects of both PHGG and its precursor intact guar gum on weight control has been recently recognized. In animal studies, slower weight gain has often been associated with ingestion of guar gum. Several reports, Calvert et al. [91], Poksay and Schneeman [92], and Shah et al. [93, 94], show significant decreases in body weight gain, and food consumption as well as food efficiency is described wherein the diets containing 5% to 10% guar gum were fed to rats for about three to four weeks. Ikegami et al. [95] reported that food consumption and body weight gain were not decreased in rats fed a diet containing 5% guar gum for two weeks. In addition, less weight gain has also been mentioned in studies of longer duration. Graham et al. [96] observed that body weights of male Osborne-Mendel rats fed diets containing 1% to 15% guar gum for 91 days were significantly lower than those of control males even though food consumption was at least 90% of control animals’ intake. Obviously, no differences were noted in total body weights of female rats in such a study. However, in a separate subchronic toxicity study, the weight gain of male Fischer 344 rats fed a diet containing 5% or 10% guar gum were depressed 7% and 16% relative to control animals. Only a slight depression in weight gain was observed for female Fischer 344 rats fed the diets containing 10% guar gum. However, in the case of a 28-day subchronic toxicity study of PHGG, Sprague-Dawley rats were fed 500 or 2500 mg/kg bw/day of PHGG by their age. A slight growth depression was observed in male rats given the higher dose of PHGG; however, these test rats also consumed somewhat less amount of food. In contrast, Takahashi et al. [97] have observed that no considerable differences were reported in body weight gain or food consumption in male weanling Wistar rats fed diets containing 0, 5%, or 10% guar gum or PHGG for three weeks. Overall, the study revealed that PHGG is effective in decreasing body fat without any reduction in protein utilization. Heini et al. [98] studied the effect of PHGG on weight control in obesity and put 25 pre- and postmenopausal obese women having average age 46 and
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average body mass index about 35 on a controlled weight-loss diet for two successive weeks, followed by giving them either 20 g/day of PHGG or a placebo for one week, followed by a one-week washout and a one-week crossover. On Days 1, 3, and 7 of the intervention weeks, measurements were made of fasting serum glucose and insulin, plasma leptin and cholecystokinin (CCK), respiratory quotient, and hunger/satiety ratings. These identical measurements were taken 0, 15, 30, 60, and 120 minutes after a test meal providing 320 kcal with or without 8 g of PHGG. No significant effect was found on fasting values of satiety, glucose, insulin, CCK, leptin, or respiratory quotient, nor on two-hour postprandial insulin, glucose, respiratory quotient, or satiety. However, PHGG significantly increased postprandial CCK levels. It was concluded that soluble fiber might play a critical role in weight control [99]. Immunological Effects of PHGG Four-week-old male Sprague-Dawley rats were given diets with water-insoluble cellulose or a water-soluble fiber: intact guar gum, PHGG, glucomannan, or highly methoxylated pectin to study the effects on serum lipids and immunoglobulin (Ig) production [43]. All soluble fibers reduced total cholesterol and triacylglycerides, but only intact guar gum and glucomannan reduced phospholipids. All soluble fibers enhanced IgA productivity in the spleen and mesenteric lymph node lymphocytes, but PHGG did not increase serum IgA. The authors concluded that the effect of soluble fiber on lipid metabolism and IgA production is dependent on the molecular size. In a follow-up to the preceding study, Yamada et al. [100] fed 25 eightmonth-old Sprague-Dawley rats diets with 5% cellulose, intact guar gum, PHGG, glucomannan, or highly methoxylated pectin for three weeks. Intact guar gum decreased food intake and weight gain and increased liver weight. PHGG increased epidydimal adipose tissue weight. Guar gum influenced IgA, IgC, and IgM, suggesting that enhancement of the immune function by dietary fiber is mainly expressed in the gut immune system, as well as corroborating the previous conclusion that the molecular weight of the fiber is an important predictor of its effect. Naito et al. [101] gave nine-week-old female BALB/c mice weighing 18 to 20 grams a control diet or a diet with PHGG for two weeks before giving them 8% dextran sulfate sodium in water to induce colitis. PHGG reduced disease activity (weight loss, stool consistency, and blood in stool) and colonic shortening was reversed. Histological examination found reduced infiltration of inflammatory cells, especially neutrophils, and less disruption of mucosal cells, as well as reduced tissue-associated myeloperoxidase activity. These findings were interpreted as inhibition of mucosal inflammatory response due to the presence of PHGG. In conclusion, the hypothesis of a beneficial immunological impact of PHGG is not well supported by the available data.
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Improved Mineral Absorption In the beginning, certain dietary fibers were thought to limit absorption of certain vitamins and minerals because they do not appear to bind minerals. Recent reports on dietary fiber’s influence on mineral absorption is somewhat controversial, as some of the research has supported the idea that certain soluble fibers can actually enhance mineral absorption and thus improve total absorption. Therefore, another health benefit of PHGG may be improved mineral absorption. High-fiber diets have been shown to reduce the balance of calcium, magnesium, and to have a negative effect on calcium transport [102, 103]. Recently, Hara et al. [104] reported that PHGG soluble fibers may enhance calcium absorption. Enterally fed patients with persistent diarrhea given 2% PHGG had significantly increased plasma calcium levels after four days of supplementation [49]. The plausible mechanism was later described by Scholz and Ahrens, as reported in Palacio and Rombeau [105]: The PHGG passes through the small intestine, approaches the colon and cecum for complete fermentation, produces short-chain fatty acids and eventually reduces the gut pH. The reduced pH improves calcium absorption in the colon and cecum. PHGG also promotes the calcium and magnesium absorption, and reduced excretion in rats. Calcium absorption in five-sixths nephrectomized (NPX) rats was considerably lower than in sham-operated rats, but the absorption in NPX rats with PHGG added to the diet were just slightly lower than in sham-operated rats with PHGG. The increase in calcium absorption was attributed to the cecum and large intestine, wherein it was suggested that nephrectomy does not influence the absorption of calcium in the large intestine induced by PHGG feeding, and the increase in ceco-colonic adsorption compensates the decreasing proximal intestinal calcium transport associated with nephrectomy. Watanabe et al. [106, 107] demonstrated the effect of a phosphorylated guar gum hydrolysate on increased calcium solubilization and improved calcium absorption in rats. In a subsequent report [108], they revealed the improving effect of feeding with a phosphorylated guar gum hydrolysate on calcium absorption impaired by ovariectomy in rats. Hara et al. [104, 109, 110] shows the difference in calcium and magnesium absorption between the normal (sham-operated for caecectomy) rats fed for seven days supplemented with 5% PHGG [104]. Further, mechanisms of calcium absorption are suggested at the villus and cellular levels, wherein at the villus crypt height, cecal vein flow number of epithelial cells per crypt and mucosal to serosal calcium fluxes were found to be improved by PHGG. The expression of calbindin-D9k stimulated at the cellular level also results in an enhanced route to the active calcium transport. In another study, the PHGG was reported to have a significant effect on decreasing the incidence of bacterial translocation compared to enteral supplemented formula without PHGG addition. Gulliford et al. [111] revealed that guar delays intestinal calcium absorption in humans.
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Iron-Sufficient (IS) diet
27.8
a
25% Iron-Deficient (ID) diet
29.1
a
50% Iron-Deficient (ID) diet
29.8
a
IS + PHGG (5%)
32.3
20% ID + PHGG (5%)
36.7
50% ID + PHGG (5%)
39.9 0
ab b b
10 20 30 40 Iron Absorption Ratio (%)
50
(p<0.05/a: b = Significant difference, a: a b = no significant difference) Figure 6.7 Enhancement of iron absorption by PHGG: Three-day iron balance test in five-week-old Wistar rats.
Iron deficiency anemia can occur as a result of many factors, such as blood loss, pregnancy, inadequate dietary intake, or malabsorption; therefore, iron absorption and utilization were investigated in growing rats fed iron-deficient diets, with or without PHGG. It was successfully demonstrated (Figure 6.7) that PHGG prevents the loss of iron from hemoglobin, serum iron, and iron storage in the liver. That was apparent in the rats fed the iron-deficient diet without fiber [112]. Further, in a three-day iron balance test in rats performed by Takahashi et al. [113], PHGG increased iron absorption. Recently, de Cassia Freitas et al. [114] found that PHGG increases intestinal absorption of iron in growing rats with iron deficiency anemia. These studies suggested that PHGG might be effective in improving the iron status in individuals with clinical iron deficiency. Although lignin and psyllium were reported to inhibit iron absorption in dogs, calcium status was not affected by consumption of a high-fiber diet in chicks [115, 116]. Similarly, no changes were found in calcium, iron, or zinc excretion in men consuming PHGG in high amounts (36 g/day) for four weeks [47]. This suggests that PHGG does not have a significant effect on Zn absorption in the large intestine and that zinc absorption is not influenced by an intestinal fermentation process [117]. PHGG: An Effective Beauty Supplementation Very recently, it was discovered that supplementation with PHGG can impose an improvement of skin conditions. In the relevant study, 12 female patients with constipation were treated with 21 g/day of PHGG for four consecutive weeks and noticeable effects on skin conditions were monitored such as reduced acne, seborrhea and xeroderma (Figure 6.8).
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Improvement, %
70
After 4 weeks
60 50 40
58.3
50.0
30
33.3
20 10 0
Acne
Seborrhea
Xeroderma
Figure 6.8 Effect of PHGG on skin improvement.
Further observations on skin condition were monitored by microscope and the skin was less dry when examined after one month of supplementation. The planar dry skin showed dead surface rashes. However, after one month of supplementation the skin appeared like steric normal skin with a smooth surface. The water content of the skin was also found to increase significantly with PHGG supplementation measured by electrostatic capacitance at low frequency at ambient temperature and under controlled humidity. The plausible mechanism of action can be related to the well-balanced physiological functions (e.g., ingestion, digestion, and excretion systems). Due to soluble PHGG dietary fiber absorbs relatively less amounts of water from the body, which allows the skin to maintain higher moisture content and a smooth surface.
Safety Issues and Toxicological Behavior of PHGG The safety of guar gum was assessed by the Joint Expert Committee on Food Additives (JECFA) in 1975 and by the EC Scientific Committee for Food (SCF) in 1978 [28, 47, 118–120], and has been considered generally recognized as safe since 1974 in numerous food applications. Because guar gum has been approved as a safe additive, partially hydrolyzed guar gum (PHGG) can also be considered a safe food additive. Various studies are available that confirm PHGG has similar properties and fundamental physiological effects as guar gum. However, PHGG also has undergone extensive toxicity testing and has been found to be safe. In vitro and animal studies performed on the acute toxicity of PHGG show that supplementation of PHGG was well tolerated, and food consumption and body weight gain were not influenced in Sprague-Dawley rats at dosage levels of 0, 0.5, and 2.5 g/kg body weight/day. In addition no differences were observed in hematology, urinalyses, ophthalmology, and histopatho-
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logical parameters showed no signs of toxicity in rats given dietary levels of up to 10% PHGG for three consecutive weeks [74, 119]. The mutagenicity was accessed upon dissolving different amounts of PHGG (0.05 to 5.0 mg/ plate) in water via microbial reverse mutation assay with Salmonella typhimurium TA100 and TA98 strains. Concentration up to 5.0 mg/plate did not reflect any effect on reverse mutation. Furthermore, an in-depth subchronic oral toxicity was carried out on Wister rats for 13 consecutive weeks. Varied portions of PHGG were fed and clinical signs, body weights, food and water intake, hematology, clinical chemistry, and pathology were studied. It was revealed that the ingestion of dietary levels of up to 10% was not associated with any adverse effects or toxicity. Suzuki and Hara [45] fed five-week-old male Sprague-Dawley rats high-fructose diets with or without 7.5% PHGG for 30 days. Glucose tolerance tests were given on Days 0, 14, and 28. It was observed that PHGG improved glucose tolerance and reduced hyperinsulinemia on Day 28. Additionally, fructose lowered the glycogen concentration in rat muscle while PHGG does not show this effect. The details are summarized in the latter part of this section. Ishihara et al. [121] summarized the preventive effect of partially hydrolyzed guar gum on infection of Salmonella enteritidis in young and laying hens. Daily consumption of PHGG at levels up to 20 g/day was proven safe. Also, PHGG is clinically proven to lower glycemic index, improve mineral absorption, and maintain digestive health. Particularly, no effects on hematologic, renal, and hepatic parameters were observed in association with PHGG intake in 10 healthy male volunteers. The subjects consumed a normal diet supplemented with a liquid formula, with or without 21 g/L PHGG. There were positive effects on stool softening but no other gastrointestinal changes were observed. An oral glucose tolerance test was performed by administration of 75 g glucose in 200 mL water. The value of blood glucose levels after the oral glucose tolerance test showed no differences between the liquid diet and its fiber-rich counterpart. Basal serum insulin levels and levels after the oral glucose load did not show any difference between diets. Blood arginine levels taken as an estimation of amino acid absorption, stool fat and fat estimation according to the 13C-Hiolein breath test, were not different between the two diet groups. The results demonstrate that PHGG does not interfere with the normal absorption of glucose, amino acid, and fat, and does not affect normal blood safety parameters, and therefore is a safe source of soluble fiber [122]. Another study also confirmed the safe use of PHGG, wherein 12 men consumed a liquid diet, alone, or with 21 g/l PHGG. This amount was well tolerated and showed no side effects. Ten obese women (n = 25) taking 20 g/day of PHGG for one week had no differences in fasting values of glucose and insulin. There was also no significant effect on twohour postprandial responses of glucose or insulin. Further, administration of PHGG (36 g/day) for four weeks to 11 adult men resulted in no side effects and no effects on mineral excretion [54]. In light of published scientific evidence, PHGG is considered safe and appropriate to use as an ingredient in
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nutritional products and liquid oral supplement products for the purpose of providing dietary fiber. The acute oral toxicity, also abbreviated as LD50, of PHGG was reported to be greater than 5000 mg/kg body-weight/day in rats [8], while the acute oral toxicity of its precursor (intact guar gum) was reported to be 9400 mg/ kg body-weight/day in rats and 8100 mg/kg body-weight/day in mice [123]. Koujitani et al. [124] of the Pharmaceutical Affairs Bureau, Ministry of Health and Welfare, Tokyo, acclimatized four-week-old mice and rats for two weeks, and fed a limited dose of 6000 mg/kg body-weight/day of PHGG via gavage of a 30% conc in water. Condition and mortality were observed at 1, 3, 6, and 24 hours, for 14 days. There were no test-article-related effects on body weights and feed consumption, no deaths, or necropsy findings during the test period. The acute oral toxicity (LD50) was >6000 mg/kg body-weight/ day in both males and females of both mice and rat species. From a subacute oral toxicity study of PHGG, Takahashi et al. [119] reported that no observed adverse effect level (NOAEL) is 2500 mg/kg body-weight/day, the highest dose tested. There were no deaths, and no statistically significant compoundrelated dose-dependent effects on body weight gain, feed consumption, general behaviour, ophthalmology, urinalysis, hematology, clinical chemistries, gross necropsy findings, absolute or relative organ weights, or histological exam. Moreover, Koujitani et al. [124] reported even higher levels of no observed adverse effect level (NOAEL) for PHGG (10% dietary concentration): 5000 and 5700 mg/kg body-weight/day for male and female rats, respectively, as this study employed a higher concentration of PHGG than the concentration used in the study of Takahashi et al. [62]. Mutagenicity tests of guar gum in several test systems showed that guar gum did not cause mutagenic changes such as signs of cellular toxicity that could probably have occurred by osmotic effects of the guar gum during these test systems. Such cellular toxicity is also known as genotoxicity. Aruga [125] performed the mutagenicity test of PHGG wherein the PHGG (50 to 5000 pg/plate) was screened for mutagenic potential in a reverse mutation assay using Salmonella typhimurium TA100 and TA98 with and without phenobarbital and 5,6-benzoflavone-induced rat S9 mix for metabolic activation. It was observed that PHGG did not increase the number of revertants and, therefore, was not mutagenic in this assay. In another study, Takahashi et al. [119] tested the mutagenic potential of PHGG in a reverse mutation assay at concentrations of 50, 100, 500, 1000, and 5000 µg/plate with Salmonella typhimurium strains TA98 and TA100, with and without S9 activation. No indications of mutagenicity were observed either with or without activation. Later, Koujitani et al. [124] performed an Ames assay with Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537, and Escherichia coli strain WP2uvrA, with and without S9 activation at concentrations of 313, 625, 1250, 2500, and 5000 µg/plate. Further, there was no evidence of mutagenicity with or without metabolic activation.
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Similarly, the chronic oral toxicity, carcinogenicity bioassay, developmental toxicity, and colonic tumorigenesis and cellular proliferation of intact guar gum are reported while no reports are available using PHGG on the aforementioned assay.
Some Possible Adverse Effects of Dietary Fiber Presenting data from a different point of view, the potential adverse effects of dietary fiber such as PHGG can also be simply listed as numbers. The likely outcome is that a healthy adult who consumes dietary fiber under the safe recommended limit may not have any adverse effect or problems with nutrient absorption. However, much more research is still needed to determine the recommended dose for children and the elderly population. One major drawback or negative effect of PHGG is the reduced absorption of vitamins, protein, and calories. However, the effect can be controlled via safe intake of the PHGG fiber. The second possible adverse effect is that fiber-rich enteral supplemented formulations may cause blockage in small diameter feeding tubes which in turn causes a problem with gums and other highly viscous fibers. Moreover, limited data are available on the effectiveness of fiberenriched formulations under long-term conditions. Also, the fermentation of dietary fiber like PHGG by anaerobic bacteria present in the large intestine creates gases such as hydrogen, carbon dioxide, methane, etc., which could be possibly related to flatulence or complaints of distention. The mechanism suggested is quite simple and tends to apply when intake content of dietary fiber is higher. The solution of this problem can be resolved with higher fluid intake when fiber content is increased. This would allow the gastrointestinal tract time to adapt the normal laxation. In general, the recommended PHGG fibers, whether added to food, or consumed as supplements, must be easily incorporated into the diet for improved compliance. Another area of particular emphasis is the effect of PHGG fiber intake on mineral bioavailability, particularly calcium, magnesium, iron, and zinc. However, now it is clinically proven that there is very little evidence that fiber itself, absent phytate, has adverse effects on mineral absorption or status, wherein it was suggested that intake of dietary PHGG fiber even at levels in excess of 40 g/ day do not result in considerable increase in gastrointestinal distress except under special circumstances such as pancreatic disease. Effects of PHGG in cecal bacterial overgrowth and increased incidence of bacterial translocation from the intestinal lumen to the draining mesenteric lymph nodes are also addressed [126]. So far, two studies on the effect of PHGG on bacterial translocation have been reported; however, they produced conflicting findings. In an unpublished study by Wells [127], it was found that supplementation of an enteral formula with 2.5% PHGG did not produce a measurable effect on the incidence of bacterial translocation in
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mice with normal cecal biota or in mice with bacterial overgrowth and high levels of bacterial translocation induced by metronidazole, but did increase bacterial translocation in mice that had high levels of bacterial translocation induced by lipopolysaccharide. However, the second study, by Wells et al. [128], has found that PHGG ingestion reduced bacterial translocation in lipopolysaccharide-treated mice. Although the evidence does not present a clear picture, there is little basis for concern that ingestion of PHGG leads to significant increase in bacterial translocation from the cecum or colon, even in the presence of substantial bacterial overgrowth.
Anticarcinogenic Properties of PHGG In a study, Weaver et al. [129] investigated the anticarcinogenic properties of PHGG, wherein 60 four-week-old female Fischer F344 rats were fed either a fiber-free diet or the same diet with 5% PHGG replacing sucrose for three weeks. They were then injected with azoxymethane subcutaneously each week for 10 weeks. Fecal in vitro fermentation rates were increased, as were butyrate concentrations in colonic contents. However, no anticarcinogenic effect was found. However, in a separate study Cihan et al. [130] explored the role of PHGG as an early postoperative enteral nutrient in colonic anastomotic healing. Fifty obese male Balb/c mice weighing 50 to 60 g were given transverse colon anastomosis, and then divided into five groups of 10 mice each and fed for seven days with early enteral nutrients using normal chow and standard enteral diets with PHGG. No differences were observed in bursting pressure. Also, other research failed to demonstrate any potential benefit of PHGG with regard to treatment of colonic anastomosis.
History of Regulatory Status of PHGG In Japan, key procedures exist that permit functional food ingredients to be recognized by a government-owned agency, which is responsible for publishing a monograph for food ingredients. A monograph reviewing the safety of PHGG and its physiological effects and food product functionality was first published by the concerned governmental agency in March 1990 [131]. Therefore, no regulatory approval is necessary for the sale of PHGG in Japan. In the U.S., the FDA has granted PHGG as Generally Recognized As Safe (GRAS) [132, 133] status. In Europe, the Belgian High Council of Health first approved PHGG in 1992. Later in 1993, the Ministry of Health approved the use of PHGG in solid foods and that further extended for its use in liquid foods in 1996. During this period, the Spanish Ministry of Health also
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accepted the use of PHGG in functional foods and supplements. The Dutch Food Authority also accepted the use of PHGG in both solid and liquid foods. In 1992, the Swiss Federal Office of Public Health also separately approved the use of PHGG since Switzerland is not a member of the European Union. In 1997, the European Union Novel Foods Regulation committee approved PHGG for food applications throughout all European Union countries.
PHGG as Food Additive: Commercial Applications Partially hydrolyzed guar gum (PHGG) appears to have little or no interaction with common food ingredients and it does not destabilize emulsions, change the viscosity of protein solutions, affect the flavor or color of products, or cause soluble materials to precipitate. In addition, PHGG prolongs the shelf life of high-starch foods, such as bread, by decreasing the turbidity of dextrin when it is added to a dextrin solution at low temperatures. PHGG is presently used in many different capacities in food and beverages. Some potential functional uses of PHGG as well as the specific chemical and physical properties of PHGG make it a unique ingredient for improving the quality of food items. As well as being a source of dietary fiber, addition of PHGG can improve processing by increasing the flowability of cereals, providing body and mellow flavor in most beverages, stabilizing the colloid system of dry and liquid meal replacements, mellowing tartness and firming texture in yogurt, stabilizing the foam system of shakes, improving the suspension of particulate matter in soups and dressings, and improving the quality of baked goods [28]. A few examples of PHGG as an additive in food applications are shown below. It was shown that PHGG remained stable in yogurt and liquid beverages. PHGG (3%) was mixed with milk and starter yogurt (20%) and incubated for 40°C for 15 hours in aerobic conditions. Dietary fiber measurements were taken after fermentation and again repeated after one week of storage at 4°C. Figure 6.9a displays the higher stability of PHGG in yogurt compared to inulin, polydextrose, and resistant dextrin after fermentation as well as after one week of storage. The stability of inulin, polydextrose, and resistant dextrin was found to decrease upon storage. The dietary fiber content data were calculated by AOAC method 985.29. Similarly, the effects of PHGG on the bacterial content of yogurt were monitored by counting the lactic acid bacteria per mL of the substance after fermentation (typically incubation) and after one week of storage (Figure 6.9b). Reduction in stability was noted in the case of inulin, polydextrose, and resistant dextrin after the one-week storage, while the PHGG showed significant stability under similar conditions. Another application that PHGG recognizes as an additive is the prevention of noodle tangling, where 5% of PHGG was added into seasoning sauce and
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Food Stabilizer (whipped cream) Alternative of Wheat Flour (cookies)
Bulking Agent (yogurt, ice cream) PHGG as a Food Additive Sugar Substitute (whipped cream, steamed bread)
Inhibitor of Starch Dispersion (rice) Coats Materials (dried fish, nuts)
Figure 6.9 (a) Fiber content stability of PHGG estimated by the AOAC Method 985.29, and (b) effect of PHGG on the bacterial content of yogurt.
kept at 5°C for 2 hours. Soaking and spray methods are recommended for the preparation. Particularly, no tangling was observed when 5% to 10% PHGG was used as an additive (Figure 6.10). An additional interesting application of PHGG as an additive is the sugar anti-caking effect, wherein PHGG and oligofructose were mixed and kept at 30°C at 70% relative humidity for two weeks. Without PHGG, the moistening effect was observed and caking was possible up to 5% PHGG doses. At higher dosages (10%) of PHGG, the anti-caking effect was significant. Simple mixing or granulation methods are recommended. The results evidently demonstrated that PHGG could be effectively employed where anti-caking properties are required. Further, masking the unpleasant taste of artificial sweeteners, especially in beverages, stabilization of whipped cream or any kind of foams, preventing of antioxidation of dry fruits (nuts, etc.) by forming film on their surface, prevention of adhesion to teeth by soft candy and improvement of texture of cookies can be successfully achieved with PHGG. The successful applications of PHGG in a number of commercial products are currently available and are being used in food, beverages, and nutritional supplements.
Summary PHGG is a functional fiber and positively recommended to be consumed in order to increase the total intake of dietary fiber. Several reports based on studies in animals, healthy humans, as well as in NIDDM (diabetic) patients,
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Dietary Fiber (%)
100
1
80
1 2 3
60
4
4
2 3
40 20 0
After 1 week (4°C)
After fermentation
Lactic Acid Bacteria (count/mL)
(a) 8.5 8.4 8.3
2 4
4 Resistant Dextrin
3 1
3 Polydextrose 2 Inulin 1 PHGG 0 No fiber
0
8.2 8.1 8
Mean (Log10) After fermentation
After 1 week (4°C) (b)
Figure 6.10 PHGG prevents noodle tangling.
evidently demonstrate that administration of PHGG is significantly effective in attenuating the postprandial rise in plasma glucose and insulin. However, the proposed effect of PHGG appears to be independent to the actual molecular weight of the guar gum (viscosity related). Further, abundant evidence supports beneficial effects of PHGG on blood cholesterol and other lipids, especially in the short term. In this context, the importance of the viscosity of the guar gum in producing a beneficial effect on blood lipids remains somewhat unclear. Further, the beneficial effects of PHGG on laxation-related properties have been well demonstrated in a number of studies with healthy adults, adults with mild illness, patients receiving enteral nutrition for particular illness, severely ill patients, and infants. There is strong evidence supporting the hypotheses of a prebiotic effect of PHGG and the role of dietary management in irritable bowel syndrome. These effects have yet to be fully elucidated. Partially hydrolyzed guar gum (PHGG) is intended to be used in conventional foods and enteral products as a functional fiber to increase the total daily intake of dietary fiber. In summary, PHGG is a functional fiber that has several health benefits such as cholesterol lowering, glycemic effects, laxative and prebiotic effects. PHGG
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Control
With PHGG
Figure 6.11 Partially hydrolyzed guar gum prevents noodle tangling.
is an ideal dietary fiber for the enrichment of fiber in food because it has reasonably low viscosity, is tasteless and odorless, and thus produces clear solutions in beverage. Also, PHGG has become a fully integrated food material without altering the rheology, taste, or appearance of products and is highly recommended for foods and supplements, primarily for nutritional purposes.
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61. Lampe, J.W., Effertz, M.E., Larson, J.L. and Slavin, J.L. (1992) ‘Gastrointestinal effects of modified guar gum and soy polysaccharide as part of an enteral formula diet’ J. Parenter Enteral Nutr., 16:538–544. 62. Takahashi, H., Wako, N., Okudo, T., Ishihara, N., Yamanaka, J. and Yamamoto, T. (1994) ‘Influence of partially hydrolyzed guar gum on constipation in women’ J. Nutr. Sci. Vitaminol., 40:251–259. 63. Yamatoya, K., Kuwano, K., Suzuki, J., Mitamura, T. and Sekiya, K. (1995) ‘Effect of hydrolyzed guar gum on frequency and feeling of defecation in humans’ J. Appl. Glycosci., 42:251–257. 64. Homann, H.H., Kemen, M., Fuessenich, C., Senkal, M. and Zumtobel, V. (1994) ‘Reduction in diarrhea incidence by soluble fiber in patients receiving total or supplemental enteral nutrition’ J. Parenter Enteral Nutr., 18:486–490. 65. Patrick, P.G., Gohman, S.M., Marx, S.C., DeLegge, M.H. and Greenberg, N.A. (1998) ‘Effect of supplements of partially hydrolyzed guar gum on the occurrence of constipation and use of laxative agents’ J. Am. Diet. Assoc., 98:912–914. 66. Fussell, S.T., Garmhausen, I. and Koruda, M.J. (1996) ‘The influence of guar gum on diarrhea in critically ill tube-fed patients’ J. Parenter Enteral Nutr. 20:26S. 67. Homann, H.H., Senkal, M., Lehnhardt, M. and Druecke, D. (2003) ‘The effects of partially hydrolyzed guar gum (PHGG) added to enteral nutrition in medical and surgical patients’ Revista Italiana di Nutrizione Parenterale ed Enterale, 21:78–81. 68. Rushdi, T.A., Pichard, C. and Khater, Y.H. (2004) ‘Control of diarrhea by fiberenriched diet in ICU patients on enteral nutrition: a prospective randomized controlled trial’ Clin. Nutr., 23:1344–1352. 69. Spapen, H., Diltoer, M., Van Malderen, C., Opdenacker, G., Suys, E. and Huyghens, L. (2001) ‘Soluble fiber reduces the incidence of diarrhea in septic patients receiving total enteral nutrition: a prospective, double-blind, randomized, and controlled trial’ Clin. Nutr., 20:301–305. 70. Alam, N.H., Meier, R., Schneider, H., Sarker, S.A., Bardhan, P.K., Mahalanabis, D., Fuchs, G.J. and Gyr, N. (2000) ‘Partially hydrolyzed guar gum: supplemented oral rehydration solution in the treatment of acute diarrhea in children’ J. Pediatr. Gastroenterol. Nutr., 31:503–507. 71. Salyers, A.A., West, S.H.E., Vercellotti, J.R. and Wilkins, T.D. (1977) ‘Fermentation of mucins and plant polysaccharides by anaerobic bacteria from the human colon’ Appl. Environ. Microbiol., 34:529–533. 72. Goldin, B.R. and Gorbach, S.L. (1976) ‘The relationship between diet and rat fecal bacterial enzymes implicated in colon cancer’ J. Natl. Cancer Inst., 57:371–375. 73. Hood, S.K. and Zottola, E.A. (1988) ‘Effect of low pH on the ability of Lactobacillus acidophilus to survive and adhere to human intestinal cells’ J. Food Sci., 53:1514–1516. 74. Alam, N.H., Meier, R., Rausch, T., Meyer-Wyss, B., Hildebrand, P., Schneider, H., Bachmann, C., Minder, E., Fowler, B. and Gyr, N. (1998) ‘Effects of a partially hydrolyzed guar gum on intestinal absorption of carbohydrate, protein and fat: a double-blind controlled study in volunteers’ Clin. Nutr., 17:125–129. 75. Velazquez, M., Davies, C., Marett, R., Slavin, J.L. and Feirtag, J.M. (2000) ‘Effect of oligosaccharides and fibre substitutes on short-chain fatty acid production by human faecal microflora’ Anaerobe, 6:87–92. 76. Pylkas, A.M., Juneja, L.R. and Slavin, J.L. (2005) ‘Comparison of different fibers for in vitro production of short chain fatty acids by intestinal microflora’ J. Med. Food, 8:113–116.
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77. Okubo, T., Ishihara, N., Takahashi, H., Fujisawa, T., Kim, M., Yamamoto, T. and Misuoka, T. (1994) ‘Effects of partially hydrolyzed guar gum intake on human intestinal microflora and its metabolism’ Biosci. Biotech. Biochem., 58:1364–1369. 78. Tuohy, K.M., Kolida, S., Lustenberger, A.M. and Gibson, G.R. (2001) ‘The prebiotic effects of biscuits containing partially hydrolysed guar gum and fructooligosaccharides: a human volunteer study’ Br. J. Nutr. 86:341–348. 79. Takahashi, H., Akachi, S., Ueda, Y., Kim, M., Hirano, K. and Yamamoto, T. (1995) ‘Effect of liquid diets with or without partially hydrolyzed guar gum on intestinal microbial flora and function of rats’ Nutr. Res., 15:527–536. 80. Rastall, B. and Gibson, G. (2006) Prebiotics: Development and Application. New York: John Wiley & Sons. 81. Miller-Fosmore, C.M., Holt, S.M. and Cote, G.L. (2002) ‘Utilization of oligosaccharides by colonic bacteria’ Illinois State Academy of Science 95(Supplement): 93. 82. Salminen, S. (2004) Lactic Acid Bacteria: Microbiological and Function Aspects, 3rd ed. New York: Marcel Dekker. 83. Giannini, E.G., Mansi, C., Dulbecco, P. and Savarino, V. (2006) ‘Role of partially hydrolyzed guar gum in the treatment of irritable bowel syndrome’ Nutr. 22:334–342. 84. Uneddu, A. (2005) ‘Diet therapy in constipation-predominant irritable bowel syndrome (C-IBS): comparison between Sardinian brown bread and soluble non-gelling fibre (PHGG) dietary supplementation’ Eur. Bull. Drug Res., 13:1–6. 85. Giaccari, S., Grasso, G., Tronci, S., Allegretta, L., Sponziello, G., Montefusco, A., Siciliano, J.G., Guarisco, R., Candiani, C. and Chiri, S. (2001) ‘Partially hydrolyzed guar gum: fiber added to treat irritable bowel syndrome’ Clinica Terapeutica, 152:21–25. 86. Parisi, G.C., Zilli, M., Miani, M.P., Carrara, M., Bottona, E., Verdianelli, G., Battaglia, G., Desideri, S., Faedo, A., Marzolino, C., Tonon, A., Ermani, M. and Leandro, G. (2002) ‘High-fiber diet supplementation in patients with irritable bowel syndrome (IBS)’ Digest Dis. Sci. 47:1697–1704. 87. Parisi, G.C., Bottona, E., Carrara, M., Cardin, F., Faedo, A., Goldin, D., Marino, M., Pantalena, M., Tafner, G., Verdianelli, G., Zilli, M. and Leandro, G. (2005) ‘Treatment effects of partially hydrolyzed guar gum on symptoms and quality of life of patients with irritable bowel syndrome: a multicenter randomized open trial’ Digest Dis. Sci., 50:1107–1112. 88. Van Nieuwenhoven, A.M., Eva Kovacs, M.R., Brummer, R.J.M., Plantenga, M.S.W. and Brouns, F. (2001) ‘The effect of different dosages of guar gum on gastric emptying and small intestinal transit of a consumed semisolid meal’ J. Am. College Nutr., 20:87–91. 89. Rose, K.E., Ishihara, N., Irimescu R. and Juneja, L.R. (2006) ‘Glycemic response, glycemic index and soluble fiber: Comparative effect of partially hydrolysed guar gum (Sunfiber) and other soluble fibers on glycemic response’ Ingredients, Health and Nutrition, 6–9. 90. Trinidad, T., Perez, E., Loyola, A., Mallillin, A., Encabo, R., Yokawa, T., Aoyama, N. and Juneja, L.R. (2004) ‘Glycemic index of sunfiber (cyamoposis tetragonolobus) product in normal and diabetic subjects’ Int. J. Food Sci. Technol., 39:1093–1098. 91. Calvert, R., Schneeman, B.O., Satchithanandam, S., Cassidy, M.M. and Vahouny, G.V. (1985) ‘Dietary fiber and intestinal adaptation: effects on intestinal and pancreatic digestive enzyme activities’ Am. J. Clin. Nutr., 41:1249–1256.
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92. Poksay, K.S. and Schneeman, B.O. (1983) ‘Pancreatic and intestinal response to dietary guar gum in rats’ J. Nutr., 113:1544–1549. 93. Shah, N., Mahoney, R.R. and Pellett, P.L. (1986) ‘Effect of guar gum, lignin and pectin on proteolytic enzyme levels in the gastrointestinal tract of the rat: a time-based study’ J. Nutr., 116:786–794. 94. Shah, N., Mahoney, R.R. and Pellett, P.L. (1987) ‘Effect of guar gum, pectin and lignin on proteolytic zymogens in the pancreas of the rat’ Nutr. Rep. Int., 36:223–228. 95. Ikegami, S., Tsuchihashi, F., Harada, H., Tsuchihashi, N., Nishide, E. and Innami, S. (1990) ‘Effect of viscous indigestible polysaccharides on pancreaticbiliary secretion and digestive organs in rats’ J. Nutr., 120:353–360. 96. Graham, S.L., Arnold, A., Kasza, L., Ruffin, G.E., Jackson, R.C., Watkins, T.L. and Graham, C.H. (1981) ‘Subchronic effects of guar gum in rats’ Food Cosmet. Toxicol., 9:287–290. 97. Takahashi, H., Yang, S.I., Kim, M. and Yamamoto, T. (1994) ‘Protein and energy utilization of growing rats fed on the diets containing intact or partially hydrolyzed guar gum’ Comp. Biochem. Physiol., 107A:255–260. 98. Heini, A.F., Lara-Castro, C., Schneider, H., Kirk, K.A., Considine, R.V. and Weinsier, R.L. (1998) ‘Effect of hydrolyzed guar fiber on fasting and postprandial satiety and satiety hormones: a doubleblind, placebo-controlled trial during controlled weight loss’ Int. J. Obesity, 22:906–909. 99. Minekus, M., Jelier, M., Xiao, J.Z., Kondo, S., Iwatsuki, K., Kokubo, S., Bos, M., Dunnewind, B. and Havenaar, R. (2005) ‘Effect of partially hydrolyzed guar gum (PHGG) on the bioaccessibility of fat and cholesterol’ Biosci. Biotechnol. Biochem., 69:932–938. 100. Yamada, K., Tokunaga, Y., Ikeda, A., Ohkura, K. I., Kaku-Ohkura, S., Mamiya, S., Lim, B.O. and Tachibana, H. (2003) ‘Effect of dietary fiber on the lipid metabolism and immune function of aged Sprague-Dawley rats’ Biosci. Biotechnol. Biochem., 67:429–433. 101. Naito, Y., Takagi, T., Katada, K., Uchiyama, K., Kuroda, M., Kokura, S., Ichikawa, H., Watabe, J., Yoshida, N., Okanoue, T. and Yoshikawa, T. (2006) ‘Partially hydrolyzed guar gum down-regulates colonic inflammatory response in dextran sulfate sodium-induced colitis in mice’ J. Nutr. Biochem., 17:402–409. 102. Kelsay, J.L., Behall, K.M and Prather, E.S. (1979) ‘Effect of fiber from fruits and vegetables on metabolic responses of human subjects’ Am. J. Clin. Nutr., 32:1876–1880. 103. Oku, T., Konishi, F. and Hosoya, N. (1982) ‘Mechanism of inhibitory effect of unavailable carbohydrate on the intestinal calcium absorption’ J. Nutr., 112:410–415. 104. Hara, H., Nagata, M., Ohta, A. and Kasae, T. (1996) ‘Increases in calcium absorption with ingestion of soluble dietary fibre, guar-gum hydrolysate, depend on the caecum in partially nephrectomized and normal rats’ Br. J. Nutr., 76:773–784. 105. Palacio, J.C. and Rombeau, J.L. (1990) ‘Dietary fiber: a brief review and potential application to enteral nutrition’ Nutr. Clin. Pract., 5:99–106. 106. Watanabe, O., Hara, H. and Kasai, T. (2000) ‘Effect of a phosphorylated guar gum hydrolysate on increased calcium solubilization and the promotion of calcium absorption in rats’ Biosci. Biotechnol. Biochem., 64:160–166.
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107. Watanabe, O., Hara, H., Aoyama, Y. and Kasai, T. (2000) ‘Increased intestinal calcium absorption from the ingestion of a phosphorylated guar gum hydrolysate independent of cecal fermentation in rats’ Biosci. Biotechnol. Biochem., 64:613–616. 108. Watanabe, O., Hara, H., Aoyama, Y. and Kasai, T. (2001) ‘Improving effect of feeding with a phosphorylated guar gum hydrolysate on calcium absorption impaired by ovariectomy in rats’ Biosci. Biotechnol. Biochem., 65:613–618. 109. Hara, H, Suzuki, T., Kasai, T., Aoyama, Y. and Ohta, A. (1999). Ingestion of guargum hydrolysate partially restores calcium absorption in the large intestine lowered by suppression of gastric acid secretion in rats’ Br. J. Nutr., 81:315–321. 110. Hara, H., Suzuki, T., Kasai, T., Aoyama, Y. and Ohta. A. (1999) ‘Ingestion of guar gum hydrolysate, a soluble fiber, increases calcium absorption in totally gastrectomized rats’ J. Nutr., 129:39–45. 111. Gulliford, M.C., Pover, G.G., Bicknell, E.J. and Scarpello, J.H.B. (1988) ‘Guar delays intestinal calcium absorption in man’ Eur. J. Clin. Nutr., 42:451–454. 112. Conrad, M.E. (1987) Physiology of the Gastrointestinal Tract, 2nd edition, Johnson, LR, Ed. Raven Press. 1437–1453. 113. Takahashi, H., Yang, S.I., Ueda, Y., Kim, M. and Yamamoto, T. (1994) ‘Influence of intact and partially hydrolysed guar gum on iron utilization in rats fed on iron-deficient diets’ Comp. Biochem. Physiol., 109A:75–82. 114. De Cassia Freitas, K., Amancio, O.M., Ferreira, N.N., Fagundes, N.U. and de Morais M.B. (2006) ‘Partially hydrolyzed guar gum increases intestinal absorption of iron in growing rats with iron deficiency anemia’ Clin. Nutr., 25:851–858. 115. Van der Aar, P.J., Fahey, G.C. Jr., Ricke, S.C., Allen, S.C. and Berger, L.L. (1983) ‘Effects of dietary fibers on mineral status of chicks’ J. Nutr., 113:653–661. 116. Fernandez, R. and Phillips, S.F. (1982) ‘Components of fiber impaired iron absorption in the dog’ Am. J. Clin. Nutr., 35:107–112. 117. Hara, H., Konishi, A. and Kasai, T. (2000) ‘Contribution of the cecum and colon to zinc absorption in rats’ J. Nutr., 130:83–89. 118. Muto, Y. (1990) Digestion and Absorption. Daiichi Shuppan Co. Ltd., Tokyo. 185–187. 119. Takahashi, H., Yang, S.I., Fujiki, M., Kim, M., Yamamoto, T. and Greenberg, N.A. (1994) ‘Toxicity studies of partially hydrolyzed guar gum’ J. Amer. Coll. Toxicol., 13:273–278. 120. Trepel, F. (2004) ‘Dietary fibre: more than a matter of dietetics. II. Preventative and therapeutic uses’ Wien. Klin.Wochenschr, 116: 511–522. 121. Ishihara, N., Chu, D.C., Akachi, S. and Juneja, L.R. (2000) ‘Preventive effect of partially hydrolyzed guar gum on infection of Salmonella enteritidis in young and laying hens’ Poultry Sci., 79:689–697. 122. Okazaki, H., Nishimune, T. and Senga, T. (1999) ‘Improvement in defecation by a beverage containing partially hydrolyzed guar gum’ J. Nutr. Food, 2:1–8. 123. Bailey, D.E., Morgareidge, K. and Collins, T.X. (1976) ‘Comparative acute oral toxicity of twelve food grade gums in the mouse, rat, hamster, and rabbit’ Toxicol. Appl. Pharmacol., 37:143. 124. Koujitani, T., Oishi, H., Kubo, Y., Maeda, T., Sektya, K., Yasuba, M., Matsuoka, N., Nishimura, K. (1997) ‘Absence of detectable toxicity in rats fed partially hydrolyzed guar gum (K-13) for 13 weeks’ Int. J. Toxicol., 16:611–623. 125. Aruga, F. (1990) ‘Reverse mutation study on Sunfiber using bacteria’ Unpublished final report: Nihon Bioresearch Center, Inc.
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126. Spaeth, C., Berg, R.D., Specian, R.D. and Deitch, E.A. (1990) ‘Food without fiber promotes bacterial translocation from the gut’ Surgery, 108:240–247. 127. Wells, C.L. (1991) ‘Effect of Impact (with and without guar/soy supplementation) and Compleat on the composition of the intestinal flora, on ileal histology, and on the translocation of intestinal bacteria’ Letter to: Sandoz Nutrition Corporation (16 May 1991). 128. Wells, C.L., Barton, R.G., Jechorek, W.P., Gillingham, K.J. and Cerra F.B. (1992) ‘Effect of fiber supplementation of liquid diet on cecal bacteria and bacterial translocation in mice’ Nutr., 8:266–271. 129. Weaver, G.Y., Tangel, C.T., Krause, J.A., Alpern, H.D., Jenkins, P.L., Parfitt, M.M. and Stragand, J.J. (1996) ‘Dietary guar gum alters colonic microbial fermentation in azoxymethane-treated rats’ J. Nutr., 126:1979–1991. 130. Cihan, A., Oguz, M., Acun, Z., Ucan, B.H., Armutcu, F., Gurel, A. and Ulukent, S.C. (2004) ‘Comparison of early postoperative enteral nutrients versus chow on colonic anastomotic healing in normal animals’ Eur. Surg. Res. 36:112–115. 131. Okamoto, T. (1990) Effective Applications for Functional Ingredients in Food and Beverages: Sunfiber. The Ministry of Agriculture, Forestry and Fisheries-Bureau of Food Distribution, Confectionary Technical Center Inc., Tokyo, Japan. 132. Angeles, R.M. (1995) ‘Letter: From Food and Drug Administration’ (23 May 1995). 133. Rulis, A.M. (1995) Federal Register 60: 36151 (13 July 1995).
7 Acacia Gum Sebastien Baray
Contents Characteristics...................................................................................................... 121 Definition..................................................................................................... 121 Safety ........................................................................................................... 122 Nutritional Aspects............................................................................................. 123 Metabolism.................................................................................................. 123 Tolerance...................................................................................................... 123 Prebiotic Effect............................................................................................ 123 Potential Health Benefits of Acacia Gum.......................................................... 125 Reduction of Diarrhea and Constipation................................................ 125 Improvement of Nitrogen Excretion........................................................ 126 Reduction of Cholesterol............................................................................ 127 Hypoglycemic Effect.................................................................................. 127 Applications of Acacia Gum in Food Products............................................... 128 Beverages...................................................................................................... 129 Bakery Products.......................................................................................... 130 Cereal Bars................................................................................................... 130 Extruded Snacks and Breakfast Cereals.................................................. 130 Confectionery.............................................................................................. 130 References............................................................................................................. 131
Characteristics Definition Acacia gum (also known as gum arabic) is an all-natural sap that exudes from stems and branches of Acacia trees (Leguminosae), which grow in the Sahel zone of Africa. The only two botanical species allowed for food applications are Acacia senegal and Acacia seyal. This natural polysaccharide is made up of neutral sugars and uronic acids (95% of the dry weight), protein (1% to 2% depending on the species), 121
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Figure 7.1 Schematic representation of acacia gum molecule (Fincher et al., 1983).
polyphenols (catechins, epicatechins, etc.), and minerals (magnesium, potassium, calcium, sodium). It has a very complex structure with an average molecular weight varying from 300 to 800 kDa. The wattle blossom model represents the highly branched and compact structure of acacia gum (see Figure 7.1): Arabinogalactans are linked with a protein skeleton. The polysaccharidic fraction is made up of a linear chain of galactose β1,3 linked. This chain is branched in position 1,6 with chains of galactose and arabinose. Rhamnose, glucuronic acid or methyl glucuronic acid units are found at the end of chains. Safety Acacia gum has been used in the food industry for decades as a food additive or ingredient. The joint FAO/WHO expert committee on food additives recognizes acacia gum as a food additive (INS 414) that can be used with no specified ADI (Acceptable Daily Intake). In the USA, acacia gum benefits from a GRAS (Generally Recognized As Safe) classification (CFR 184.1330).
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In Europe, acacia gum is listed as a food additive (E414) under the quantum satis principle.
Nutritional Aspects Metabolism Acacia gum generally contains more than 70% soluble dietary fiber on dry extract basis by the internationally recognized and official AOAC 985.29 method. Fibregum™ (a range of branded acacia gum products from Colloides Naturels International) has a guaranteed soluble dietary fiber content of more than 90% on dry basis. Acacia gum is not metabolized in the upper digestive tract and is not hydrolyzed in the small intestine, due to a lack of proper depolymerizing enzymes such as galactanases or arabinases. It will only be fermented by lactic acid bacteria in the large bowel. Upon arrival in the colon, acacia gum represents an extra carbon source providing fuel for microbial fermentation. After a few days of adaptation, no acacia gum is found in rat [1] or human [2] feces, meaning that acacia gum is totally degraded by colonic flora and then fermented. For that reason, its actual caloric value has been estimated at about 1.5 kcal/g [3]. Acacia gum’s mechanical roles, such as increasing satiety rate or transit time in the upper intestinal tract, are minimal, as compared with viscous soluble fibers and with insoluble fibers having a high water-retention capacity. However the influence of acacia gum, on gastric emptying time for instance, could be an indirect influence through its colonic fermentation metabolites such as the short-chain fatty acids (SCFAs). Tolerance Contrary to other low-viscosity fibers, such as oligosaccharides, studies on human subjects showed that acacia gum does not exhibit laxative side effects at dosages up to 50 grams per day (see Figure 7.2) [4]. Thanks to its high molecular weight and its complex structure, acacia gum is slowly fermented and does not disturb the osmotic pressure of the gut. It is thus very well tolerated in the human diet. Prebiotic Effect Fermentation of acacia gum in the large bowel stimulates the growth of lactic acid bacteria (Lactobacilli and Bifidobacteria), which is beneficial for human health and wellness. More than 20 studies support the prebiotic effect of acacia gum.
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% 100
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Figure 7.2 Tolerance of acacia gum vs. FOS in human.
First in vitro studies showed that among different genus of bacteria from human feces, Bifidobacteria strains [5], more specifically from the B. longum and B. adolescensis [6] species, were able to use acacia gum for their growth. In an in vitro system batch, May et al. [7] were able to demonstrate an increase in the total anaerobes quantity with acacia gum. With a continuous system, Michel et al. [8] showed that the Lactobacilli count was increased by 6.75 times and the Clostridium count was decreased by 1.8 log with acacia gum compared to a control and the decrease was even better compared to fructooligosaccharides (FOS). In rats, 10% of acacia gum added to the diet allowed to increase the diaminopimelic acid index in the cecum and feces, measured as an indicator of the total bacterial mass, compared to a control and wheat bran [9]. In a female volunteer consuming 10 g/d of acacia gum during 18 days, the proportion of bacteria able to ferment acacia gum rose from 6.5% at the beginning of the study to 53.6% at the end of the treatment indicating an adaptation of the microflora [10]. After cessation of the consumption, this proportion decreased slightly to come back to initial value after 45 days. In a single-blind controlled study performed on 10 healthy volunteers consuming either Fibregum™ or sucrose as control at the dose of 10 g/d during 10 days, concentrations of Bifidobacteria, Lactobacilli, and total lactic acid bacteria groups were significantly increased with Fibregum™ at the dose of 10 g/d compared to control without affecting neutral groups as Bacteroides [4]. The bifidogenic effect was even more pronounced (+1 log) in subjects having low initial Bifidobacteria count (<9.5 log). In a randomized double-blind controlled study involving 96 healthy volunteers [11], an intake of 6 g/d of Fibregum™ induced a 0.7 log increase of fecal Bifidobacteria after one week of consumption. Moreover, this effect was greater compared to FOS that induced a 0.3 log increase at the same dosage. A mix of 3 g of Fibregum™ plus 3 g of FOS had a synergetic bifidogenic effect (+1.38 log increase). Acacia gum is widely fermented and results in greater production of total short-chain fatty acids (SCFAs) when compared to other sources of oligo- or polysaccharides, including pectin, psyllium, xylooligosaccharides, fructo-
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oligosaccharides, and others, as seen in the in vitro model [7, 8, 12–16] using either fecal bacteria from human or pig origin. Increased total pool and concentration of SCFAs were also demonstrated in cecum, feces, cecum blood flow, and hepatic portal venous plasma of rats [1, 17–23]. Acacia gum is considered one of the most soluble and most fermentable polysaccharides. However, because SCFAs are progressively absorbed in the colon, it is rather difficult to detect a variation in their concentration in human feces. McLean Ross et al. [2] and Rochat et al. [11] were not able to demonstrate a SCFA fecal concentration increase after a daily intake of respectively 25 g and 6 g of acacia gum. The shift from acetate to higher proportions of propionate and butyrate with acacia gum compared with control period and with other sources of fiber (for example pectin) has been described many times in vitro [7, 8, 14–16], in rats [1, 18–23] as well as in humans [2]. This shift probably partly explains the health benefits on the gut epithelium (stimulation of intestinal mobility, reduction of inflammation, and colorectal cancer risk for instance), but also the possible effects on lipid metabolism.
Potential Health Benefits of Acacia Gum Reduction of Diarrhea and Constipation Benefits of acacia gum on water/electrolyte absorption and on recovery from diarrhea have been well detailed in studies on malnourished rats or animals with diarrhea induced by use of cathartics [24–26]. In rat intestine exposed to cholera toxin, acacia gum reduced chloride secretion and normalized sodium transport [27]. The mechanisms of action of acacia gum have not been fully elucidated. Evidence suggests that acacia gum may be an indirect regulator of nitric oxide (NO) metabolism, scavenging some of the NO diffused from the enterocyte into the lumen and thereby promoting fluid absorption [28]. Alternatively, acacia gum may modify bulk transport by enhancing diffusive mechanisms but has no effect on sodium-dependent carriers [29]. The efficacy of acacia gum might derive, at least in part, from regulation of NO-dependent gating of the basolateral membrane potassium channel [30]. However, considering that acacia gum is not absorbed at all in the upper gastrointestinal tract, the possible linkage might be exerted via a purely physical mechanism, such as NO gas adsorption or scavenging. Additional studies indicate that acacia gum, in addition to its ability to remove NO diffused into the intestinal lumen, may also partially inhibit intestinal NO synthase and thus modulate intestinal absorption through these mechanisms [31, 32].
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Several in vivo studies clearly showed that supplementation with acacia gum reduces fecal incontinence and improves stool consistency [33–35]. In addition, acacia gum, from the dose of 15 g/d, allows increasing stool wet weight and stool humidity in healthy adults [10]. More than a drug, acacia gum is interesting because it behaves as a regulator: It is able to reduce diarrhea and, alternatively, reduce constipation risk. Improvement of Nitrogen Excretion In a prospective single-blind crossover study, a greater nitrogen excretion in stools and lower serum urea nitrogen has been measured on 16 patients (male and female) with chronic renal failure when 50 g/d of acacia gum was added to a hypo-proteic diet during four weeks [36]. Significant decrease of plasma urea (–11%, p < 0.05) was also observed in patients with slowly progressive uremia with 30 g acacia gum daily [37]. This could be dependent on an increase in bacterial growth and activity in the gut. More recent studies, in rat models of acute renal failure, suggest that acacia gum may also improve renal function independently of its action on fecal bacterial ammonia metabolism [38, 39]. Acacia gum may act by reducing the amount of urea nitrogen excreted in urine and by increasing urea disposal in the large intestine, where it is degraded. It has been also reported that acacia gum can decrease urea nitrogen excretion, urea production, and urea cycling in rats [40, 41] without having a net effect on nitrogen balance. Latest data support the hypothesis that dietary supplementation with acacia gum may have a potential beneficial effect in renal disease, by increasing systemic levels of butyrate and thus suppressing the profibrotic cytokine TGF-β1 activity [42]. The regular intake of acacia gum in addition to a low-protein/high-calorie diet can contribute to the postponement of the need for hemodialysis or peritoneal dialysis in children with end-stage renal disease [43]. More recently, the use of acacia gum in adult patients with symptomatic uremia has been investigated in 11 patients [44]. Assimilation of acacia gum was associated with amelioration of the uremic symptoms and improvement of general well-being as long as patients were compliant with the therapeutic protocol. The most significant finding in this study is the achievement of hemodialysis freedom in two patients, both of whom had a previous vascular access [45]. These effects enable lowering of the kidneys’ workload with the objective of decreasing adverse clinical symptoms such as nausea, anorexia, and fatigue associated with renal failure. Acacia gum could also be used to prevent renal damage that could be associated with a high-protein diet. Moreover, acacia gum can help normalize parameters such as increase in urine volume, in serum creatinine, or in urea induced by nephrotoxicity [46]. Acacia gum has notably been shown to protect the kidneys from gentamicininduced nephrotoxicity in rats [47]. Its administration lessened the negative effects of this nephrotoxicity possibly by inhibiting a free-radical-mediated
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process and preventing histological changes in renal tissues [47]. Acacia gum can thus help the body to detoxify or eliminate deleterious components and thus prevent tissue damage. Reduction of Cholesterol Physiological effects of acacia gum from human studies include the lowering of serum triglyceride and cholesterol levels [48, 49]. A study in five healthy human volunteers taking 25 g/d of acacia gum shows a significant reduction of total serum cholesterol concentrations [50, 51]. Another study in seven non-obese hypercholesterolemic men consuming 15 g acacia gum twice a day along with their main meals, during 30 days, indicates that acacia gum causes a significant decrease in serum total cholesterol levels, especially LDL and VLDL fractions [52], which confirms previous results obtained in rats [53]. But other studies come to different conclusions either in normal [54] or in hypercholesterolemic subjects [55]. In the same way, some studies in rats exhibit contradictory conclusions on the ability of acacia gum to reduce plasma cholesterol levels. Those variations among studies are possibly due to the variability of acacia gum used or the dose and the duration of consumption. The potential ability of acacia gum to decrease serum cholesterol may be linked to its globular structure and its emulsifying and film-forming properties [56]. The production of SCFAs (especially propionate) and also possible binding with cholesterol and bile acids in the small intestine may be responsible for this outcome. Hypoglycemic Effect Acacia gum not only has a negligible impact on blood glycemia, but it also has been proven to globally reduce the Glycemic Index (GI) of food products. Glucose tolerance test was conducted in 12 healthy subjects. The addition of 20 g acacia gum to 100 g load of glucose resulted in a significant reduction of plasma glucose response (–18.6%) and serum insulin (–12.4%) [57]. Twelve healthy Japanese males consumed consecutively in a random order a sucrose loading (100 g) plus 0, 5, or 10 g of acacia gum dissolved in 300 mL of water [58]. Blood samples were taken from each subject before examination, and at intervals of 30 minutes during 150 minutes after supplementation. Blood glucose level was determined by glucose oxidase method using Glutest Ace. Blood glucose concentration reached peak level 30 minutes after the supplementation with sucrose and acacia gum. Compared to the peak glucose level after taking the placebo (171.1±7.65 mg/dL), the level was significantly lowered after taking 5 g or 10 g acacia gum (153.5±7.5 and 146.0±9.8 mg/dL, respectively). Similarly, the glucose concentration at 60 minutes after
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supplementation was significantly decreased in test groups compared to placebo group. Additionally, a dose-response relationship was observed in the blood glucose lowering effect of acacia gum. Fourteen overweight or obese women suffering from type 2 diabetes consumed 50 g of available carbohydrate from white bread (100 g) as reference food, and seven days later the same reference product plus 15 g of Fibregum™ dissolved in 180 mL of water [59]. Addition of Fibregum™ to the diet allowed a significant GI reduction (–18.6%). The glycemic and insulin index of three crispbreads proportionally decreased in a group of 12 healthy people when increasing quantities of Fibregum™ (0, 6%, and 11% by weight) were added to the breads [60]: Glycemic Index of crispbread decreased from 78 for the standard product to 69 when 6% Fibregum™ was added and 65 with 11% Fibregum™.
Applications of Acacia Gum in Food Products Acacia gum is available in the form of a highly soluble and pure powder that is tasteless and odorless. Acacia gum requires no heating or shearing for activation, but it is resilient to high shear and also temperature or pH extremes. Thanks to its low viscosity and high solubility, it is very easy to add a significant amount of acacia gum into many food products without altering their original characteristics. The acacia gum can simply be added to an existing formulation with no negative interaction or unwanted increase in viscosity (see Figure 7.3). In the human mouth, acacia gum resists hydrolysis by salivary enzymes and local flora, which allows it to be classified as non-cariogenic and makes it safe for teeth [61]. Acacia gum can be used in dietetic products and can safely be used in sugar-free formulations.
Viscosity (cP)
5000 4000 3000 2000 1000 0
0
10
20
30
Concentration (%) Figure 7.3 Influence of concentration on viscosity of acacia gum (at 75°F).
40
50
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Acacia Gum No Heat Treatment
% Remaining Fibre
120 100 80 60 40
Fibregum FOS
20 0
0
15
30
45
60
Time (days) Heat Treatment 5 min at 85°C/185°F
% Remaining Fibre
120 100 80 60 40
Fibregum + T°C FOS + T°C
20 0
0
15
30
45
60
Time (days) Figure 7.4 Fiber stability of acacia gum vs. FOS against low pH (3.8) and temperature.
Due to its highly branched structure, acacia gum is extremely resistant to heat treatments, acidic conditions, and yeast fermentation; it remains stable against the most severe temperatures, even at very low pH for several months (see Figure 7.4). Acacia gum not only brings nutritional benefits but it also provides many technical functionalities to food applications such as beverages (fruit juice blends, smoothies, etc.), dairy products (milk, yogurt, etc.), baked goods (breads, muffins, cookies, wraps, etc.), confectionery, extruded snacks, cereals, sauces and dressings, nutrition bars (cereal, high protein, etc.), meal replacement shakes and powders, or nutraceutical tablets. Beverages Acacia gum is being widely used in reduced-sugar or low-juice beverages because the roundness and mouthfeel it provides perfectly matches the texture brought by sucrose or fruit juice. Studies on rats clearly showed that water, glucose, and mineral absorption were significantly enhanced when acacia gum was added into oral rehydration solutions or sports drinks [24–27].
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Bakery Products Thanks to its moisture regulation and film-forming properties, acacia gum brings many benefits to baked goods in terms of processing, texture, and shelf life. Addition of acacia gum to bakery products has been proven to enhance their texture (smoothness and fullness), especially in freeze/thaw or freeze/ bake applications. Those benefits lead to a reduced staling effect and a shelf life extension. For instance, studies carried out by The Food Development Group in Toronto, Canada, clearly showed that the texture of bakery products such as soft cookies or muffins was improved at increased acacia gum levels (0 to 3% by weight). In the meantime, superior eating qualities over the standard cookie without acacia gum were noted during the entire duration of the shelf life. The softness brought by the addition of acacia gum is perceived by the consumer as freshness. Cereal Bars Acacia gum develops unique binding and sticking properties that enable a partial or total replacement of sugar, glucose syrup, and high-fructose corn syrup (HFCS) in the binding solution. Addition of 4% to 8% acacia gum is usually required to effectively bind the dry components of the formula (fruits, cereals). Its high moisture stabilization properties and its film-forming ability favor extending the shelf life and delaying the hardening of the bar. Extruded Snacks and Breakfast Cereals Acacia gum acts as a lubricant during the extrusion process, which leads to a more consistent shape and texture of the snacks. During extrusion, the addition of acacia gum into the snack dough has been reported to help decrease the mechanical energy while increasing both efficiency and output of the extruder. Such benefits have been obtained with addition of 2% to 5% acacia gum, but optimum reduction of electrical intensity, engine torque, and heat buildup have been observed with 3.5% acacia gum. At the same time, acacia gum’s high moisture-control properties help increase crispiness and reduce the staling effect during storage. Confectionery Acacia gum is not considered a thickening hydrocolloid when dissolved in water at low concentration (up to 30%). Meanwhile, when used in sucrose or sugarless systems (polyols and artificial sweeteners) at high levels of dry substances, acacia gum provides a unique texture to European-type molded confectionery products such as jujubes or gum pastilles.
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In coated sweet goods, acacia gum is used for its film-forming ability in order to improve the physical and mechanical properties of the centers and make the hard and soft coating layers more effective. The addition of a low level (1% to 3%) of acacia gum in a sugarless hard candy based on sorbitol, maltitol, or mannitol, slightly increases the amount of residual water (1% to 3%) after cooking and therefore decreases the cooking temperature from 40 to 60°F. Hygroscopicity of the candy is reduced, recrystallization of polyols is avoided, and wrapped sweets are not sticky. Acacia gum is used as a binder for tabletting by direct compression or wet granulation in food and pharmaceutical products. For the direct compression, purified and agglomerated acacia gum is mixed with the other powders (having the same mesh size) before filling the die. In the wet granulation, acacia gum in solution is added to the powders to make a slurry, which is dried and sieved to produce a free-flowing material that is then compressed.
References
1. McLean Ross AH, Eastwood MA, Brydon WG, Busuttil A, McKay LF. A study of the effects of dietary gum arabic in the rat. Br.J.Nutr. 1984; 51:47–56. 2. McLean Ross AH, Eastwood MA, Brydon WG, Anderson JR, Anderson DM. A study of the effects of dietary gum arabic in humans. Am.J.Clin.Nutr. 1983; 37:368–75. 3. Phillips GO. Acacia Gum (gum Arabic): a nutritional fibre; metabolism and calorific value. FoodAddit.Contam. 1998; 15:251–64. 4. Cherbut C, Michel C, Raison V, Kravtchenko TP, Meance S. Acacia Gum is a bifidogenic dietary fiber with high digestive tolerance in healthy humans. Microbial.Ecol.HealthDis. 2003; 15:43–50. 5. Salyers AA, Palmer JK, Wilkins TD. Degradation of polysaccharides by intestinal bacterial enzymes. Am.J.Clin.Nutr. 1978; 31:S128–S130. 6. Crociani F, Alessandrini A, Mucci MM, Biavati B. Degradation of complex carbohydrates by Bifidobacterium spp. Int.J.Food Microbiol. 1994; 24:199–210. 7. May T, Mackie RI, Fahey GC, Jr., Cremin JC, Garleb KA. Effect of fiber source on short-chain fatty acid production and on the growth and toxin production by Clostridium difficile. Scand.J.Gastroenterol. 1994; 29:916–22. 8. Michel C, Kravtchenko T, David A, Gueneau S, Kozlowski F, Cherbut C. In vitro prebiotic effects of Acacia gums onto the human intestinal microbiota depend on both botanical origin and environmental pH. Anaerobe 1998; 4:257–66. 9. Walter DJ, Eastwood MA, Brydon WG, Elton RA. Fermentation of wheat bran and gum arabic in rats fed on an elemental diet. Br.J.Nutr. 1988; 60:225–32. 10. Wyatt GM, Bayliss CE, Holcroft JD. A change in human faecal flora in response to inclusion of gum arabic in the diet. Br.J.Nutr. 1986; 55:261–66. 11. Rochat F, Baumgartner M, Jann A, Rochat C, Nielsen G, Reuteler G, and Ballèvre O. Synergistic effect of prebiotics on human intestinal microflora. 2001. Ref type: personal communication.
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12. Tomlin J. Which fibre is best for the colon? Scand.J.Gastroenterol.Suppl 1987; 129:100–4. 13. Adiotomre J, Eastwood MA, Edwards CA, Brydon WG. Dietary fiber: in vitro methods that anticipate nutrition and metabolic activity in humans. Am.J.Clin. Nutr. 1990; 52:128–34. 14. Mortensen PB, Hove H, Clausen MR, Holtug K. Fermentation to short-chain fatty acids and lactate in human faecal batch cultures. Intra- and inter-individual variations versus variations caused by changes in fermented saccharides. Scand.J.Gastroenterol. 1991; 26:1285–94. 15. Titgemeyer EC, Bourquin LD, Fahey GC Jr., Garleb KA. Fermentability of various fiber sources by human fecal bacteria in vitro. Am.J.Clin.Nutr. 1991; 53:1418–24. 16. Bourquin LD, Titgemeyer EC, Fahey GC Jr., Garleb KA. Fermentation of dietary fibre by human colonic bacteria: disappearance of, short-chain fatty acid production from, and potential water-holding capacity of, various substrates. Scand.J.Gastroenterol. 1993; 28:249–55. 17. Walter DJ, Eastwood MA, Brydon WG, Elton RA. Fermentation of wheat bran and gum arabic in rats fed on an elemental diet. Br.J.Nutr. 1988; 60:225–32. 18. Storer GB, Illman RJ, Trimble RP, Snoswell AM, Topping DL. Plasma and caecal volatile fatty acids in male and female rats: effects of dietary gum arabic and cellulose. Nutrition Research 1984; 4:701–7. 19. Topping DL, Mock S, Trimble RP, Storer GB, Illman RJ. Effects of varying the content and proportions of gum arabic and cellulose on caecal volatile fatty acid concentrations in the rat. Nutrition Research 1988; 8:1013–20. 20. Topping DL, Illman RJ, Trimble RP. Volatile fatty acid concentrations in rats fed diets containing gum arabic and cellulose separately and as a mixture. Nutrition Reporter 1985; 32:809–14. 21. Tulung B, Remesy C, Demigne C. Specific effect of guar gum or gum arabic on adaptation of cecal digestion to high fiber diets in the rat. J.Nutr. 1987; 117:1556–61. 22. Walter DJ, Eastwood MA, Brydon WG, Elton RA. An experimental design to study colonic fibre fermentation in the rat: the duration of feeding. Br.J.Nutr. 1986; 55:465–79. 23. Annison G, Trimble RP, Topping DL. Feeding Australian Acacia gums and gum arabic leads to non-starch polysaccharide accumulation in the cecum of rats. J.Nutr. 1995; 125:283–92. 24. Wapnir RA, Teichberg S, Go JT, Wingertzahn MA, Harper RG. Oral rehydration solutions: enhanced sodium absorption with gum arabic. J.Am.Coll.Nutr. 1996; 15:377–82. 25. Wapnir RA, Wingertzahn MA, Moyse J, Teichberg S. Gum arabic promotes rat jejunal sodium and water absorption from oral rehydration solutions in two models of diarrhea. Gastroenterology 1997; 112:1979–85. 26. Teichberg S, Wingertzahn MA, Moyse J, Wapnir RA. Effect of gum arabic in an oral rehydration solution on recovery from diarrhea in rats. Journal of Pediatrics, Gastroenterology and Nutrition. 1999; 29:411–17. 27. Turvill JL, Wapnir RA, Wingertzahn MA, Teichberg S, Farthing MJ. Cholera toxin-induced secretion in rats is reduced by a soluble fiber, gum arabic. Dig. Dis.Sci. 2000; 45:946–51. 28. Wingertzahn MA, Teichberg S, Wapnir RA. Jejunal nitric oxide (NO) levels are reduced by gum arabic (GA). J.Am.Coll.Nutr. 1998; Abstract 52:509 (abstr).
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29. Wingertzahn MA, Teichberg S, Wapnir RA. Stimulation of non-sodium-dependent water, electrolyte, and glucose transport in rat small intestine by gum arabic. Dig.Dis.Sci. 2001; 46:1105–12. 30. Rehman KU, Wingertzahn MA, Harper RG, Wapnir RA. Proabsorptive action of gum arabic: regulation of nitric oxide metabolism in the basolateral potassium channel of the small intestine. J.Pediatr.Gastroenterol.Nutr. 2001; 32:529–33. 31. Rehman KU, Codipilly CN, Wapnir RA. Modulation of small intestinal nitric oxide synthase by gum arabic. Exp.Biol.Med. (Maywood.) 2004; 229:895–901. 32. Rehman KU, Wingertzahn MA, Teichberg S, Harper RG, Wapnir RA. Gum arabic (GA) modifies paracellular water and electrolyte transport in the small intestine. Dig.Dis.Sci. 2003; 48:755–60. 33. Bliss DZ, Jung HJ, Savik K et al. Supplementation with dietary fiber improves fecal incontinence. Nurs.Res. 2001; 50:203–13. 34. Korula J. Dietary fiber supplementation with psyllium or gum arabic reduced fecal incontinence in community-living adults. ACP J.Club. 2002; 136:23. 35. Campbell S. Dietary fibre supplementation with psyllium or gum arabic reduced incontinent stools and improved stool consistency in community living adults. Evid.Based.Nurs. 2002; 5:56. 36. Bliss DZ, Stein TP, Schleifer CR, Settle RG. Supplementation with gum arabic fiber increases fecal nitrogen excretion and lowers serum urea nitrogen concentration in chronic renal failure patients consuming a low-protein diet. Am.J.Clin. Nutr. 1996; 63:392–8. 37. Rampton DS, Cohen SL, Crammond VD et al. Treatment of chronic renal failure with dietary fiber. Clin.Nephrol. 1984; 21:159–63. 38. Ali BH, Al Qarawi AA, Haroun EM, Mousa HM. The effect of treatment with gum Arabic on gentamicin nephrotoxicity in rats: a preliminary study. Ren Fail. 2003; 25:15–20. 39. Ali BH, Alqarawi AA, Ahmed IH. Does treatment with gum Arabic affect experimental chronic renal failure in rats? Fundam.Clin.Pharmacol. 2004; 18:327–9. 40. Assimon SA, Stein TP. Digestible fiber (gum arabic), nitrogen excretion and urea recycling in rats. Nutrition 1994; 10:544–50. 41. Younes H, Garleb K, Behr S, Remesy C, Demigne C. Fermentable fibers or oligosaccharides reduce urinary nitrogen excretion by increasing urea disposal in the rat cecum. J.Nutr. 1995; 125:1010–6. 42. Matsumoto N, Riley S, Fraser D et al. Butyrate modulates TGF-beta1 generation and function: potential renal benefit for Acacia(sen) SUPERGUM (gum arabic)? Kidney Int. 2006; 69:257–65. 43. Al Mosawi AJ. Acacia gum supplementation of a low-protein diet in children with end-stage renal disease. Pediatr.Nephrol. 2004; 19:1156–9. 44. Al-Mosawi AJ. Continuous renal replacement in the developing world: is there any alternative? Therapy 2006; 3:265–72. 45. Al-Mosawi AJ. Acacia gum therapeutic potential: possible role in the management of uremia — a new potential medicine (8 articles). Therapy 2006; 3:301–21. 46. Al-Mosawi AJ. The challenge of chronic renal failure in the developing world: possible use of acacia gum. Pediatr.Nephrol. 2002; 17:390–1. 47. Al-Majed AA, Mostafa AM, AL RIKABI AC, Al Shabanah OA. Protective effects of oral Arabic gum administration on gentamicin-induced nephrotoxicity in rats. Pharmacol.Res. 2002; 46:445–51.
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48. Meyer D, Tungland B. Non-digestible oligosaccharides and polysaccharides: their physiological effects and health implications. In: McCleary BV, Prosky L, eds. Advanced Dietary Fibre Technology. 2006:464. 49. Schneeman BO, Lefevre M. Effects of Fiber on Plasma Lipoprotein Composition. In: Vahouny GV, Kritchevsky D, eds. Dietary Fiber — Basic Clinical Aspects. 1984:309–21. 50. McLean Ross AH, Eastwood MA, Brydon WG, Anderson JR, Anderson DM. A study of the effects of dietary gum arabic in humans. Am.J.Clin.Nutr. 1983; 37:368–75. 51. McLean Ross AH, Eastwood MA, Brydon WG, McKay LF, Anderson DM, Anderson JR. Gum arabic metabolism in man. Proc.Nutr.Soc. 1982; 41:64A. 52. Sharma RD. Hypocholesterolemic effect of gum acacia in men. Nutrition Research 1985; 5:1321–6. 53. Sharma RD. Hypocholesterolemic activity of some Indian gums. Nutrition Research 1984; 4:381–9. 54. Haskell WL, Spiller GA, Jensen CD, Ellis BK, Gates JE. Role of water-soluble dietary fiber in the management of elevated plasma cholesterol in healthy subjects. Am.J.Cardiol. 1992; 69:433–9. 55. Jensen CD, Spiller GA, Gates JE, Miller AF, Whittam JH. The effect of acacia gum and a water-soluble dietary fiber mixture on blood lipids in humans. J.Am.Coll.Nutr. 1993; 12:147–54. 56. Eastwood MA, Brydon WG, Anderson DM. The effect of the polysaccharide composition and structure of dietary fibers on cecal fermentation and fecal excretion. Am.J.Clin.Nutr. 1986; 44:51–5. 57. Sharma RD. Hypoglycemic effect of gum acacia in healthy human subjects. Nutrition Research 1985; 5:1437–41. 58. Castellani F. Fibregum (acacia gum) helps reduce the glycemic index of food products. AgroFood Industry Hi-tech 2006; 16:24–6. 59. Meance S, Mescheriakova VA, Charaphétdinov CC, Plotnikova OA. Glycemic Index with a supplementation of acacia gum or a viscous acacia gum mix in type 2 diabetic women 2004; Ref type: personal communication. 60. Fremont, G. Glycemic Index and Insulin Index values of Fibregum enriched crispbreads 2006; Ref type: personal communication. 61. Imfeld T, Meance S. Evaluation of the safety for teeth of the acacia gum Fibregum at different concentrations in humans 2003; Ref type: personal communication.
8 Pectin Hans Ulrich Endress and Frank Mattes
Contents Technological Aspects......................................................................................... 136 Introduction................................................................................................ 136 Chemical Structure.................................................................................... 136 Physical Properties..................................................................................... 138 Commercial Pectins................................................................................... 140 Nutritional Aspects............................................................................................. 141 Metabolism of Pectin................................................................................. 141 Fermentation of Pectin............................................................................... 142 Prebiotic Nature.......................................................................................... 143 Role of Pectin in Weight Management.................................................... 144 Affinity to Metal Ions and Excretion of Toxic Metals........................... 145 Influence of Pectin on Jejunal and Ileal Morphology............................ 147 Medical Aspects................................................................................................... 148 Reduction of Symptoms of Dumping, Short Bowel Syndrome, and Short Gut Syndrome.................................................................. 148 Effects on Acute Intestinal Infections..................................................... 148 Effects on Atherosclerosis......................................................................... 149 Effects on Cholesterol and Lipid Metabolism........................................ 150 Effects on Glucose Metabolism................................................................ 152 Effects on Cancer........................................................................................ 154 Application of Pectin in Food Products............................................................ 156 Fruit Spreads............................................................................................... 157 Industrial Fruit Preparations.................................................................... 157 Confectionery Articles............................................................................... 158 Dairy Products............................................................................................ 158 Beverages and Sorbet................................................................................. 158 Condiments and Spreads.......................................................................... 159 Bakery Products, Cereal Products........................................................... 159 Capsules and Other Nutraceutical Products.......................................... 159 References............................................................................................................. 160
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Technological Aspects Introduction Pectin is a well-known ingredient used to form gels, to stabilize acidified milk beverages, or simply to act as a viscosifier in beverages. Besides its technological properties, pectin is also a dietary fiber since pectin is not digested by the human body and can be categorized as such by the AOAC methods 985.29 and 991.43 [1]. Pectins are consumed every day, as they are either used as an ingredient in different food products or as protopectin found in the cell wall of fruits and vegetables. The term protopectin is used to describe the native pectin in plant tissues, which cannot be purified without using destructive methods. With cellulose, hemicelluloses, glycoproteins, and lignin, pectins form the cell wall of all higher plants. The concentration of pectin is highest in the middle lamella, a tissue which connects cells. In plant physiology, pectin takes part in water retention, ion transport, and therefore is involved in growth, size, and shape of cells. Pectin content is less in primary cell walls and almost absent in secondary cell walls [2]. Chemical Structure Pectin is a polysaccharide consisting of galacturonic acid, which forms a linear chain by α-(1,4)-d glycosidic links (Figure 8.1). In the polygalacturonic acid chain, α-(1,2)-l-rhamnopyranose units are inserted, which forms kinks interrupting the linear chain resulting in a zigzag-shaped molecule. d-GalacCarboxyl-group O
O C O
Amid-group
C
OH O O
OH OH
Methylester-group O
O NH2 O
C O
OH OH
C
OCH3 O O
OH
O
OH
O
O
C=O
C=OH
CH3
CH
Acetyl-group
CH
MeO
Figure 8.1 Chemical structure.
OCH3 O
HO Ferolyl-group
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turonic acid units are partially esterified with methanol, so that a degree of esterification (DE) or degree of methylation (DM) can be defined. The degree of esterification is plant specific and is also influenced by pectin-degrading enzymes during the ripening process of fruits and vegetables by the action of pectinesterases. The degree of esterification can also be influenced during the extraction process of commercial pectin types. Per definition pectins with a DE of higher than 50% are called high methylester pectins, HM pectins, and pectins with a lower DE than 50% are called low methylester pectins, LM pectins. Unesterified pectin is called pectinic acid and its salts pectates. In most plants, HM pectin is found, and pectins isolated from apples have a degree of esterification of up to 80%. In lemon fruits or sugar beet, pectin with lower DE is found: 75% and 60%, respectively. Sunflower heads contain pectin with a lower DE than 50%. Also the distribution of methylester is plant specific as plant pectinesterases de-esterify pectin block-wise during maturation. Pectin, which is de-esterified during the extraction process, has randomly distributed methylester groups. Pectins are rarely esterified with ethanol. Pectins in sugar beet plants have a high content of acetyl groups. Acetic acid is esterified mainly with C-2 and C-3 of the galacturonic acid units. Bound to rhamnose units are so-called neutral sugar side chains consisting mainly of l-arabinose and d-galactose, which form complex structures. From many fruits and vegetables (e.g., apples, apricots, cabbage, carrots, onions, pears, and sugar beet), pectins containing arabinan side chains can be isolated. Arabinans are polysaccharides consisting of α-(1,5)-linked arabinofuranosyl units to which α-(1,2)- and α-(1,3)-linked arabinofuranosyl are attached as side chains. In other plants (e.g., citrus fruits, grapes, onions, potatoes, soy beans, tomatoes, and apples), additionally heteropolysaccharide side chains containing L-arabinose and L-galactose can be found and are commonly named arabinogalactans. Two structurally different arabinogalactans have been found. Type 1 consists of an α-(1,4)-linked linear chain of d-galactopyranosyl residues with short chains of linear α-(1,5)-arabinans. Type 2 is a highly branched polysaccharide with ramified chains of α-(1,3)and α-(1,6)-linked d-galactopyranosyl residues terminated by L-arabinofuranosyl and to a small extent by L-arabinopyranosyl residues. Other neutral sugars (d-xylose, d-glucose, d-mannose, d-apiose) form single unit side chains or short side chains. d-fucose can be found at the terminal end of sugar side chains. The distribution of rhamnose units and therefore also neutral sugar side chains is uneven. Areas having low rhamnose content are called homogalacturonan or smooth regions. Areas of high rhamnose content are named rhamnogalacturonan, and because of being highly branched these areas are also called hairy regions [3]. The molecular weight of pectin molecules depends on the type of plant and the maturation stage. It is influenced by pectin degrading enzymes, for example polygalacturonase which split linkages between the galacturonosyl residues of the pectin main chain. Pectin with very high molecular weight is found in apples in citrus fruits, which is, besides the availability, the reason
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why commercial pectins are produced out of these fruits. Commercial pectin types that are used as gelling agents and thickeners have a molecular weight of about 100,000 dalton. Commercial pectin with high molecular weight is limited in its application as dietary fiber because of its viscosity-forming property. For dietary fiber enhancement pectin types with low molecular weight, for example 30,000 dalton, are produced. Not all galacturonic-acid-containing polysaccharides can be called pectin. As food additive the term pectin may be used only for polysaccharides containing at least 65% galacturonic acid [4–6]. According to United States Pharmacopeia pectin has to have a minimum content of galacturonic acid of at least 74% [7]. Physical Properties Pectin is soluble in water, but not soluble in organic solvents. By having carboxylic acid groups pectin is a polyelectrolyte and a weak organic acid. Added to water carboxylic acid groups dissociate and the pectin molecule becomes negatively charged. Pectin is very stable at acidic pH values from pH 2 to pH 4.5. The stability of pectin additionally depends on the degree of esterification. At pH values below pH 2 pectin gets de-esterified; for example, high-methylester pectins turn into low-methylester pectins. At higher pH values than pH 4.5 pectin degrades by a process called β-elimination. In this reaction the pectin chain is split next to methylester-containing galacturonic acid units. β-elimination is a process driven by hydroxide ions leading to a stronger reaction at neutral pH value. Low-methylester pectins are more stable at higher pH values than high-methylester pectins. At very high pH values additional saponification occurs. Having no methylester groups, pectinic acid and its salts show the highest stability. Pectin lyase, a pectin-degrading enzyme, also splits pectin molecules by the β-elimination mechanism. Because of its molecular weight and molecular structure, pectin is capable of binding water. Pectin molecules also form convolutions due to the linear characteristic of the molecules and interactions between pectin molecules. This causes increased friction leading to shear thinning flow behavior of pectin solutions containing pectin molecules with high molecular weight and used in high concentration. Diluted pectin solutions or pectin solutions made with low-molecular-weight pectin show Newtonian flow behavior. Divalent metal ions increase cross-linking of pectin molecules by interacting with carboxylic acid groups of the pectin molecules leading to increase of viscosity. Interactions with divalent metal ions are also possible when high methylester pectins with a block-wise distribution of non-esterified carboxylic acid groups are used. The most important commercial application of pectin is gelation. Under certain conditions pectin forms a three-dimensional network, which is stabilized by interactions between pectin molecules. For initiating the gelation process a minimum concentration of the pectin is necessary. Important
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factors influencing the gelation process and pectin concentration needed to set are molecular structure of pectin, concentration and type of total soluble solids, pH value, ionic strength, valency and kind of ions, and temperature in the manufacturing process [8–10]. The gel structure is formed during cooling down from high temperature in which the product is in a so-called sol status. Gel formation is turning a liquid sol into a solid structure. The point at which a structure is formed is characteristic to a certain temperature, which can be defined as setting temperature. The setting temperature of pectin gels is highly influenced by the pectin type, pH value, content of total soluble solids, and divalent metal ions. Minor influences are ionic strength, type of total soluble solids, pectin dosage, etc. A reason for commercially distinguishing high-methylester pectin from low-methylester pectin is their different ability to form gels for different application areas. High-methylester pectin form gels at total soluble solids higher than 55% and pH values below pH 3.5. Junction zones stabilizing the gel structure are formed by hydrophobic interactions between methylester groups and hydrogen bonds between hydroxyl groups. Therefore highmethylester pectins are used as gelling agent for traditional jams, jellies, and marmalades. The addition of total soluble solids reduces the water activity for making a shelf stable product, but also reduces the firm hydrate cover surrounding pectin molecules. Acidic conditions are required to reduce the dissociation of the carboxylic acid groups reducing the negative charge density of pectin molecules. By reducing negative charge density repulsion of pectin molecules is reduced, and once attracting forces grow stronger than repelling forces junction zones are formed. In the food industry this is achieved by adding acidifying ingredients, for example citric acid or lemon juice. While high-methylester pectin forms gels only at the above described conditions, low-methylester pectin is able to form gels relatively independent from the content of total soluble solids content and pH value by forming junction zones under the influence of divalent metal ions. Low-methylester pectins may find enough ions to establish firm junction zones already present, or ions, for example calcium, are added separately to the system. Due to the glycosidic bonds of the galacturonic acid units a folded structure of the pectin molecules forms. As a result two galacturonic acid units form a hollow body. Into the hollow body a positively charged calcium ion can be imbedded, which reduces the negative charge density. Sterically seen only 50% of the size of the calcium ion is imbedded, allowing another pectin molecule to attach to the calcium ion. In these hollow spaces calcium ions are bound as metal complexes. The calcium content influences the gel strength formed as well as the affinity of the pectin molecules to divalent metal ions. The affinity of pectin to divalent metal ions depends on the amount of free carboxylic acid groups, so that typically low-methylester pectins show interactions with calcium ions. But also high-methylester pectins can interact with calcium ions, if they have areas that have several consecutive free carboxylic acid groups, for example high-methylester citrus pectin. The amount of calcium needed
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to form gels increases with reduced content of total soluble solids, increasing pH value and increasing ionic strength. Higher concentration of calcium is also needed when products are made with sugar alcohols than with sucrose as total soluble solids. A gel is formed during the cooling process at a certain temperature, the socalled setting temperature. The setting temperature can be measured by an oscillating rheometer and it is influenced also by the pectin type, especially by pH value, content of total soluble solids, and calcium content. The setting temperature depends on the degree of esterification, and it is reduced from high degree of esterification to 60% DE, and setting temperature increases again when the degree of esterification is further decreased. Due to their different setting temperature and therefore different setting speed respectively setting time high-methylester pectins can be classified as rapid set, medium rapid set, to extra slow set pectin. Reducing the pH value change of a product increases the setting temperature as well as increasing total soluble solids, and, in the case of low-methylester pectins, the calcium content. In products that are deposited above setting temperature, slowly a network is formed stabilized by junction zones. If products are deposited below setting temperature in general a softer gel is formed with a rough gel structure. This process is also named pre-gelation as the gel is formed during the manufacturing process. And because of incurring process steps the gel structure will be partially destroyed, not able to re-form. Commercial Pectins Pectin is produced by extraction from plants, and despite the wide occurrence of pectin in nature only a few materials are used as sources for manufacturing of commercial pectin. For the industrial process raw material has to be available in sufficient quantities as well as in stable conditions to prevent pectin-degrading processes in the raw material. Citrus peels, apple pomace, and sugar beet pulp are commercially used for pectin production. These materials are obtained after juice and sugar production. To get storeable and transportable conditions, citrus peels, apple pomace, and sugar beet pulp are immediately dried after processing. Citrus peels are additionally washed to prevent browning and to separate citrus oil. Citrus pectin can also be produced from fresh processed citrus peels. The yield of citrus pectin from dried peels is about 30%, whereas from apple pomace approximately 15% pectin can be extracted. In the manufacturing process the pectin-containing extract is produced by treating the raw material with inorganic acid at elevated temperature. Under these conditions the bonds of the side chains that bind the pectin molecule to the cell wall network are clinched releasing the molecule into the aqueous solution. In the next steps the pectin-containing extract is separated from the insoluble raw material, which mainly contains cellulose, followed by clarification and concentration. Pectin is isolated by alcoholic precipitation.
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The alcohol-water mixture is separated from the precipitated pectin, which is then dried, ground, and sieved to defined particle size. Pectin with different degrees of esterification can be obtained by adjusting the extraction conditions accordingly. Another possibility is to use extracted high-methylester pectin, which is in a second step de-esterified under acidic conditions. A de-esterification process under alkaline condition with ammonia is used to introduce amide groups. Pectin types obtained in such a process are also called low-methylester-amidated pectins. Pectin extracted from apple pomace or citrus peel typically has high molecular weight and high water-binding capacity. High water-binding capacity presents itself as an obstacle, because of getting very high viscosity levels, which would limit the amount of pectin that could be added to enhance products with soluble dietary fiber. Pectins with reduced molecular weight, hence reduced viscosity, can be produced by ball milling or treating pectin with oxidizing agents. Low viscosity pectins can also be produced by enzymatic treatment, for example with pectin lyases (PL; EC 4.2.2.10), which don’t change the degree of esterification. By treating pectin with a combination of pectin esterase (PE; EC 3.1.1.11) and endo-polygalacturonase (endo-PG; EC 3.2.1.15) pectin with reduced degree of esterification and reduced molecular weight will be obtained. Certainly it is possible to produce pectin with low molecular weight by choosing the respective raw material. Pectin in sugar beet pulp naturally has a lower molecular weight than pectin made from apple pomace or citrus peels.
Nutritional Aspects Metabolism of Pectin Due to its molecular structure pectin is not digested by the human body, as there are no enzymes excreted that are able to degrade the molecule. However certain bacteria of the gut flora are able to use pectin as substrate. Without the fermentation process pectin would pass almost unchanged through the digestive system. Pectin is quite stable under the acidic conditions of the stomach. However, it cannot be overlooked that a slight de-esterification process occurs. A certain degradation at the alkaline conditions of the ileum is discussed [11] as well as microbial degradation [12, 13], which would explain increased levels of uronic acids in blood, liver, and urine, when pectin was applied [14, 15]. In patients with an ileum syrinx, applied pectins were recovered by from 100% to only 70%. But studies have also excluded fermentation at this early stage of digestion [16]. Pectins reduce amylase activity by 10% to 40%, lipase activity by 40% to 80%, and trypsin activity by 15% to 80% [17,–21]. The activity of pancreatic
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Fiber Ingredients: Food Applications and Health Benefits
enzymes is reduced by an increase of viscosity of the digestive fluids, which reduces the contacts between enzymes and substrates. Pectin may also inhibit enzyme activity, for example lipase [22, 23], by interacting with substrates inhibiting the adsorption of enzyme to the substrate. Based on this knowledge a patent for pectin-containing health food was filed, which is supposed to reduce lipase activity to reduce obesity, hyperlipidemia, and arteriosclerosis. Fermentation of Pectin Fermentation of pectin mainly occurs in cecum, colon ascendens, and colon transversum. In these sections a microbial flora exists that is able to produce pectin-degrading enzymes (pectin esterase, endo-polygalacturonase, and pectin lyase). Microorganisms, for example Bacteriodes, E. coli, Lactobacillus, and Bifidobacterium, are able to use pectin as substrate and these organisms are able to degrade pectin by 90% to 95% [24, 25]. When grown on a mixture of polysaccharides Bacteroides ovatus preferred to utilize starch and pectin, which showed that these carbohydrates are important substrates for the bacterium located in the large intestine [26]. Studies with rats showed that pectin degradation is reduced in the digestive system of rats and degradation is influenced by degree of esterification and adaptation time of the pectin-containing diet [27, 28]. Studies showed that pectin degradation increases with decreasing degree of esterification [29] and duration of adaptation time [30]. Products of the fermentation process in the human body are the shortchain fatty acids: acetate, propionate, and butyrate with a molar proportion of 84:14:2 [15, 31] and gases like methane, carbon dioxide, and hydrogen. The pectin concentration seems to have an influence on the molar proportion of short-chain fatty acids that are formed. At low pectin concentration (2.5 mg/ ml), the molar proportion of short-chain fatty acids of 81:10:9 are formed, and once high pectin concentrations (30 mg/mL) were applied a molar proportion of 74:7:20 was formed [32]. The formed short-chain fatty acids are utilized by the host macroorganism and are nutrients for colon cells. Homogenates of human feces were incubated anaerobically with pectin resulting in an increase of short-chain fatty acids by 6.5 mmol/g pectin or 1.05 mol/ mol hexose equivalents [33]. Pectin might be partially fermented to oligo-galacturonic acid with different degree of polycondensation. Non-reducing ends of these oligomers can bear ∆-4,5-double bonds due to β-elimination or by action of pectin and pectate lyases. By incubating pectic acid with human feces galacturonic acid, ∆-4,5-unsaturated di- and tri-galacturonic acids were formed with di-galacturonic acid as the main product [34]. The respective enzymes were also found in animal feces [35–37]. Products obtained by further degradation of galacturonic acid were furan-2,5-dicarbonic acid and galactaric acid, which further are transformed into acetoacetic acid. Studies investigating the fermentability of pectin showed that in the fermentation process a time lag in degrading of the substrate is seen. The fer-
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mentability of complex substrates, for example dietary fibers, is influenced by adaptation of cecum and colon flora [38]. By using fresh human feces, pectin was degraded by 97.4% [39]. Using in vitro fermentation with inocula made from white Wistar rats, pectin was degraded by 92% to 95% and the digestible energy of high ester pectins were found to be between 9.9 and 10.4 KJ/g dry weight [40]. Compared to high methylester pectin, low methylester pectin seems to ferment faster [41]. In vitro studies comparing the ability to ferment pectin of a complete human fecal flora with cultures of defined species isolated from human feces showed that isolated cultures have limited ability to ferment pectin. While the spectrum of intermediate products of the pectin fermentation, for example unsaturated oligo-galacturonic acids, changed permanently in the culture, leading to the formation of short-chain fatty acids, with complete fecal flora, while in pure cultures of E. coli no pectin degradation was found. Also the pectin-degrading activities of Bacteroides thetaiotaomicron as well as co-cultures of B. thetaiotaomicron and E. coli were lower [42]. Using conventional and germ-free rats the fermentation process of pectin was studied. In this study [43] these rats were fed for three weeks with a 6.5% pectin-containing diet using pectin with different degrees of esterification (34.5%, 70.8%, 92.6%). The molecular weight of pectin that was isolated from the small intestine of germ-free rats was unaffected by the diet. It passes the small intestine as a macromolecule. In most of the conventional rats no galacturonan was found in cecum, colon, or their feces, but in the colon diand tri-galacturonic acid was found. In all pectin-fed groups the concentration of short-chain fatty acids in cecum or feces was higher than in the reference group, without having been fed with pectin. The groups fed with pectin showed higher total anaerobic and Bacteroides counts. And the groups of conventional rats that were fed with pectin with lower degree of esterification showed increased formation of short-chain fatty acids. The pectin-fed rats showed increased ileum, cecum, and colon weights. Also during in vitro fermentation of pectin with fecal flora obtained from rats unsaturated oligogalacturonic acids were formed and pectin with lower degree of esterification was fermented faster than pectin with higher degree of esterification. Pectin-fed rats also showed increased total bacterial population in the cecum as well as increased weight of cecal wall and its contents [44]. Prebiotic Nature Strains of Bifidobacteria are able to ferment pectin by 10% [45]. But not all Bifidobacteria are able to utilize pectin [46]. Bifidobacterium pseudolongum P6, which was isolated from rabbit cecum, fermented pectin via a modified Entner-Doudoroff pathway. Pectin was degraded by extracellular endopolygalacturonase. The enzyme 2-keto-3-deoxy-6-phosphogluconate (KDPG) aldolase (EC 4.1.2.14) has an important role in the fermentation process of pectin. KDPG aldolase activity has been seen in pectin-fermenting organisms, for example Treponema saccharophilum [47], Butyrivibrio fibrisolvens, Pre-
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Fiber Ingredients: Food Applications and Health Benefits
votella ruminicola [48], and Lachnospira multiparus [49], while no KDPG activity was seen in cell extracts obtained from Bifidobacterium species or Streptococcus bovis [46] that are not able to utilize pectin. B. pseudolongum P6 fermented pectin to acetate, lactate, succinate, and ethanol (3.22 ± 0.23; 6.01 ± 0.64; 1.58 ± 0.25; 0.66 ± 0.10; 0.32 ± 0.10; mmol/g pectin). In the fermentation process no carbon dioxide was formed. Bifidobacterium lactis showed good growth rates with high methylester pectin as substrate. Low methylester pectins were better growing media than high methylester pectin for B. pseudolongum, B. bifidum Bb12, Lactobacillus plantarum 0207, L. casei Shirota, and L. acidophilus. Bifidobacterium angulatum and B. infantis were not able to utilize high methylester pectin but were able to ferment low methylester pectin. Comparing different pectin types, greater fermentation selectivity was seen with decreasing degree of esterification as well as reduced molecular weight [50]. Role of Pectin in Weight Management By just consuming pectin weight reduction might be questionable, although it has been seen that consuming 36 g pectin per day increased excretion of fatty acids by 80% [51]. Pectins decrease bile acid concentration in the small intestine. If the bile acid concentration is too low, fat absorption is significantly reduced, so that pectin is recommended as a useful adjuvant in the treatment of disorders related to overeating [52]. With results of other studies conducted with the U.S. Army using high methylester apple pectin, it was concluded that pectin may have an important adjunct role in human nutrition and especially in obese persons [53]. Another hint for the role of pectin in weight management might come from studies with HIV-positive patients [54]. Lipodystrophy has been described with increasing frequency in patients infected with HIV. Differences in the diets of HIV-positive men, who developed fat deposition, and those who did not were studied. The patients who did not develop fat deposition had overall greater energy intake and greater consumption of total protein, total dietary fiber, soluble fiber, insoluble fiber, and pectin than patients who developed fat deposition. Playing an important role in weight reduction can be traced back to pectin’s properties to: • Delay gastric emptying half time [55–58] • Increase mouth-cecum transit time • Bind high amounts of water into a gel matrix • Prolong the feeling of satiety • Reduce food consumption • Reduce absorption of food components from the stomach [59] • Immobilize nutrients
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Pectin • Reduce formation of enzyme-nutrient complexes [60–63) • Reduce degradation and digestion of macromolecules [63) • Increase unstirred water layer [64] • Delay/reduce resorption of nutrients • Increase nutrient excretion
Pectin might also be able to support weight management by viscosity and gel formation. Pectin and pectin-containing systems can partially replace sugar or fat as bulking agent for developing calorie-reduced food. Affinity to Metal Ions and Excretion of Toxic Metals As a polyelectrolyte, pectin is able to bind and exchange cations. The stability of the respective complexes is significant for the type of cation [65–71]. The affinity of sodium pectinate to different metal ions from high affinity to low aaffinity is shown below [67]:
Na-pectinate: Pb > Ba > Cd > Sr > Zn > Cu > Co > Ni > Fe > Hg > Cr > Mn > Mg
Metal ions can be bound inter-molecularly between two pectin molecules as well as intra-molecularly. The affinity of pectin to metal ions is influenced by the degree of esterification [68, 70, 71], distribution of free carboxylic acid groups [72], pH value [73–75], ionic strength, and concentration of affinity of other present cations. Supplemented pectin had no negative effect in short-term studies with humans [76,–79] on Fe, Cu, and Zn balances. Similar results were seen in studies lasting five to six weeks on Ca and Mg levels [51, 80]. Also in studies with workers who were exposed to high levels of lead they showed no significant change of Cu, Fe, Mg, and Zn when they took 8 g/d pectin over a period of six weeks in order to increase excretion of lead by binding to pectin [81]. The pH value influences the binding of cations. For essential minerals Ca, Cu, and Zn, the strongest binding was seen in the pH range of pH 4 to 6. Strongest binding with Fe was seen at pH 7.0 to 7.5 [73–75]. Therefore it can be concluded that bioavailability for Ca, Cu, and Zn is not reduced, as the pH value in the jejunum, where minerals are absorbed, is pH 6 to 7. Fe availability is discussed as studies show results of significant reduced availability [82, 83), slight reduction [74, 75, 84–86], or no change of bioavailability [74, 87, 88]. Degrees of esterification and molecular weight have an influence on iron absorption [89, 90, 91]. Rats fed with pectin with low molecular weight (89,000 dalton) and degree of esterification of 75% showed iron absorption of 57% compared to 48% in the control group. Serum iron, transferring saturation, hematocrit and liver and spleen iron were increased compared to the control
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group or the groups fed with pectin with high molecular weight (low DE and high DE) or the group with low DE and low molecular weight. Studies also have shown a negative influence of pectins and other negatively charged dietary fibers on the availability of minerals once dietary fiber was consumed in the form of fruits, vegetables, and cereals. This effect can be caused by other factors, for example phytates or lignin [16]. Another factor that has to be considered is the duration of consumption or the length of study. In a study with rats, there was a reduced resorption of Zn, Cu, Cr, and Co in the beginning of the study supplementing 10% dietary fiber in the diet [92]. But after 21 weeks neither a deficit of these minerals nor a difference to the control group was reported. It has been discussed that the gut mucosa undergoes an adaptation process once the diet is changed. This process was investigated with rats fed with a diet containing 15% dietary fiber (pectin, cellulose, MCC, bran). During the first two weeks, size and form of jejunal villi changed and were again more uniform after another three weeks. In general the number of villi increased with increasing dietary fiber content of the food and duration of supplementation [93]. Negative reports from shortterm studies should be reviewed with some caution as the negative results may be caused by adaptation procedures in the gut. Essential mineral salts of pectins and especially oligo-galacturonic acids can be used for supplementing these elements, for example Fe, Zn, and Mg with good bioavailability [94]. Interestingly strong complexes are formed with lead and other toxic metal ions [67], and excretion is increased by pectins [82, 95–100]. Except for one publication [101] a significant increase of lead excretion after pectin consumption is reported in animal [67, 96, 97–99] and human studies [91, 95, 102, 103]. A pectin supplementation of 8 g per day for six weeks significantly increased renal lead excretion (p < 0.001) by 130% from 55 to 127 ng Pb/ml urine which resulted in a significant decrease (p < 0.01) of blood lead level from 760 ng to 530 ng Pb/mL blood. In this study, cadmium was also decreased and levels of Cu, Fe, Mg, and Zn remained unchanged. The high affinity of pectin to lead is almost independent of the DE of pectin if the DE is less than 50%. This is not the case for the affinity to Cd [69], Zn [102], and Ca [103]. Even high methylester pectin forms relatively stable complexes [70]. This selective and strong binding takes place at higher pH values, similar to the conditions of the small intestines. Weak binding was found at low pH values. Pectin cannot be absorbed as a macromolecule, so that as active substances in this detoxification process galacturonic acid oligomers that were formed by microorganisms are discussed. In vitro and in vivo studies, in which the binding affinity of saturated galacturonic acid oligomers with a degree of polymerization from DP 1 to DP 9 towards cations was investigated, showed that binding affinity increased with increasing degree of polymerization [104]. Ca, Sr, and Zn were bound very weakly by electrostatic interactions, while strong complexes were formed with Cd, Cu, and Pb. The strongest complex was formed by lead with galacturonic acid oli-
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gomer DP 5, which had almost the same strength as a complex formed with a polymeric chain. Binding of Ca, Sr, and Zn with mono-galacturonic acid was negligible, while Cu and Pb showed significant degrees of association. An even more effective excretion of lead could be observed by intravenous application of mixtures of ∆-4,5-unsaturated galacturonic acid oligomers (10 mg/kg body weight per day). The excretion of lead improved by 400% with a mixture containing mainly tri- and tetra-unsaturated oligogalacturonates and by 600% with a mixture of mainly unsaturated di-, less unsaturated tri-, and almost no saturated tetra-galacturonates. It was stated that the double bond could be contributing to excretion of lead by providing an additional binding possibility. Influence of Pectin on Jejunal and Ileal Morphology As previously discussed, pectin influences morphology and ultra-structure of the intestines. The effects of pectin on jejunal and ileal morphology were studied with adult male mice fed a semisynthetic diet containing 8% cellulose or pectin for 30 days. No significant differences in the jejunal villus height between the two groups were found, but the jejunal crypt depth and both the ileal villus height and crypt depth of the mice fed the pectin diet were significantly greater than those of the mice fed the cellulose diet. Numerous intercellular spaces were observed in the jejunal absorptive cells of the mice fed the pectin diet, but not the cellulose diet. Moreover, the ileal absorptive cells of mice fed the pectin diet contained numerous peroxisomes, whereas there were few in these cells of mice fed the cellulose diet [105]. Male Wistar rats were fed an elemental diet containing 2.5% pectin for 14 days. Pectin feeding included a significant increase in the villus height and crypt depth in the small intestine. These effects correlated with a significant increase in plasma enteroglucagon levels [106]. Pectin supplementation resulted in significant increases in the length, weight, and number of Ki-67-positive cells in the ileum, cecum, and colon [107]. In the cecum of Sprague-Dawley rats, the concentration of SCFA was positively associated with the number of cells per crypt column, total cells per crypt, and the proliferative zone. In contrast, in the distal colon, there was no significant correlation between SCFA concentration and measurements of cell proliferation. The data suggest that pectin stimulates cecal cell proliferation through the production of SCFA [108]. In the proximal colon of rats, the effect of pectin on cell proliferation was also highly dependent on the source of fat in the diet. Pectin exerted a hyperproliferative effect when the source of fat in the diet was corn oil, but pectin had no effect when beef tallow or fish oil was the fat source. This indicates that pectin and fat modulate cell proliferation of the colon in an interactive site-specific manner [109].
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Medical Aspects Reduction of Symptoms of Dumping, Short Bowel Syndrome, and Short Gut Syndrome The dumping syndrome consists of early postprandial abdominal and vasomotor symptoms, resulting from osmotic fluid shifts and release of vasoactive neurotransmitters, and late symptoms secondary to reactive hypoglycemia. Effective relief from symptoms of dumping can be achieved with dietary modifications to minimizing ingestion of simple carbohydrates and to exclude fluid intake during ingestion of the solid portion meal. More severely affected individuals may respond to agents such as pectin, which increase the viscosity of intraluminal contents [110–115]. Short bowel syndrome is characterized by weight loss, diarrhea, and malabsorption. Pectin improves small and large bowel mucosal structure, prolongs intestinal transit, and decreases diarrhea in rats. Pectin significantly increased stool solidity, and improved colonic water absorption following resection without significantly altering mucosal structure [116]. Patients with reduced length of remaining small bowel after bowel surgery due to mesenteric thrombosis or Crohn’s disease responded well to the approach of a pectin-supported diet program instead of total parenteral nutrition [117]. The effect of pectin-supplemented diet in short gut syndrome was investigated in a three-year-old boy [118]. Nitrogen absorption was higher and stomach-to-anus transit time was prolonged during pectin supplementation of the enteral feed. Effects on Acute Intestinal Infections Patients who receive tube-feeding formulas very often show diarrhea. By adding pectin to these formulas, liquid stools are significantly reduced and a normalization of colonic fluid composition can be achieved [119]. This was also achieved when tube-fed patients receiving antibiotics additionally were fed with pectin [120]. In literature there are products containing pectin, for example in combination with agar, tannic substances, iodine, kaolin, bentonite, alkyl polyalcohols, aluminium phosphate, activated charcoal, sweet whey, and nickel-pectinate [121]. Clinical studies showed that pectin has the potential to reduce acute intestinal infections by inhibiting the growth of Shigella, Salmonella, Klebsiella, Enterobacter, Proteus, and Citrobacter. A rapid suppression of diarrhea and other symptoms of acute infections were observed, once 5% pectin solutions were given to patients [122]. A preparation, given to children having acute, non-complicated diarrhea, of apple pectin and chamomile extract reduced the duration of diarrhea significantly by at least 5.2 hours. After three days of treatment the diarrhea had ended significantly more (33 out of 39 patients) than in the placebo group (23 out of 40 patients) [123]. The product used in
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the study was commercially available as Diarrhoesan. A study with a pectinsupplemented rice-based diet or green-banana-supplemented rice-based diet showed reduction of diarrhea in infants compared to the group who received a non-supplemented rice-based diet [124]. Positive effects were also achieved in children with persistent diarrhea with a green banana or pectin enriched diet. After three days of treatment significantly more children recovered (green-banana-group: 59%, pectin-group: 55%, control-group: 15%). By day 4 these proportions increased correspondingly (82%, 78%, 23%). The study showed that besides reducing diarrhea duration green banana or pectin significantly reduced amounts of stool, oral rehydration solution, intravenous fluid, and frequency of vomiting [125]. Effects on Atherosclerosis An important risk factor for atherosclerosis, stroke, and coronary heart disease is fibrinogen, and not only its concentration; it is also believed that the quality of fibrin networks may be an important risk factor for the development of coronary heart disease. The risk is increased with high serum cholesterol levels. Coronary heart disease and stroke caused by atherosclerosis and its related problems of hyperinsulinemia, hyperlipidemia, and hypertension are strongly related to the diet [126]. In a study with two groups of 10 male hyperlipidemic volunteers the effect of pectin on fibrinogen and fibrinogen networks was studied. For four weeks each volunteer of one group received a pectin supplement of 15 g per day and the effects compared to the group that received a placebo were studied. The group that received pectin supplementation showed significant decrease in total cholesterol, LDL, and apolipoprotein A and B. Also the fibrin network became more permeable and it had lower tensile strength, which is believed to be less atherogenic. In this study it was suspected that pectin modified network characteristics by a combination of its effects on metabolism and altered fibrin conversion. An in vivo study comparing the effect of pectin with acetate showed that acetate, which is also formed in the fermentation of pectin, showed that acetate may be responsible in part for the pectin supplementation. Fibrinogen levels in the acetate group remained almost unchanged and like the pectin group fibrin networks were more permeable, had lower tensile strength, and were more lyseable [127]. In the Los Angeles Atherosclerosis Study [128] the intima-media thickness (IMT) of the common carotid arteries in humans (aged 40 to 60 years, n = 573), 47% of women were measured ultrasonographically. A significant inverse association was observed between IMT progression and the intakes of viscous fiber (P = 0.05) and pectin (P = 0.01). The ratio of total to HDL cholesterol was inversely related to the intakes of total dietary fiber (P = 0.01), viscous fiber (P = 0.05), and pectin (P = 0.01). The intake of viscous fiber, especially pectin, appears to protect against IMT progression. Serum lipids may act as a mediator between dietary fiber intake and IMT progression.
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Frequent and long-lasting high insulin concentrations promote vascular lesions, the primary stadium of atherosclerosis. Suppression of postprandial insulin levels by pectins may therefore have an anti-atherogenetic effect [129]. Dietary fibers like pectin may also increase peripheral insulin sensitivity in young and old adults [130]. Effects on Cholesterol and Lipid Metabolism Pectin increases the viscosity of the chymus leading to a reduced turnover of large molecules, for example fat molecules, bile acid, cholesterol, etc. But pectin shows more properties. With low density lipoproteins (LDL) pectin forms complexes, which leads to a reduction of lipid resorption and an increased excretion of lipid with the pectin molecules. It has been seen that the interaction is electrostatic [131] and the binding of LDL depends on the degree of esterification of pectin. High methylester pectin can bind LDL by a ratio of 1:4, whereas low methylester pectin is able to bind less LDL [132]. The positive influence of pectin was already described in 1961. It has been shown that consuming food containing pectin leads to serum cholesterol reduction [133]. Most studies carried out with a wide variety of subjects and experimental conditions showed the potential of cholesterol reduction by consuming 6 to 15 g pectin per day [133–149]. In the liver, bile acids are synthesized from serum cholesterol, which is bound to serum LDL, and secreted into the small intestine. Bile acid then is re-absorbed during digestion. In the chymus pectins bind bile acids and therefore lead to increased excretion of bile acids, which in turn reduces the re-absorption of bile acids from the gut back into the liver. This increases bile acid synthesis in the liver, reducing cholesterol and most importantly LDL, which has the highest atherogenic potential. Pectins have almost no influence on the level of high density lipoproteins (HDL) leading to a healthier LDL:HDL ratio. In discussion is the influence of degree of esterification of pectin on the potential of pectin to reduce cholesterol. Studies [150] indicating that a minimum degree of esterification of 10% is needed for a pectin to have cholesterol-reducing properties were not able to be reproduced [145]. Studies published since 1985 are summarized in Table 8.1. Synergistic effects on reducing cholesterol with other substances were found and by combining the dose of 15 g pectin with 20 g fish oil per day the cholesterol ester fraction of plasma lipids were reduced further by 44% [158]. Another beneficial effect was a 30% decline in the fatty acid fraction. Studies with rats showed an increased reduction of plasma cholesterol and plasma triglycerides by combining apple pectin with polyphenols from apples [159]. By comparing 67 different studies that were carried out between 1966 and 1996 in which the effects of pectin, psyllium, oat fiber, and guar gum on levels of cholesterol, triglycerides, and lipoproteins were studied, it has been seen that pectin showed highest effectiveness in lowering total cholesterol, LDL, and triglycerides. All applied substances significantly reduced total choles-
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Pectin Table 8.1 Influence of Pectins on Lipid Metabolism Pectin g/d + a, b, c
Subjects
Time
30 c 15 s 27 ?
3 wk 3 wk 4 wk
15
54 55 47
90 d
15 + a
90 d
10 40
Cholesterol Total
LDL
HDL
TG
Reference
–17 –12 –15
–21 –14 n.d.
+4 +12 n.d.
n.d. n.d. n.d.
15 + b
–34,4 –34,5 –36
n.d. n.d. –23,5
+24,6 +34,0 +36,3
–24,6 º 26,2 –18,8
4 wk
15
–11,6
–11,5
+21,3
n.d.
4 wk
10 + c
–44
–45,5
+14
–55
Schuderer (151) Cerda et al. (152) Grudeva (153) Grudeva et al. (154) Veldman et al. (155, 156) Bartz et al. (157)
2020
Notes: c = controlled, s = self-served, n.d. = not determined, a = + sorbitol 1:1, b = + sorbitol 2:1, c = 1,5 g omega-3-fatty acid.
terol and LDL level without changing the HDL level significantly. This metaanalysis also showed that increasing the pectin dosage to more than 10 g per day didn’t further improve the effects [160]. Studies showed that the effect of pectin to reduce cholesterol is proportional to the level of serum cholesterol, so that cholesterol reduction was higher in patients who had increased cholesterol level [161, 162]. Table 8.2 gives a summary of the meta-analysis. Regarding the effectiveness of pectin it appears that high molecular weight or high viscosity has a minor influence on the cholesterol-reducing properties of pectin. The ability to form hydrophobic interaction seems to be more important. In a study with several sugar beet pectins, the beet pectin, which was de-acetylated and had a low molecular weight, showed highest cholesterol reduction. Sugar beet pectin with reduced neutral sugar content showed lowest cholesterol reduction. However, apple pectin with high methylester content and high viscosity showed strongest cholesterol reduction in this study [163]. Other studies showed the molecular weight as an important factor for cholesterol reduction [164]. In some research work it was postulated that by higher production of short-chain fatty acids from pectin the pH value in the lower intestine is lowered changing microbial cholesterol synthesis, which positively affects excretion of cholesterol and bile acid. In in vitro studies pectin showed limited potential to bind bile acid. Comparing different pectin substances at different conditions resulted in the finding that low methylester pectin and acetylated pectin interacted less with bile acids. Best binding properties of bile acid showed pectin with very high methylester content at pH 6 [165]. Studies on triglyceride excretion didn’t
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Table 8.2 Change of Lipid Parameters under Consumption of Soluble Dietary Fibers (Meta-analysis) [160] Soluble Dietary Fibers Cholesterol Oat products Psyllium Pectin Guar LDL cholesterol Oat products Psyllium Pectin Guar HDL cholesterol Oat products Psyllium Pectin Guar Triglycerides Oat products Psyllium Pectin Guar
Number of Studies
Participants
Change per g Fiber [mg/dL]
26 17 7 17
1600 757 277 341
– 1,43 – 1,08 – 2,71 – 1,00
22 17 4 12
1439 757 117 218
– 1,23 – 1,12 – 2,13 – 1,28
24 17 7 15
1542 757 277 302
– 0,07 – 0,07 – 0,14 – 0,11
20 16 6 17
1374 720 247 338
+ 0,7 + 0,3 – 1,8 – 0,9
show a specific effect of pectin. An unspecific increase of triglyceride was noticed, which can be explained by increased viscosity of the chymus. Increased viscosity of the chymus results in reduced mobility of large molecules, especially enzymes, so that excretion is increased. Another physical effect pectin shows is to increase the unstirred water layer, which reduces resorption of large molecules. Lipids and lipid-degrading enzymes are bound into the matrix hindering the formation of enzyme-substrate complexes [166]. The addition of pectin increased the activity of cholesterol-7-α-hydroxylase in rats. This enzyme activates bile acid synthesis from cholesterol and might also lead to a reduction of the level of LDL [167]. Effects on Glucose Metabolism Blood glucose level is strongly affected by carbohydrate-rich food and causes a peaking glycemic response. Because of gel formation and increasing chymus viscosity pectin delays the absorption of glucose and other monosaccharides, as well as reduction of degradation of complex carbohydrates.
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Pectin Table 8.3 Influence of Pectins on Serum Glucose and Serum Insulin
Subjects
Amount Pectin Added in g
8 d3 i
1010
13 n
10
5 g dumping syndrome
10,5
6d 6d 6n 23 g 3h
14,5 9/sqma 14,5 10–20 5
8i 7i 6n 6n 13 d 5n, 6o, 5d
15 7 10 10 10 10 + guar
7n
20
Time Interval (min.) of Significant Decrease of Serum Serum Glucose Insulin 30–90 30–120 at 15 min. n.s. 30–90 at 30 min improved retention of load in stomach n.s. 30–60 30–45 at 30 min Hypoglycemia Overted 15–90 60–90 n.s. 60–90 at 60 min. Significant decrease in all but greatest change in obese and diabetic subjects n.s.
Reference
30–120 — 15–45
Jenkins et al. (168)
—
Leeds et al. (170)
n.s. n.s. — — —
Jenkins et al. (171) Monnier et al. (172) Holt et al. (173) Labayle et al. (174) Labayle et al. (174)
— >180 min. n.s. n.s. n.s.
Vaaler et al. (175) Poynard et al. (176) Gold et al. (177) Gold et al. (177) Williams et al. (178) Kanter et al. (179)
—
Schwartz et al. (180)
Jenkins et al. (169)
Note: d = diabetics; n = normal subject;s g = gastric surgery; h = hypoglycemic; o = obese; i = insulin dependent diabetics; n.s. = not significant. a Square meter body surface.
Pure pectin has a glycemic index of almost zero. Sugar, which is added to standardize commercial food-grade pectin, increases the glycemic index respectively. This also means that pectin and other soluble fibers reduce the glycemic index in case of combined consumption. Studies showed that pectin lowers blood glucose and insulin levels after consuming carbohydraterich food. A summary is shown in Table 8.3 [168–183]. In a test with diabetic and non-diabetic consumers, pectin flattened the glycemic response and reduced the insulin demand for both groups. That led to less urinary glucose loss and improved control of diabetes [184]. Several studies suggested that the addition of pectin as a gel and viscosity providing soluble fiber has an influence on the unstirred water layer, which
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reduced the absorption of large molecules such as fatty acids or glucose. With increasing pectin dosage the unstirred water expanded resulting in reduced absorption of glucose and fatty acids [185, 186]. Gastric inhibitory polypeptide, which reduces gastric motility and insulin secretion, is reduced by pectin [187, 188]. There are indications that gastric motility has an influence on gastric emptying half time. Insulin reduction could result in reduced activity of α-hydroxy-α-methylglutaryl (HMG)CoA-reductase. HMG-CoA-reductase is involved in an early step of the endogenous cholesterol synthesis. Since its activity also depends on insulin concentration, cholesterol level could be reduced. Effects on Cancer Insoluble fiber increases excretion and therefore also accelerates the excretion of mutagenic substances. Under certain conditions, for example when too small amount of liquid is consumed, soluble fiber can prolong excretion. But studies that focus on the influence of pectin on carcinogenesis show benefits of pectin. A project in which the effect of several pectin types on azoxymethaneinduced colon carcinogenesis in rats was investigated showed decreased multiplicity of colon tumors. The diet was supplemented with 20% apple pectin and 20% citrus pectin. The number of tumors was significantly reduced in the group fed apple pectin. Apple pectin decreased fecal glucuronidase and tryptophanase levels, with a significant decrease in the activity of glucuronidase during the initiation stage [189, 190]. Diet supplementing by 20% apple pectin also decreased the number of tumors in 1,2-dimethylhydrazine-induced colon carcinogenesis [191]. Prostaglandin E2 (PGE2) level in distal colonic mucosa was lower than in basal-diet-fed rats. Again at the initiation stage fecal glucuronidase activities were significantly lower than in the control group. Glucuronidase is considered a key enzyme in the metabolism and carcinogenic activation of 1,2-dimethylhydrazine in the colonic lumen. The ability of apple pectin to decrease PGE2 was dose dependent [190]. However these results indicate an anti-inflammatory effect in the bowel. Rats also showed significant reduced incidence of hepatic metastasis, once the diet was supplemented with apple pectin. Supplementing the diet with apple pectin reduced the amount of colorectal tumors induced by 1,2-dimethylhydrazine significantly in a study with transgenic mice carrying human c-Haras genes [192]. Studies concluded that pectin and its degraded products, for example butyrate, are important contributing factors of the protective effects of fruits against colon cancer. The colonic crypt contains highly proliferative cells in its base and differential cells on its luminal surface. Carcinogenesis significantly affects this orderly cellular distribution. Important mechanisms against colorectal cancer are anti-proliferative effects on the human colonic adenocarcinoma cell line HT 29 induction of apoptosis in tumor cells. A significant reduction in attached cell numbers by pectin and pectic-oligosaccharides were obtained after three days incubation. Increased apoptosis
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frequency after incubation with 1% (w/v) pectin and/or pectic oligosaccharides was seen by caspase activity and DNA laddering on agarose gel electrophoresis [193]. A pectin-enriched diet induced up-regulation of active caspase-1 (20 kDa) and caspase-3 precursor in rats that have been treated with 1,2-dimethylhydrazine (DMH). The average number and volume of tumors per rat were lower in rats fed with pectin. In general, pectin enhanced caspase-3 activity in all colonocyte populations. The luminal colonocytes exhibited higher caspase-3 activity than proliferative colonocytes of rats fed a standard diet. In pectin-fed non-DMH-treated rats, equal activity was measured among all colonocyte populations. In luminal colonocytes of rats that have undergone DMH treatment cleaved poly (ADP-ribose) polymerase subunit [89 kDA] was detected. In the group that was fed the standard diet detection was less compared to the group that received a pectin enriched diet. BAK was equally expressed in isolated colonocytes from rats of both dietary groups treated with DMH and in the group of rats fed with pectin without having received DMH treatment. In the group without DMH treatment and standard diet a higher expression in differentiated colonocytes was obtained. Within the DMH treated group Bcl-2 expression was lower in colonocytes in rats fed with pectin compared to rats fed the standard diet. Apoptotic index in the DMH treated groups was higher in rats receiving the pectin diet in both types of colonocytes. The production of butyrate as one of the products obtained in the fermentation process of pectin might be important for these effects [194]. In animal studies modified citrus pectin (MCP) inhibited spontaneous pulmonary metastases [195]. Pathogenic organisms or cell destructive substances have to bind to the surface of a cell to cause harm. The ability of cells to metastasize appears to be related in part to the cohesiveness of cells. Cellular interactions are mediated by a carbohydrate-binding protein at the cell surface called galectin-3. Human studies showed a correlation of the level of galectin expression and tumor stage. In agarose cell cultures, anti-galectin monoclonal antibodies inhibited the growth of tumor cells [196]. Oral consumption of modified citrus pectin (MCP) interfered with cell-to-cell interactions mediated by galectin-3 molecules. In vitro tests with rats showed a time-dependent and dose-dependent inhibition of cell adhesion by tumor cell lines and significantly reduced occurrence of metastases [197]. Tumor growth, angiogenesis, and spontaneous metastasis in vivo were significantly reduced in mice fed with modified citrus pectin. In vitro, modified citrus pectin inhibited the binding of galectin-3 to human umbilical vein endothelial cells (HUVECs). The effect depended on the dosage, but with a concentration of 0.25% MCP the binding of galectin-3 (1 µg/mL) to HUVECs was inhibited to 100% [198]. A phase II pilot study showed that prostate specific antigen doubling time from 7 out of 10 men increased after taking MCP for 12 months compared to before taking MCP [199]. Other studies also showed the potential of modified citrus pectin on reducing the growth of solid primary tumors [200–207]. However, modified
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citrus pectin is not a clearly defined molecule. In studies it was described as a galactosyl-rich pectin fragment with low molecular weight, high pH value, and a degree of esterification of less than 5% [195, 197]. It was discussed that mono-galacturonic acid units have no activity and that activity is reduced with increased molecular weight [208, 209]. It is also claimed that active substances are carbohydrates, which have a terminal ∆-4,5-unsaturated galacturonic acid at its non-reducing end [209]. The application and production of modified citrus pectin is also described in several patents. Patent EP 0 716 605 B1 (WO 95/07084), a carrot soup, describes using α-1,4-galacturonic acid units derived from pectin with a degree of esterification of 20% to 80% [210]. Other patents are WO 01/60378 A2 [209] and WO 02/42484 [211] and claim different activity mechanisms. However, in common are a rather low degree of polymerization and a content of unsaturated galacturonides.
Application of Pectin in Food Products By consuming fruits and vegetables in our daily diet we eat pectin. Dietary fiber produced from fruits, for example apple fiber, contains pectin. Commercial pectin is produced by an extraction process from plant raw material [10]. Different pectin types are obtained by using different raw material sources, for example apple pomace, citrus peels, and through various stages of the extraction process in which high methylester and low methylester pectins are obtained. Depending on raw material and manufacturing process, pectins with different molecular weight can be obtained. Crude pectin varies in its gel strength. In order to produce pectin that guarantees the same gelling properties, batches of pectin are mixed and crude pectin is standardized with sugar to certain gel strength. For certain application areas, for example confectionery products, pectins are additionally standardized with buffer salts. Standardized pectin that is used as a food additive has high molecular weight to obtain the requested high water-binding capacity. To calculate the amount of soluble fiber contributed by adding standardized pectins to food, the amount of added ingredients to standardize the commercial pectin has to be considered. To use 100% pectin crude pectin also can be obtained from the pectin manufacturers. Due to the high water binding there are limits for certain products to the amount of high molecular weight pectin that can be added. Low-molecular-weight pectin provides low viscosity. It can be used in high dosages without having major influences on the texture of the desired product.
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Fruit Spreads Fruit spreads are a traditional application for pectin as commercial pectin is used to supplement naturally occurring pectin in fruit. With industrial production of fruit spreads it became even more important to use a gelling agent that would provide control in the production of fruit spreads and consistent quality for consumers. Fruit spreads are traditional jams, jellies, and marmalades with high sugar content. In these products sugar acts as a preservative, sweetener, and filler. Fruit spreads with self-preserving properties must have a minimum content of total soluble solids of 62 °brix. In these products typically high methylester pectin is used with a dosage of 0.1% to 0.4%. Pectin dosage depends on the type of fruit product used and the fruit type itself. Gel-forming properties of pectin depend on the amount of total soluble solids present in the finished product and the pH value of the fruit spread. High methylester pectin forms gels at a total soluble solids content of at least 60 °brix and a pH value of below pH 3.4. Fruit spreads that have a reduced content of sugar are manufactured with low methylester conventional or low methylester amidated pectins. The pectin dosage lies in a range of 0.6% to 1.2% and depends highly on the amount of sugar that is used. By using commercial pectin it is possible to create a variety of different textures. Apple pectin will provide a smooth gelled texture, whereas gels with a brittle texture are obtained once citrus pectin is used. Industrial Fruit Preparations Sweet bakery products and fermented dairy products often use fruit preparations to add a fresh taste to the products. And by using different fruits it is possible to create a line of products offering a variety of flavors. Glazings are a form of fruit preparations that enhance the appearance of fruit cakes. Fruit preparations are specialized products and tailor-made to the respective application. Fruit preparations for baked products give biscuits and cookies a fresh note and serve as a source of moisture to prevent drying of the cookie. Pectin provides the desired structure of the fruit preparation and thermal stability once the product passes through the baking process. Depending on firmness and required baking stability in bakery fillings up to 1.5% pectin is used. In dairy fruit preparations typically low methylester pectin is used. Such a pectin forms shear thinning gel structures, which is an important quality aspect as shear thinning ensures maintaining fruit integrity without the tendency to form syneresis. Additionally good mixing behavior with the dairy product is seen to maintain mouthfeel and stability. The usage level is between 0.5% and 1.5% and depends mostly on the content of total soluble solids in the fruit preparation. Molecular-weight-reduced pectin can be added to fruit preparations to increase the respective product with soluble dietary fiber.
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Confectionery Articles Pectin is used as gelling agent for a variety of confectionery products. It is possible to produce acidic fruit jellies with firm and brittle texture and also products with a gummy texture. Also aerated products can be manufactured using pectin as gelling agent. Typically high methylester pectins are used that have been standardized to constant setting temperature in order to prevent pre-gelling. In order to standardize the production of confectionery products buffer salts that have retarding properties, for example sodium citrate, are added to the manufacturing process. For manufacturing fruit jellies 1.3% to 1.7% pectin is used and with a dosage of about 2.5% products with a gummy texture are obtained. Dairy Products Low-fat or fat-free fermented dairy products, for example yogurt, fresh cheese, etc., might lack mouthfeel and viscosity. Low methylester pectin is used to enhance firmness, mouthfeel, and transport stability with a dosage of 0.2%. In the manufacturing process pectin is added to non-fermented milk before homogenizing. Low methylester can be used as gelling agent for dairy dessert products. High methylester pectin has the ability to stabilize protein at acidic conditions. It is now widely used to stabilize acidified milk drinks, yogurt smoothies, and soy beverages. The amount of pectin that is used depends on the amount of protein that has to be stabilized and the pH value of the finished product. Within the pH range of 4.0 to 4.2, strong stabilization is seen, so that it is possible to run the beverage through heat treatment for producing a product with long shelf life. Pectin that is designed for protein stabilization has limitations to be used for providing a source of soluble fiber. More suitable would be molecular-weightreduced pectin, which might be used in addition to other soluble fibers, for example inulin. Beverages and Sorbet Low caloric soft drinks or juice drinks show a lack of mouthfeel, because of the use of non-nutritive high-intensity sweeteners. However, mouthfeel contributes decisively to flavor transfer of a beverage. By adding high methylester pectin the viscosity and mouthfeel of low caloric beverages will be enhanced. The enhanced aroma transfer will create a better impression of the intensive flavor. To create a juicy mouthfeel a pectin dosage of 0.1% is used. High methylester pectin also stabilizes pulp particles of juices and juice drinks. The addition of a large amount of pectin with high molecular weight results in full bodied products thus limiting the amount of pectin for this application. By being very stable at acidic conditions pectin is an ideal source for soluble fiber. In order to be able to produce fiber enriched beverages, it is possible to use molecular-weight-reduced pectin. With such
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a pectin type it is possible to develop beverages that contain 3% soluble fiber without noticing the high fiber content. Being very stable at acidic conditions pectin ensures high fiber content even at the end of the shelf life of a shelf stable product as it is not degraded. In sorbets high methylester pectin is used to provide mouthfeel, and, with strong water binding, pectin controls the growth of large ice crystals. Typically 0.5% pectin is used in sorbet products. Condiments and Spreads Tomato sauces often need to be thickened, and pectin is a suitable ingredient. Medium methylester and low methylester pectins give similar textures as the natural tomato pectin. Between 0.6% and 1.0% pectin is used to thicken tomato based sauces. Condiments, like mint sauce or other fruit condiments, can also be textured with pectin. Fat-reduced spreads have relative high water content. Pectin is able to thicken the water phase of fat-reduced spreads in order to obtain a stable emulsion. Depending on the fat content, either high methylester pectin or low methylester pectin is used. Bakery Products, Cereal Products With its high water-binding property, pectin is suitable to be used in bakery products to control moisture content. By using about 0.1% high molecular weight pectin stalling is reduced, which increases the shelf life of bakery items, for example rolls. The properties of high-molecularweight pectin limit the amount of pectin that can be added to dough, but molecular-weight-reduced pectin offers possibilities to enhance items with soluble fiber or be part of a dietary fiber blend. Carbohydrate reduction can be achieved by suitable dietary fiber blends. With its water binding properties, pectin can play a distinctive role obtaining the desired dough rheology. Pectin can also be used to enhance the soluble fiber content of pasta and cereal products. Capsules and Other Nutraceutical Products Pectin can be dry mixed with other ingredients into a blend, which is compressed to tablets or sold as dry powder for beverages or other products. Manufacturing pectin tablets or capsules is a way to offer consumers the possibility to consume pure high-molecular-weight pectin as similar amounts that are applied to food will have major influences on water binding and texture. High-molecular-weight pectin and low-molecular-weight pectin, including modified citrus pectin, can be easily added to dry mixes for beverages that are prepared by the consumer.
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189. Ohkami H, Tazawa K, Yamashita I, Shimizu T, Murai K, Kobashi K, Fujimake M, Effects of apple pectin on fecal bacterial enzymes in azoxymethane-induced rat colon carcinogenesis, Jpn. Cancer Res. 1995, 86 (6), 523–29. 190. Tazawa K, Yatuzuka K, Yatuzuka M, Koike J, Ohkami H, Saito T, Ohnishi Y, Saito M, Dietary fiber inhibits the incidence of hepatic metastasis with the antioxidant activity and portal scavenging functions (Japanese), Hum. Cell. 1999, 12 (4), 189–96. 191. Tazawa K, Okami H, Yamashita I, Ohnishi Y, Kobashi K, Fujimaki M, Anticarcinogenic action of apple pectin on fecal enzyme activities and mucosal or portal prostaglandin E2 levels in experimental rat colon carcinogenesis, J. Exp. Clin. Cancer Res. 1997, 16 (1), 33–38. 192. Ohno K, Narushima S, Takeuchi S, Itoh K, Mitsuoka T, Nakayama H, Itoh T, Hioki K, Nomura T, Inhibitory effect of apple pectin and culture condensate of Bifidobacterium longum on colorectal tumors induced by 1,2-dimethylhydrazine in transgenic mice harbouring human prototype c-Ha-ras genes, Exp. Anim. 2000, 49 (4), 305–07. 193. Olano-Martin E, Rimbach GH, Gibson GR, Rastall RA, Pectin and pectic-oligosaccharides induce apoptosis in in vitro human colonic adenocarcinoma cells, Anticancer Res. 2003, 23 (1A), 341–46. 194. Avivi-Green C, Madar Z, Schwartz B, Pectin-enriched diet affects distribution and expression of apoptosis-cascade proteins in colonic crypts of dimethylhydrazine-treated rats, Int. J. Mol. Med. 2000, 6 (6), 689–98. 195. Raz A, Pienta KJ, Method for inhibiting cancer metastasis by oral administration of solubile modified citrus pectin, US Patent 1998, 5 834 442. 196. Raz A, Lotan R, Endogeneous galactoside-binding lectin: A new class of functional tumor cell surface molecules related to metastasis, Cancer Metastasis Rev. 1987, 6, 433–52. 197. Pienta KJ, Naik H, Akhtar A, Yamazaki K, Replogle TS, Lehr J, Donat TL, Tait L, Hogan V, Raz A, Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin, J. Natl. Cancer Inst. 1995, 87 (5), 348–53. 198. Nangia-Makker P, Hogan V, Honjo Y, Baccarini S, Tait L, Bresalier R, Raz A, Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin, J. Natl. Cancer Inst. 2002, 18, 94 (24), 1854–62. 199. Guess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI, Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study, Prostate Cancer Prostatic Dis. 2003, 6 (4), 301–04. 200. Platt D, Raz A, Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin, J. Natl. Cancer Inst. 1992, 18, 84 (6), 438–42. 201. Inohara H, Raz A, Effects of natural complex carbohydrate (citrus pectin) on murine melanoma cell properties related to galectin-3 functions, Glycoconj J. 1994, 11 (6), 527–32. 202. Naik H, et al., Inhibition of in vitro tumor cell-endothelial adhesion by modified citrus pectin: a pH modified natural complex carbohydrate (meeting abstract), Proc. Am. Assoc. Cancer Res. 1995, 36, A377. 203. Hsieh T, Wu JM, Changes in cell growth, cyclin/kinase, endogenous phosphogroteins and nm 23 gene expression in human prostatic JCA-1 cells treated with modified citrus pectin, Biochem. Mol. Biol. Int. 1995, 37, 833–41.
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204. Strum S, Scholz M, McDermed J, McCulloch M, Eliaz I, Modified citrus pectin slows PSA doubling time: a pilot clinical trial (meeting abstract), International Conference on Diet and Prevention of Cancer, 28.05.-02.06.1999, Tampere, Finland. 205. Weiss T, McCulloch M, Eliaz I, Modified citrus pectin induces cytotoxicity of prostate cancer cells in co-cultures with human endothelial monolayers (meeting abstract), International Conference on Diet and Prevention of Cancer, 28.05.02.06.1999, Tampere, Finland. 206. Hayashi A, Gillen AC, Lott JR, Effects of daily oral administration of quercetin chalcone and modified citrus pectin on implanted colon-25 tumor growth in Balb-c mice, Altern. Med. Rev. 2000, 5 (6), 546–52. 207. Zhu HG et al., Enhancement of MHC-unrestricted cytotoxic activity of human CD56+ CD3- natural killer (NK) cells and CD3+ T cells by rhamnogalacturonan: target cell specificity and activity against NK-insensitive targets, J. Cancer Res. Clin. Oncol. 1994, 120 (7), 383–88, 5. 208. Guggenbichler JP, Blockierung der Anlagerung von Keimen an menschlichen Zellen, European Patent 1998, 0 716 605 B1. 209. Stahl B, Boehm G, Antiadhesive Carbohydrates, International Patent 2001, WO 01/60378 A2. 210. Guggenbichler JP, De Bettignies-Dutz A, Meissner P, Schellmoser S, Jurenitsch J, Acidic oligosaccharides from natural source block adherence of Escherichia coli on uroepithelial cells, Pharmaceutical and Pharmacological Letters 1997, 7, 35–38. 211. Kunz M, Munir M, Vogel M, Method for Producing Pectin Hydrolysis Products, International Patent 2000, WO 02/42484 A2.
9 Polydextrose Julian D. Stowell
Contents Introduction.......................................................................................................... 174 Manufacture, Structure, and Specifications..................................................... 175 Manufacture................................................................................................ 175 Structure....................................................................................................... 175 Specification................................................................................................. 177 Polydextrose as Fiber........................................................................................... 177 Regularization of Bowel Function............................................................ 178 Impact on Blood Lipids.............................................................................. 178 Attenuation of Blood Glucose Responses................................................ 179 Polydextrose as a Prebiotic................................................................................. 180 Other Physiological Aspects............................................................................... 183 Oral Health.................................................................................................. 183 Energy Contribution................................................................................... 183 Satiety........................................................................................................... 183 Toleration...................................................................................................... 183 Safety ........................................................................................................... 184 Polydextrose Analysis......................................................................................... 184 Technological Functionality............................................................................... 185 Sweetness and Sweetness Enhancement................................................. 185 Moisture Management............................................................................... 186 Physical Nature of Polydextrose – Glass Transition Temperature (Tg).................................................................................................... 186 Physical Nature of Polydextrose — Its Affinity for Water.................... 188 Stability......................................................................................................... 191 Food Applications................................................................................................ 193 Confectionery Applications...................................................................... 193 Chocolate Confectionery........................................................................... 194 Baked Goods................................................................................................ 194 Frozen Dairy Desserts................................................................................ 194 Cultured Dairy Products........................................................................... 194 173
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Beverages and Dairy Drinks..................................................................... 195 Fruit Spreads and Fruit Fillings................................................................ 195 Meat Applications....................................................................................... 195 Pasta and Noodles...................................................................................... 195 Pharmaceuticals.......................................................................................... 196 Regulatory Status................................................................................................. 196 Conclusions........................................................................................................... 196 Acknowledgments............................................................................................... 196 References............................................................................................................. 197
Introduction Polydextrose was originally developed in the 1970s by scientists at Pfizer seeking a low-calorie bulking agent. The objective was to develop an ingredient that could be used in conjunction with intense sweeteners when replacing fully caloric carbohydrates in processed foods. It is a highly branched low-molecular-weight randomly bonded polysaccharide of glucose having an average degree of polymerization of approximately 12 glucose units. It resists digestion in the upper gastrointestinal tract and is partially fermented in the colon, contributing an energy value of 1 kcal/g. Polydextrose was first used commercially in the early 1980s. It rapidly found favor as a convenient means of reducing calories and fat in a wide variety of processed foods. In the Asia-Pacific region the physiological benefits of polydextrose were recognized early on and the product has been used extensively there to enhance the dietary fiber content of foods since the mid1980s. The scientific research on polydextrose has continued, and a number of physiological benefits are now well documented. These include: • Oral health benefits – polydextrose has been shown to be noncariogenic • Dietary fiber properties • Reducing glycemic impact – polydextrose can be used to replace glycemic carbohydrates to reduce the overall glycemic response to foods and diets • Prebiotic properties Today polydextrose is added to foods for its physiological effects as well as for technological reasons. Earlier work on polydextrose technology and food applications has been reviewed elsewhere [1, 2]. This chapter provides an update on the physiological aspects of polydextrose and other new data will be included as appropriate.
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Manufacture, Structure, and Specifications Manufacture Polydextrose is prepared by the bulk melt polycondensation of glucose and sorbitol in conjunction with small amounts of food-grade acid in vacuo. Further purification steps are then involved to generate a range of products with improved organoleptic properties. Pfizer has patented a partially hydrogenated version of polydextrose, which is suited for high inclusion rates, for sugar-free applications, and where Maillard reactions are not required. The improved family of polydextrose products is currently marketed by Danisco Sweeteners Ltd. under the brand names Litesse® and Litesse®UltraTM. Auerbach et al. [2] have described the comparative properties of the family of polydextrose products. Structure A representative structure of polydextrose is given in Figure 9.1. Craig et al. [3] describe the earlier analytical work that has led to the conclusion that polydextrose is a highly branched glucose polymer containing various types of glycosidic bonds, with -1,6 bonds predominating. The average degree of polymerization of polydextrose is approximately 12 (weight average molecular weight of ~2,000 Daltons, with a range of 162 to ~20,000). Stumm and Baltes [4) also determined that polydextrose is a highly branched material. Recent efforts by Danisco Sweeteners have been aimed at further elucidating the polydextrose structure. Glycosyl linkage analysis was undertaken using the protocol described by York et al. [5]. Samples were prereduced, permethylated, depolymerized, reduced, and acetylated, and the resultant partially methylated alditol acetates (PMAAs) analyzed by gas chromatograCH2OH
CH2OH
O
O OH
O
O
HO
OH CH2OH O OH
HO
OH
CH2 HO O
HO O
O OH
CH2 OH
HO
O O
OH
O OH
CH2OH
CH2
O O
CH2
O
O OH
OH
OH
CH2OH OH
O OH
OH HO
OR OH
R = H, sorbitol or more polydextrose
O OH
O
HO
O
HO CH2OH
OH
HO
CH2
O
O OH OH
Figure 9.1 Representative structure for polydextrose. R = H, sorbitol, sorbitol bridge, or more polydextrose.
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Fiber Ingredients: Food Applications and Health Benefits Branching, Furanoses, Branch/Terminal Ratio and Linkage Positions
45 40 35
Area %
30 25 20 15 10 5
ed
ed 2-
Li
nk
ed 3-
Li
nk
ed 4-
Li
nk
al
nk
in
Li
rm Te
bl
Tr
6-
e b ch r ip anc le h br an So ch rb Fu itol ra s no To se ta s lb ra nc To h p ta oi Br l te nts rm an ch i /te nal rm in al
ed
an
br
le
ou
ng
Si
D
in
an
rm
br
N
on
Te
ch
al
0
Type of Linkage or Branching Figure 9.2 Linkage analysis of polydextrose.
phy-mass spectrometry (GC-MS). Prereduction was carried out on the polydextrose to prevent degradation of the reducing ends by beta-elimination in the presence of base. A solution of polydextrose in D2O was treated with NaBD4 at room temperature overnight. After neutralizing with acetic acid, the borate was removed by repeated dissolution in and evaporation of 9:1 methanol:acetic acid. Borate was converted to the more volatile methyl borate and removed by evaporation. An aliquot of the dried prereduced sample was permethylated by method of Ciukanu and Kerek [6]. This involved treatment with sodium hydroxide and methyl iodide in dry DMSO. Following sample workup, the permethylated material was hydrolyzed using 2 M trifluoroacetic acid (2 hr in sealed tube at 121°C), reduced with NaBD4, and acetylated using acetic anhydride/trifluoroacetic acid. The resulting PMAAs were analyzed on a Hewlett-Packard 5890 GC interfaced to a 5970 MSD (mass selective detector, electron impact ionization mode); separation was performed on a 30 m Supelco 2330 bonded phase fused silica capillary column. The results, shown in Figure 9.2, confirm the highly branched nature of polydextrose and the presence of a complete spectrum of glycosidic linkages. The degree of polymerization (DP) of polydextrose was determined by MALDI-TOF (Matrix-assisted Laser Desorption/Ionization – Time-of-Flight) mass spectrometry. MALDI-TOF was performed with a Hewlett-Packard 2025A mass spectrometer operated in the positive ion mode. The spectrometer was calibrated
177
Polydextrose DP Distribution of Polydextrose by MALDI-TOF Spectroscopy
9.00 8.00 7.00
Peak Height
6.00 5.00 4.00 3.00 2.00 1.00 0.00
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 31 32 33 34 35 36 37 38 39 40 Degree of Polymerization
Figure 9.3 Polydextrose degree of polymerization (DP) distribution.
with a mixture of glucose oligmers (degree of polymerization between 3 and 20). Aqueous solutions of polydextrose were diluted 1:1 with aqueous 50% acetonitrile containing 100 nM 2,5-dihydroxylbenzoic acid and 0.5μl was applied to the sample plate of the mass spectrometer. Samples were desorbed from the plate with a nitrogen laser (λ337nm) having a pulse width of 3ns and delivering approximately 16 μJ of energy per laser pulse. The results given in Figure 9.3 confirm earlier studies that indicated that polydextrose is comprised of components having a complete spectrum of DPs up to DP 30 and above. Specification Polydextrose is manufactured and marketed in accordance with the Food Chemical Codex (FCC) Specification, currently in its fifth edition [7].
Polydextrose as Fiber The absence of a consistent globally accepted fiber definition has allowed confusion to persist regarding what is and what is not considered to be a fiber. Polydextrose is widely accepted as a fiber ingredient in most major countries where the prevailing definition is based on physiological effects or chemical
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composition. Only in those few countries where fiber is still more narrowly defined as intrinsic plant material would polydextrose not be considered a fiber. The main physiological benefits of fibers have been described by the U.S. Institute of Medicine as laxation or regularization of bowel function, normalization of blood lipid concentrations, and attenuation of blood glucose responses [8]. Polydextrose offers some benefits under each of these headings. Regularization of Bowel Function Biomarkers of improved bowel habit and/or health have been described by Cummings et al. [9] in their report on gut health and immunity included in PASSCLAIM (process for the assessment of scientific support for claims on foods). These include increased stool weight, decreased transit time, improved stool consistency as evidenced by ease of defecation, and reduced fecal pH. Five human studies [10–14] and one study in rats [15] have all reported increased fecal weight in conjunction with dietary supplementation with polydextrose. Nakagawa et al. [16] and Tomlin and Read [12] reported stool softening, and Jie et al. [11] reported improved ease of defecation in conjunction with polydextrose supplementation. Two human studies have reported increased stool frequency on consumption of polydextrose [10, 11] while two other studies have shown no effect [12, 16]. A rat study [15] showed reduced transit time in association with polydextrose consumption while two human studies showed no effect [12, 13]. Decreased colonic pH, associated with the increased production of shortchain fatty acids, has been consistently reported in studies in humans [10, 11], rats [17, 18], and in two in vitro studies simulating human colonic digestion [19, 20]. Hence, the ability of polydextrose to favorably affect gut pH is well documented. Impact on Blood Lipids Earlier studies on polydextrose suggest a favorable impact on plasma cholesterol in animals and humans [11, 21–23], although the body of data is equivocal. Saku et al. [21] found in a human study that serum apo A-I, A-II, HDL-C, and HDL2-C were lowered, and HDL3-C was raised. Total cholesterol, triglycerides, and LDL were unchanged. Choe et al. [22] studied rats and found that serum triglycerides and cholesterol were lowered, and HDL was raised. Liu and Tsai [23] studied humans and found that serum total cholesterol and LDL were decreased. HDL was unchanged. Polydextrose may act within the large intestine somewhat like other soluble fibers, such as pectin or cereal beta-glucan. Short-chain fatty acids (acetic, propionic, and butyric) are produced by fermentation of fiber by large bowel bacteria. These acids have a beneficial influence on gut mucosa and some may be absorbed to inhibit liver cholesterol synthesis. Another proposed effect is the incorporation of cholesterol into bacterial biomass, thus reducing reabsorption in the colon.
Polydextrose
179
More recently Pronczuk and Hayes [24] studied the effectiveness of polydextrose in lowering plasma and liver cholesterol in gerbils, a diet-sensitive model for the manipulation of plasma lipids [25, 26]. In one experiment, gerbils were fed purified diets containing 0.15% cholesterol and either 0% or 6% PDX for four weeks. In the second, gerbils received a cholesterol-free diet with 0% or 6% PDX for three weeks, after their endogenous cholesterol pools were expanded by cholesterol supplementation. The gerbil studies demonstrated that 6% PDX (about 30 grams per day human equivalent) significantly lowered plasma and liver cholesterol in both cholesterol-fed gerbils and those with expanded pools of endogenous cholesterol. Based on favorable gerbil results, a pilot study with hyperlipemic humans was also conducted. Volunteers consumed drinks providing either 15 g or 30 g polydextrose per day for four weeks followed by a four-week washout period. In the human study, an intake of 30 g/d polydextrose significantly lowered LDL cholesterol (about 6%) in a subgroup of responders. The combined studies suggest that polydextrose may lower LDL cholesterol as effectively as other soluble fibers when supplemented at 30 g/d human equivalent. Schwab et al. [27] investigated the physiological effects of polydextrose in 44 middle-aged subjects with abnormal glucose metabolism in a placebocontrolled, randomized, and double-blind study. The intervention lasted 12 weeks. The first week involved adaptation with a dose of 8 g/d followed by a dose of 16 g/d. Blood samples were obtained at 0, 4, 8, and 12 weeks. During the polydextrose intervention the concentrations of high-density lipoprotein cholesterol (HDL) increased by 0.07 mmol/l (p < 0.05, 0 wk vs. 12 wk) and those of low-density lipoprotein cholesterol (LDL) decreased. LDL also decreased in the control group. This positive increase in HDL cholesterol is usually difficult to achieve by dietary means. In summary these animal and human data suggest that polydextrose has a moderate beneficial effect on serum and liver cholesterol metabolism not unlike that of other soluble fermentable dietary fibers. It is not possible to be more specific about the magnitude of the effect. Recently Vasankari and Ahotupa [28] found that the ingestion of 12.5 grams of Litesse® polydextrose along with a hamburger meal reduced the total postprandial hypertriglyceridemia by 25%. It has been postulated that the polydextrose passing through the lumen of the intestine interferes with fat uptake in some way. Further investigations are required to confirm the effect and clarify the mechanism. Postprandial effects are becoming acknowledged as independent disease risk factors and this represents a promising new line of research. Attenuation of Blood Glucose Responses Polydextrose itself elicits a negligible glycemic and insulinemic response. Figure 9.4 gives a comparison between polydextrose and glucose. The International Table of Glycemic Index and Glycemic Load Values [29] lists Litesse (Danisco’s branded polydextrose) as follows:
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Fiber Ingredients: Food Applications and Health Benefits Glycemic Load (per serving)
Litesse II
7±2
1
Litesse III Ultra
4±2
0
300
Plasma Insulin conc. (uU/ml)
Plasma glc. conc. (mg%)
591
Glycemic Index (versus glucose)
250 200 150 100
0
1
2
3
4
Time (h) GLC
5
80 60 40 20 0
0
1
2
3
4
5
Time (h) PDX
GLC
PDX
Figure 9.4 A comparison of postprandial plasma glucose and insulin response to either glucose or polydextrose ingestion. The mean response has been calculated from 10 subjects (55).
As a non-digestible carbohydrate it is not strictly appropriate to assign a glycemic index as such to polydextrose. However, the comparison with glucose indicates the potential for polydextrose to reduce the glycemic response of foods when used as a replacement for high or medium glycemic carbohydrates. In addition to this, polydextrose has been shown to attenuate the blood glucose raising potential of glucose itself. Jie et al. [11] reported that 12 grams of polydextrose reduced the glycemic index of glucose from 100 down to 88. Shimomura30 similarly found that the area under the plasma glucose and insulin curves was reduced by 28 ± 12% and 26 ± 10% respectively when glucose was ingested with 14 grams of polydextrose.
Polydextrose as a Prebiotic The concept of prebiotics was first described by Gibson and Roberfroid in 1995 [31]. Prebiotics are non digestible food ingredients that selectively stimulate a limited number of bacteria in the colon, to improve host health.
181
Polydextrose
Since then, the concept has been further developed [32] and in order to qualify for prebiotic classification, a compound is required:
1. To resist gastric acidity, hydrolysis by mammalian enzymes and gastrointestinal absorption
2. To be fermented by the gastrointestinal microflora
3. To stimulate selectively the growth and/or activity of intestinal bacteria associated with health and well-being
Hence, dietary fiber and prebiotics are overlapping but distinct concepts. Recent studies confirm that polydextrose is fermented slowly throughout the colon, mediating a prebiotic effect not only in the proximal colon but in the distal colon where significant risk for disease exists. The unique arrangement of glycosidic linkages of polydextrose makes it resistant to hydrolysis by human digestive enzymes. This has been determined using [14C] labelled polydextrose in rat and human intervention studies [33, 34] and confirmed in the measurement of glycemic effect, reported above. After ingestion polydextrose passes intact into the colon where it is partially fermented by the colonic microflora. The slow and consistent fermentation of polydextrose was first demonstrated using an in vitro colon simulator [19, 20] and subsequently confirmed in a study on pigs (Figure 9.5) [35]. Ishizuka et al. [36], using a rat model, showed that polydextrose considerably reduced the formation of aberrant crypt foci (ACF) in the presence of a carcinogen. The effect was most pronounced in the rectum where the reduction was up to 65%. The authors concluded that ingestion of polydextrose may prevent colorectal carcinogenesis. 80 PDX mg/g Dry Matter
70 60 50 40 30 20 10 0
Distal small intestine
Caeeum
Proximal colon Middle colon
Figure 9.5 Progressive fermentation of polydextrose in the pig colon.
Distal colon
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A study by Hara et al. [37] showed that dietary polydextrose increased calcium absorption and bone mineralization in rats. The effect may partly have been due to colonic acidification, which would be expected to increase calcium solubility. However, the main positive effect was, unexpectedly, seen in the small intestine. Jie et al. [11] conducted a double-blind intervention study involving 120 healthy males. This demonstrated that polydextrose enhanced both Bifidobacteria and Lactobacilli in a dose-dependent manner with the effect being seen with a dose as low as 4 grams per day. Increasing doses of polydextrose resulted in a reduction in fecal pH, indicative of a shift from proteolytic to saccharolytic fermentation. The lower pH serves to inhibit pathogen growth. Fecal butyrate was also enhanced in a dose-dependent manner. This enhancement of butyrate was also seen in the colon simulator studies of Mäkivuokko et al. [20]. With regard to short-chain fatty acid production, Wang and Gibson [38] reported that polydextrose generated a high percentage of propionate and butyrate compared to some other fermented carbohydrates. The molar ratio of acetate to propionate to butyrate was 61:25:14. The bifidogenic effect of polydextrose was confirmed in a recent human intervention study in which polydextrose at 5 grams per day was combined with a probiotic. An almost 100-fold increase in Bifidobacteria was seen from a starting level of 107 [39]. Fermentation of polydextrose has beneficial effects for mucosal functions. Enhanced butyrate production serves as an important energy source, not only for epithelial cells, but also for mucosal immune cells. Polydextrose has been shown to increase production of immunoglobulin A (IgA) in the large intestine of rats, and a synergistic effect was seen with a polydextrose:lactitol combination [40]. Balancing immune responses in the large intestine is especially important for reducing the risk of colon cancer development. A possible mechanism for reduction in cancer development involves the regulation of mucosal gene expression. Overexpression of the cyclooxygenase 2 (cox-2) gene is related to early stages of colon cancer development and chronic inflammatory diseases in the intestine. Mäkivuokko et al. [20] combined two different in vitro systems, namely a four-stage simulator of colonic fermentation and a cell-culture-based model of human intestinal epithelial function, in order to study the effects of polydextrose on colon cancer development. A dose-dependent decreasing effect on cox-2 expression was observed in Caco-2 cells (a human colon cancer cell line). This reduction of cox-2 expression associated with the colonic fermentation of polydextrose further suggests a protective role of polydextrose against colon cancer. This study is a good example of the emerging science of nutrigenomics, the impact of nutrition on gene expression. Efforts are ongoing to further elucidate the role of polydextrose in gut health.
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183
Other Physiological Aspects Oral Health The polydextrose forms Litesse®II and Litesse®UltraTM have passed the plaque pH telemetry test and are recommended for the production of confectionery with “tooth-friendly” properties [40]. Of course products as consumed would need to be tested before such a claim could be substantiated on an individual basis. Energy Contribution A wide range of animal and human studies have been undertaken to determine the energy contribution of polydextrose. These studies have been summarized by Auerbach et al. [2]. Techniques used include isotope label distribution and energy balance. The studies have shown that 45% to 50% of the glucose equivalents of polydextrose are excreted in the feces while 45% to 50% are fermented in the colon. The data support a caloric availability for polydextrose of 1 kcal/g and this value is widely accepted for labelling purposes around the world. An exception to this is Germany where, for products both manufactured and marketed in Germany, an energy value of 2 kcal/g is currently used. This is an anomaly based on early rat studies using questionable methodology. It is hoped that this situation will be resolved when the European Union (EU) updates the Nutrition Labelling Directive. Satiety Polydextrose is not proposed as a magic bullet for satiety. However, foods containing polydextrose have been shown to encourage consumers to eat less calories overall in an ad libitum situation. King et al. [41] studied the independent and combined effect of polydextrose and xylitol on appetite. Xylitol (25 g), xylitol:polydextrose (50:50; 25 g), or polydextrose (25 g) in yogurt ingested at breakfast three hours before lunch suppressed combined calorie intake by between 5% and 8% versus a sucrose control. Polydextrose can facilitate the development of foods that have a lower caloric density. The positive effect of lowering caloric density on satiety has been extensively documented by Rolls and coworkers (see, for example, [42]). Toleration Polydextrose has a relatively high molecular weight compared to other specialty carbohydrates such as polyols. Hence, it has a minimal osmotic effect as it passes through the gastrointestinal tract. In addition, as noted above, polydextrose is fermented slowly throughout the colon. This is in contrast to some other non-digestible carbohydrates that have a regular, linear structure
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and are fermented rapidly in the proximal colon. These factors contribute to polydextrose being well tolerated at typical consumption levels. Flood et al. [43] have reviewed nine clinical studies designed to evaluate the gastrointestinal symptoms mediated by polydextrose in both adults and children. The Joint Food and Agriculture Office of the United Nations (FAO) and World Health Organization (WHO) Expert Committee on Food Additives (JECFA) and the European Commission, Scientific Committee on Food (EC/SCF) evaluated the same data and concluded that polydextrose has a mean laxative threshold of ~90 grams per day (1.3 g/kg body weight) or 50 grams in a single dose [44, 45]. Safety Confirmation of the safety of polydextrose was, of course, a prerequisite for approval of the ingredient for use in foods around the world. Comprehensive studies were undertaken in a range of animal species and these were complemented by human intervention studies with doses of up to 150 grams per day, in other words, far in excess of likely consumption. Based on a review of the data, both JECFA in 1987 [44] and the EC/SCF in 1990 [45] assigned an acceptable daily intake (ADI) “not specified,” meaning that polydextrose can be added to foods at the level needed to achieve the desired functionality. The polydextrose safety data have been reviewed by Burdock and Flamm [46].
Polydextrose Analysis The original AOAC official method for determining total dietary fiber in foods, the enzyme-gravimetric method AOAC 987.29, does not quantify polydextrose. This method includes an 80% ethanol precipitation step that discards polydextrose, which is largely soluble in 80% ethanol. A dedicated method has been developed for the determination of polydextrose in foods, which involves extraction from food matrices, ultrafiltration, enzyme treatment, and subsequent HPLC measurement [47]. A collaborative study confirmed the robustness of this method [48], and it was subsequently published as Method AOAC 2000.11 in the Official Methods book of AOAC International [49]. Fiber measured by AOAC 2000.11 can be added to that determined by AOAC 987.29 to give the total fiber content of foods. The method has been listed as an approved method for determining dietary fiber in the CODEX consultation document of January 2007 (CL 2007/3-NFSDU).
185
Polydextrose 1.2 1 0.8 0.6 0.4 0.2 in ul In
Xy lit ol M al tit ol Er yt hr ito l So rb ito l M an ni to l Is om al t La ct ito Po l ly de xt ro se
Su
cr os
e
0
Figure 9.6 The relative sweetness values of some commonly used carbohydrates (sucrose = 1).
Technological Functionality Polydextrose has been developed to meet a wide range of application needs, and the technological functionality of polydextrose in food systems has been well documented [1, 2]. Polydextrose is used in many food applications, from beverages through to confectionery products, for both its physiological and technological benefits. Some of the more recent technological information is presented here. Sweetness and Sweetness Enhancement Although polydextrose possesses many of the functional properties of carbohydrates such as sugar, glucose syrups, and maltodextrin, essentially it is not sweet (Figure 9.6). However, polydextrose can be used to balance and reduce the sweetness level of food products and is also suitable for savory applications or in products that require bulk, with a less sweet profile. When used in combination with sugars and polyols, polydextrose has a sweetness-enhancing effect and very often an appropriate level of sweetness can be achieved without the need for high potency sweeteners. For example, in flavored milk drinks with 4% w/v fructose or sucrose, a sweetness enhancement is observed with increasing levels of polydextrose addition, as seen in Figure 9.7. This sweetness-enhancing effect is also experienced in confectionery and bakery applications. This effect is not unique to polydextrose and is also seen with mixtures of sugars and starches [55–57]. An explanation based on increased viscosity of carbohydrate solutions in the mouth was investigated and found not to be the cause of this effect [58].
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Fiber Ingredients: Food Applications and Health Benefits
Increase in Sweetness “score” Compared to Control
18 16 14 12
3% w/v Polydextrose
10
6% w/v Polydextrose
8 6 4 2 0
4% w/v Sucrose
4% w/v Fructose
Figure 9.7 Sweetness enhancement of 4% w/v fructose and sucrose sweetened, flavored milks at 3% and 6% w/v addition of polydextrose.
Moisture Management Moisture management is one of the most important properties in the development of food products as it influences texture, flavor, shelf life, consumer acceptability, and food safety. Polydextrose can act both as an humectant and as a crisping agent in foods. This may seem contradictory, but this multifunctional aspect of polydextrose has been demonstrated in many practical applications. The functionality of polydextrose is strongly influenced by the amount of water in the food system and the subsequent effect on the glass transition temperature of the composite food. In order to understand this more fully it is important to understand the chemical and physical nature of polydextrose in certain foods. Physical Nature of Polydextrose — Glass Transition Temperature (Tg) Polydextrose powder is an amorphous glass with an anhydrous glass transition temperature of 110ºC. This is significantly greater than that of most other carbohydrates and is partly a function of molecular weight. Heating above the glass transition temperature (Tg) leads to a flowable melt which after cooling produces a clear glass with a brittle texture. The high Tg of polydextrose can be helpful in raising the composite Tg of a food. Polydextrose can also protect the structure of frozen and thawed materials. Products stored in a freezer can undergo deleterious changes in texture (e.g., ice- and solute-crystallization, starch retrogradation), structure (e.g., collapse and shrinkage), and chemical composition (e.g., oxidation flavor/ color degradation). Polydextrose may do this by interrupting sugar or polyol re-crystallization and/or starch retrogradation, by providing structure and/
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Polydextrose 125 100 75
Tg (°C)
50 25 0
0
5
10
15
20
25
30
35
–25 –50 –75
Water Content % wb
Figure 9.8 Glass transition temperature (Tg) of polydextrose versus moisture content.
or raising the composite Tg which is the glass transition temperature of a maximally freeze concentrated solution [50]. The Tg values (where ice can no longer form) of lactose (–28ºC), sucrose (–32ºC), fructose (–42ºC), glucose (–43ºC), and sorbitol (–43.5ºC) are all lower than polydextrose (–24ºC) [51]. This means that replacement of these sugars with polydextrose raises the composite Tg of a food. Freezer storage stability improves when the difference between Tg and storage temperature (typically –18ºC for a home freezer) is minimized. The concepts of water as a plasticizer of foods and how this affects the stability of foods were introduced in the 1980s. When water increases the free volume around large food polymers such as polydextrose, the molecules are given room to move more freely. The flexibility and mobility of molecules is influenced by the proportions of plasticizer (water) molecules in the system. Water, via this action, can influence whether a food polymer is in a glassy or rubbery state through its effect on glass transition temperature. The relationship between Tg and moisture content for polydextrose is shown in Figure 9.8. In a glass-like state polydextrose is so viscous that it cannot flow under its own weight and the water molecules, for all practical purposes, are immobile and stable as in hard candy or in low moisture systems such as pastry and some biscuits. Increasing the amount of water present in a system will decrease the glass transition temperature, and a food is more likely to return to a “rubbery” state as in higher moisture applications such as some cookies and cakes. Both water activity and glass transition concepts can contribute to a better understanding of water management in foods [60].
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1,0
Water Activity
0,8 0,6 Sucrose
0,4
Polydextrose
0,2 0,0
0
20
40 60 Concentration w/w%
80
100
Figure 9.9 Water activity (Aw) at various concentrations of sucrose and polydextrose.
Sorption Desorption
Water Content % wb
40
30
20
10
0
0
20
40
RH %
60
80
100
Figure 9.10 Sorption-desorption isotherm for polydextrose.
Physical Nature of Polydextrose — Its Affinity for Water Figure 9.9 shows the water activity of polydextrose relative to sucrose. At higher concentrations polydextrose is more effective at reducing Aw. This is because sucrose crystallizes at high concentrations and these crystals do not interact with the water to lower Aw. Polydextrose can function as an humectant in foods to slow undesirable changes in moisture content as is shown in the sorption-desorption isotherm in Figure 9.10. This figure shows the moisture stability of polydextrose at various relative humidities. On desorption to 0% humidity polydextrose still contains 10% w/w moisture. This indicates that polydextrose is able to retain
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The control sample shows that more protein was dispersed to form a network linking the starch. The protein structure forms a continuous network around the starch grains. Figure 9.11 Light microscopy control sample.
moisture and thus positively affects texture and shelf life in a range of applications, including confectionery, baked goods, and reformed meat products [61, 62]. The use of polydextrose in shortcrust pastry is a practical example of the unique water management properties of this polymer. Polydextrose is known to improve the texture and appearance of reducedfat/reduced-sugar shortcrust pastry. How this is achieved is not fully understood. However, polydextrose may interact with the protein, starch, or fat in the pastry and/or may preferentially absorb water, reducing the hydration of the flour. Light and electron microscopy methods have been used to examine the structure of raw and cooked samples of reduced-fat pastry containing polydextrose compared with a control sample [59]. Light microscopy: Pieces of the pastry were fixed and prepared in an aqueous protein cross-linking fixative, dehydrated, and embedded in resin. In this case the fat and the water are removed and probably the polydextrose also. The 2–4 µm sections were cut and stained with light green to show the protein and diluted iodine to stain the starch. The control sample as shown in Figure 9.11 indicates that more protein was dispersed to form a network linking the starch. The protein structure forms a continuous network. In Figure 9.12 the effects of the addition of just 2.5% (dough weight basis) can be demonstrated. Polydextrose seems to inhibit the dispersion of the protein. Starch grains can be seen embedded in a less continuous protein matrix, resulting in a coarser, less homogenous structure than the control. Cold-stage Scanning Electron Microscopy (CryoSEM): This method involves freezing small pieces of the pastry rapidly in a liquid nitrogen flush and examining in an electron microscope while at a –185ºC. The samples are intact, meaning that all the fat, water, protein, and starch is present. In a gluten/flour model system, samples were etched to sublimate some of the
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The effects of the addition of polydextrose to the pastry were seen as low as 2.5% level (dough weight basis), but were most marked at the 10% level. The polydextrose inhibits the dispersion of the protein. Starch grains can be seen embedded in a less continuous protein matrix, resulting in a coarser, less homogenous structure than the control. Figure 9.12 Light microscopy – polydextrose sample (2.5% dough weight).
Figure 9.13 CryoSEM – control – gluten/flour model.
water away, which leaves a lacy network structure where less bound water is present. As illustrated in Figures 9.13 and 9.14, the addition of polydextrose to the flour/gluten model resulted in a more icy matrix than the control, indicating less hydration of the gluten. In traditional and organoleptically acceptable shortcrust pastry, the fat in the recipe acts as a shortening agent, interrupting and preventing the continuous development of gluten structure producing a “short” texture. When polydextrose is used in reduced-fat pastry, it hydrates, and this rapid absorption of water reduces the amount of water available for gluten development, producing the same “short” texture as the full fat product. On baking and
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Figure 9.14 CryoSEM – polydextrose sample (more icy matrix, less hydration of the gluten).
TGA Vigo 011-30
100
Weight %
80 60 40 20 0
20
60
100
140
180
220 260 300 Temperature (°C)
340
380
420
460
Figure 9.15 Heat stability of 70% w/w polydextrose solution.
cooling, polydextrose forms a stable glass structure that provides a short, crisp texture. Stability Polydextrose is very stable in solution. In Figure 9.15 the change in weight of a 70% w/w polydextrose solution over a temperature range of 20ºC to 460ºC has been measured and it can be seen that over the temperature range 20ºC to 160ºC moisture is lost from the solution as would be expected and it is not until 260ºC that gross changes begin to take place. Similar behavior can be seen when the polydextrose powder is heated over the same temperature range (see Figure 9.16). Polydextrose remains stable until
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100
Weight %
80 60 40 20 0
20
60
100
140
180
220 260 300 Temperature (°C)
340
380
420
460
Figure 9.16 Heat stability of polydextrose powder.
Table 9.1 Percentage Increase in Free Monomers in a 5% w/v Solution after Incubation at pH 2.6, 100ºC for 5 Hours % Increase in Free Monomers Polydextrose (Litesse Two) Polydextrose (Litesse® Ultra) Fructo-oligosaccharide (Av DP 10) ®
Time in Hours 0
1
5
0.02
0.02
2.28
0.08
0.3
2.38
0.2
45.42
100
approximately 300ºC when it begins to melt and decompose. These temperature conditions far exceed those that are found in normal food processes. The predominant α-1,6 glycosidic linkages in polydextrose are more than two to four times as resistant to hydrolysis than α-1,2, α-1,3, or α-1,4 bonds. Table 9.1 indicates how bonding type and molecular shape can affect the acidic hydrolysis rate of carbohydrate polymers. Polydextrose is very stable at low pH and high temperature compared to linear and regular polymers such as fructo-oligosaccharides. Model systems containing polydextrose have indicated very good stability against hydrolysis over a broad range of pH and temperature making it ideal for use in many beverage applications, even those at lower pH. No significant
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hydrolysis would be expected at any storage temperature when the pH is higher than 4.0 [63]. Commercial experience with polydextrose in beverages over the last 10 years has indicated the ease of formulation and stability in use of high levels of fiber in this application. In summary, polydextrose is a low-calorie specialty carbohydrate that has a variety of useful properties including high water solubility, high glass transition temperature, and good stability at elevated temperatures and over a broad range of pH. These technological properties allow its use in a wide variety of foods including baked goods, beverages, confections, and frozen dairy desserts. Polydextrose is a functional ingredient that can play a variety of roles in food formulations. Identifying and understanding these important contributions is the first step to developing new and improved foods with polydextrose.
Food Applications Polydextrose allows the development of food products with a wide variety of nutritional improvements such as prebiotic, fiber fortification, calorie reduction, reduced glycemic load as well as sugar and fat reduction. The technological properties of polydextrose facilitate the production of products with a taste and texture profile similar to that of standard products. Confectionery Applications The combination of high water solubility and high solution viscosity of polydextrose facilitates the processing of sugar-free and reduced-sugar candy of excellent eating quality. Polydextrose is a great choice for calorie and sugar reduction in hard and chewy candies and caramels as well as pectin and gelatine jellies. As noted above, polydextrose is amorphous and does not crystallize at low temperatures or high concentrations so it can be used to control the crystallization of polyols and sugars and therefore the structure and texture of the final product. This is analogous to conventional sugar confectionery production where glucose syrups are used to prevent or control sucrose crystallization. Selection of the appropriate polydextrose form offers greater flexibility in terms of color and taste depending on the extent of Maillard reaction desired. Its non-cariogenic properties can be useful in tooth friendly confectionery. Polydextrose has a positive heat of solution (no mouth cooling effect), which allows versatility in delicately flavored confectionery [65].
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Chocolate Confectionery The development of chocolate and composite chocolate products with reduced calories, sugar, and fiber enrichment is possible with polydextrose. Polydextrose functions to replace sucrose and provide a warm, creamy texture in the chocolate matrix without contributing a mouth cooling effect or scratchy aftertaste. Polydextrose completes the chocolate flavor through the formation of small amounts of caramel during processing. Its low residual acidity ensures that the delicate cocoa and sweet flavors are brought forward and maintained [65]. Baked Goods Polydextrose replaces sugars and some of the fat in baked goods applications. Its humectant properties and water activity (similar to sucrose) allow shelf life to be maintained or improved. Polydextrose is used as a bulking agent to control the sweetness of many baked items. Since it is not significantly sweet itself it may also be used in savory applications such as pastry and bread. The addition of polydextrose to pastry at low levels decreases gluten formation and increases the crispness of short pastry doughs, improving the machineability of very thin sheets of dough and reducing pastry shrinkage [66]. Polydextrose is also useful as a non-sweet binder in cereal bars to build solids without adding sweetness. Frozen Dairy Desserts Polydextrose replaces the bulk, creaminess, smoothness, and mouthfeel of sugar and fat, enabling the formulation of high-quality, lower-calorie and reduced-fat products [67]. It has greater viscosity in solution than sucrose or sorbitol at equivalent concentrations and its role in freezing-point depression helps in achieving creamy, palatable frozen desserts. Cultured Dairy Products Polydextrose in yogurt improves the creaminess, mouthfeel, taste, and flavor of yogurt white base, when used at low levels (3% w/w) and has been shown to contribute greatly at low use levels to the formation of soft white cheeses. Its key benefits in low-fat and non-fat systems are the prevention of syneresis, the ability to provide viscosity without gumminess, and improved creamy mouthfeel [68]. Fruit preparations with polydextrose improve creaminess and mouthfeel in fruit yogurt.
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Beverages and Dairy Drinks Polydextrose is used in dairy drinks; neutral or flavored, or low pH, pasteurized, or UHT and in many other clear beverage formats. Polydextrose will improve the mouthfeel, giving the taste experience of a product of a much higher fat content; this is particularly noticeable in low-fat dairy drink applications [69]. Polydextrose is also added to beverages as a source of dietary fiber as it is very soluble, forming clear solutions, and is very stable over shelf life. Fruit Spreads and Fruit Fillings Polydextrose is used in fruit spreads and fruit fillings to replace all or part of the sugars and to build solids. Its high water solubility and high viscosity are ideal to reduce sugar content and the calorie value. Polydextrose helps prevent migration of moisture from fruit fillings into dough and pastry, increasing the shelf life in a combination product [70]. Meat Applications Polydextrose can be used in meat products such as chicken nuggets to bind moisture in the meat patty. Moisture loss is reduced during cooking as well as moisture migration to the batter and breadcrumb coating. This has the effect of keeping the chicken nugget moist and juicy while the crispiness of the coating is improved and stays crispier for longer after cooking [71]. In surimi and reformed meat products polydextrose may be used as a cryoprotectant to modify the Tg (glass transition) of the frozen matrix without contributing sweetness. This leads to the development of frozen fish and meat products with improved flavor and texture. In burgers, meat patties, and homogenized sausage applications polydextrose is able to replace some of the fat without compromising mouthfeel and flavor to make reduced-fat and -calorie products. Pasta and Noodles Fiber enhancement of noodle and pasta products is possible with polydextrose as well as some process improvement benefits to the mechanical properties of the dough. The addition of polydextrose to the dough improves firmness that can aid forming of noodle or spaghetti strands or pasta shapes. The texture of the cooked product is not significantly altered by the addition of polydextrose and 95% of the added polydextrose remains in the pasta or noodles after cooking [72].
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Pharmaceuticals Its primary use in pharmaceuticals is as a solid dosage form. In tableting, polydextrose solutions can be used as binders in wet granulation processes and may also be used in conjunction with other materials as a film and tablet coating agent. Polydextrose is used in the manufacture of directly compressible tableting excipients [73]. It also acts as a bulking agent in the formulation of sugar-free confectionery type dosage forms. In conjunction with isomalt, lactitol, or maltitol, it can be used in the manufacture of sugar-free hard candies and gum arabic lozenges or pastilles.
Regulatory Status Polydextrose is widely approved for use in foods around the world. It was first approved in the USA in 1982 as a food additive for several food applications under 21 CFR 172.841. It is approved in the European Union (EU) under the auspices of the Miscellaneous Additives Directive (MAD) as a bulking agent for use at quantum satis, in all foods except where specifically precluded by standards of identity. In Japan the Ministry of Health and Welfare (MOHW) recognizes polydextrose as a food. Polydextrose is recognized as a fiber in a growing number of countries although, as noted above, the absence of a formally adopted fiber definition makes this a complicated subject. It is important to check local labeling regulations before including polydextrose in new food products.
Conclusions Polydextrose is a versatile food ingredient that can be used to improve the nutritional profile of a wide variety of processed foods. The consumption of foods based on polydextrose can help consumers to increase their fiber intake to levels recommended by health professionals [54], while at the same time helping them to reduce caloric intake and reducing the overall glycemic impact of the diet. Polydextrose has much to offer the emerging science of prebiotics and investigations are ongoing.
Acknowledgments The data summarized in this chapter represent a team effort sustained over a period of many years. The baton has been handed from Pfizer to Cultor to
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Danisco but many of the scientists have been involved right from the early days. I would particularly like to acknowledge the efforts of Mike Auerbach, Stuart Craig, Ken Knoblock, Chris Krüger, Harri Mäkivuokko, Helen Mitchell, Chuck Nichols, Geoff O’Sullivan, Nina Rautonen, and Kirsti Tiihonen among others. We also gratefully acknowledge the contribution of the many universities and research institutes with whom we have collaborated.
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66. Umesh K, Amarjeet K, Padda GS and Kamaljit K (2006) Studies on development of low calorie baked products using polydextrose as fat replacers. Advances in Food Sciences 28(1): 7–3 67. Kappas J (1998) Polydextrose, fat replacers and functional ingredients in frozen dairy applications. in: Ice cream: proceedings of an international symposium, Athens, September 1997, pp 75–82 Publisher: IDF 68. Honer C and Ruland S (1995) Weighing in. Dairy Field 178(1): 42–47 69. Anon (1991) Polydextrose — Applications of bulk sweeteners. Food Marketing and Technology 5(6): 19–20 70. Anon (1981) New bulking agent for reduced-calorie foods. Manufacturing Confectioner 61(7): 217 71. Satsuba H and Okuma K (1995) Matsutani Chem Ind Ltd. Production of sausages. Japanese Patent Application, Patent number: 7-132067. Publication date: 23.5.95, 19950523; Application filing date: JP, 10.11.93, 19931110. 72. Matsuda I, KatsutaY, Shimada K and Kiyoshima T (2006) Water-soluble dietary fiber-containing composition and method for preparing same. Patent Assignee: Matsutani Kagaku Kogyo KK, Patent Number: JP 2006254901 A, Japanese Patent Application 73. Woznicki E and Grillo SM (1987) Coatings based on polydextrose for aqueous film coating of pharmaceutical, food and confectionery products. Patent Assignee: Colorcon Inc. Patent Number: WO 8707902 A1, PCT International Patent Application
Section II
Resistant Starch
10 Resistant Starch E. Terry Finocchiaro, Anne Birkett, and Monika Okoniewska
Contents Introduction.......................................................................................................... 206 Background to Natural RS: Starch and RS Chemistry.......................... 206 Classification................................................................................................ 206 Resistant Starch 1 (RS1).................................................................. 207 Resistant Starch 2 (RS2).................................................................. 208 Resistant Starch 3 (RS3).................................................................. 208 Resistant Starch 4 (RS4).................................................................. 208 RS in Food and the Diet............................................................................. 208 Commercially Available Natural RS, A Chronological Perspective... 209 Commercially Available Non-Traditional RS: Soluble Dextrins, Chemically Modified Starch......................................................... 210 Analysis of RS: AOAC and Non-AOAC Methodologies................................. 216 Food Applications: Key Functional Properties in Low- and HighMoisture Systems........................................................................................ 224 Overview of Health Benefits.............................................................................. 226 Introduction................................................................................................. 226 Digestive Health.......................................................................................... 227 Fermentation.................................................................................... 227 Prebiotic............................................................................................ 230 Colonic Cell Health......................................................................... 231 Intestinal Function.......................................................................... 231 Nutrient Interactions...................................................................... 232 Glycemic Management............................................................................... 232 Weight Management.................................................................................. 237 Available Calories........................................................................... 237 Satiety Hormone Production......................................................... 238 Body Composition.......................................................................... 238 Energy Partitioning........................................................................ 238 Conclusion............................................................................................................. 239 Acknowledgments............................................................................................... 240 References............................................................................................................. 240 205
206
Fiber Ingredients: Food Applications and Health Benefits
Introduction Background to Natural RS: Starch and RS Chemistry Starch is a glucose polymer, with the glucose units arranged either in a straight chain called amylose or in a highly branched chain called amylopectin. Starch is largely a digestible polymer; however, some starch, called resistant starch (RS), is able to resist digestion in the small intestine and pass to the large intestine, where it can act as a fiber in the body. A variety of factors can influence the digestion (and resistance to digestion) of native starches, including the precise granular structure, the ratio of amylose to amylopectin, and the starch source. Amylopectin is easily attacked by amylases and tends to be less resistant to digestion than straight-chain amylose. Amylopectin generally has a lower melting point (vs. straight-chain amylose), which also contributes to its lack of resistance in heat-processed foods. High amylose corn starch is one of the more resistant native starches and a logical source when selecting a base material for manufacturing high-RS ingredients. High amylose corn starch is more resistant to amylase digestion than dent corn starch, which contains approximately 25% amylose, or waxy corn starch, which contains less than 1% amylose. Further, native high amylose corn starch has a more resistant crystalline pattern (known as the B configuration) when compared to other starches such as wheat (Haralampu 2000; Annison and Topping 1994; Sajilata et al. 2006). Thermal treatment of starch represents a key processing variable in the manufacturing of highly resistant starches. Typically, heating starch in the presence of excess water disrupts the inherent crystalline structure. The granules swell to the point of disruption of the native crystal structure, a process known as gelatinization. Thus gelatinization is a function of temperature, moisture, and time, and occurs when certain conditions are met. As the gelatinized starches cool, re-crystallization into a resistant B pattern occurs, forcing water out from between the starch chains. This process is known as retrogradation (Haralampu 2000; Annison and Topping 1994; Sajilata et al. 2006). High amylose corn starch does not readily gelatinize at normal cooking temperatures (Annison and Topping 1994). Upon gelatinization at more extreme conditions the starch will readily retrograde to a resistant form called the V pattern, and RS can be further enhanced with repeated heating and cooling (Annison and Topping 1994). Classification Scientists typically refer to four classes of resistant starch, which are defined based on their reason for resistance (Brown et al. 1995; Sajilata et al. 2006) (Table 10.1). RS1, RS2, and RS3 are either found in nature or can be produced
207
Resistant Starch (RS) Table 10.1 Classes of RS (Brown et al. 1995; Sajilata et al. 2006) RS Starch Type
Characteristic
Properties
Foods
RS1
Trapped in food matrix
Whole or partially milled grain, sweet corn, parboiled rice, legumes
Affected by milling, pureeing, chewing, and gelatinization
RS2
Granular, with highly crystalline regions Retrograded amylose and amylopectin
Not completely swollen, gelatinized, or dispersed. Matrix is not easily penetrated by digestive enzymes. May or may not test as dietary fiber Granular. May or may not test as dietary fiber
Raw potato, green banana, high amylose corn Cooked and cooled starches in potatoes, rice, tortillas, bread crumbs
RS content reduced if starch is gelatinized Increased with certain processing techniques. Occurs more readily at 32°F–40°F More evidence of physiological effects is required
RS3
RS4
Chemically modified starches
Non-granular. May or may not test as dietary fiber
May or may not test as dietary fiber. Could be soluble or insoluble
Does not occur in nature or in naturally occurring foods
Other
during normal food processing/handling, so have been considered “natural” for the purpose of this review. High amylose corn starch is an example of a natural RS. RS4 refers to chemically modified starch (i.e., starch that is chemically converted with existing techniques). Resistant dextrins are starchbased soluble ingredients produced by acid and heat treatment (Ohkuma et al. 1994; Fouache et al. 2003). This induces chemical rearrangement(s), so resistant dextrins have also been classified by some as RS4. Together, RS4 and resistant dextrins comprise the class of “non-traditional” RS, and serve as alternate commercial approaches to natural RS. The four types of RS are defined as follows (Sajilata et al. 2006). Resistant Starch 1 (RS1) This type of RS is trapped by the food matrix (such as whole kernels and whole grain), which can physically block enzymes from reaching the starch (Tovar 1996). Mastication, milling, grinding, and other food-processing treatments that reduce particle size will generally reduce the amount of RS1 in a food.
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Fiber Ingredients: Food Applications and Health Benefits
Resistant Starch 2 (RS2) This type of RS occurs in raw starch granules partly due to crystalline starch structures and partly due to the nature of the granule. Loss of crystallinity by gelatinization will decrease the amount of RS2 in a food. High amylose corn starch does not fully gelatinize at temperatures reached in conventional cooking (154ºC to 171°C); hence it is an ideal source for process-tolerant natural RS (Annison and Topping 1994). Resistant Starch 3 (RS3) This is non-granular crystalline starch that occurs naturally when cooked (gelatinized) starches cool and crystallize (retrograde). Cooling profiles can significantly impact the crystalline pattern of the retrograded starch, and RS3 formation is enhanced with successive heating and cooling. Consequently, commercial RS3 ingredients are generally based on this process, sometimes in combination with amylase treatment to increase starch crystallinity and further enhance RS yields (Iyengar et al. 1991; Chiu et al. 1994; Henley and Chiu 1995). RS3 forms in processed foods (e.g., in baked goods), particularly in the crumb of breads that have been subsequently refrigerated, and in cooked and cooled tortillas, rice, and potatoes (Kulp and Ponte 1981; Agama-Acevedo et al. 2004; Shamai et al. 2004). Resistant Starch 4 (RS4) RS4 is produced using standard chemical modification techniques such as cross-linking, substitution, or a combination of various chemistries (Seib and Woo 1999; Wolf et al. 1999). Pyrodextrinization can also produce RS4 (Ohkuma et al. 1994; Fouache et al. 2003). When compared to the more traditional (natural) classes of RS, these materials may differ significantly with respect to physiochemical properties and physiological impact (Wolf et al. 1999; Annison et al. 2003; Brown 2004). RS4 represents a broad group: Some materials measure as dietary fiber using total dietary fiber methodology while others do not (Proksy et al. 1985; Prosky et al. 1994), and others are analyzed using RS-specific methodology (McCleary and Monaghan 2002; McCleary et al. 2002). RS4s can also vary considerably in solubility. Limited nutritional studies on the physiological effects of RS4s are available for review, so clearly more research is needed to determine their physiological impact and potential benefits. RS in Food and the Diet Diets high in relatively unprocessed foods contain high quantities of RS. For example, intact whole grain foods and legumes are naturally high in RS. However these foods typically do not maintain high levels of RS after food processing, so some food manufacturers choose to augment their products
Resistant Starch (RS)
209
with commercially prepared, relatively stable forms of RS. Typically, less than 10% of dietary starch is resistant to digestion in foods not supplemented with commercial RS ingredients; however, studies have shown that much higher quantities of RS can be tolerated without experiencing undesirable digestive side effects commonly associated with more traditional types of fibers (Kendall et al. 2003). The RS content of food is not always easy to predict because RS is defined by its physiological nature. That is, RS is defined as “the sum of starch and products of starch degradation not absorbed in the small intestine of healthy individuals” (Asp 1992). Total RS content could be influenced by numerous factors including starch characteristics (described previously), food processing, the amount of starch consumed, other dietary components, and physiological factors such as the amount of mastication and gut transit time (Haralampu et al. 2000). Many processed foods, unless fortified with commercial (more stable) RS ingredients, will tend to have lower amounts of RS than the native unprocessed counterparts. Cooking, soaking, and milling tends to disrupt the physical or botanical structure of the plant thereby decreasing the amount of RS (Bednar et al. 2001; Henningsson et al. 2001; Siddhuraju and Becker 2001). For example, native whole grain wheat contains 14% RS, while milled wheat flour contains only 2% RS (Bednar et al. 2001). The same trend is true of other starch sources. Certain processing techniques can increase RS through retrogradation and re-crystallization. This can be enhanced by controlling environmental factors such as water content, pH, thermal input, temperature cycling (heating and cooling), freezing, and drying. Cooking and cooling (which promotes gelatinization and retrogradation) causes the formation of RS3 in potatoes and other foods (Liljeberg - Elmstahl 2002). Extrusion, utilized to make commercial snacks and cereals, also causes retrogradation, and can increase RS content. Commercially Available Natural RS: A Chronological Perspective Commercially manufactured RS3 ingredients, considered to be the first generation of RS ingredients, have been available since the early to mid-1990s with the 1993 commercialization of NOVELOSE® starch by National Starch Chemical Co. (Chiu et al. 1994; Henley and Chiu 1995), and the 1994 commercialization of Crystalean® by Opta Food Ingredients (Iyengar et al. 1991). Both ingredients are prepared from high amylose corn starch, with approximately 30% dietary fiber (dry basis), and retain their resistance through most common cooking processes. RS3 ingredient manufacture typically involves completely cooking out the starch granule, with successive heating and cooling steps and optional amylase treatment to enhance the crystallization of amylose (Iyengar et al. 1991; Chiu et al. 1994; Henley and Chiu 1995). Some RS3s test as dietary fiber according to official methods, and can be labeled as dietary fiber in certain countries where regulatory definitions and local
210
Fiber Ingredients: Food Applications and Health Benefits
official methods allow. These ingredients have been used by food companies worldwide to formulate healthier foods such as cereals and beverages. Although these first-generation commercial RS3 ingredients were considered novel at their time of release, a relatively large particle size and low RS yield tended to limit widespread usage in foods, particularly in bakery and high-moisture foods. Second-generation RS2 ingredients were commercially introduced in the mid to late 1990s, with higher RS contents and smaller particle size, and were more successful, particularly in bakery products. High fiber/relatively process tolerant RS2 ingredients are natural granular starches manufactured using a simple heat/moisture treatment (Shi 2003; Shi and Trzasko 1997). For example, Hi-maize® 260 starch from high-amylose cornstarch is produced without chemical or enzyme treatment and contains a minimum of 60% dietary fiber. Hi-maize® 260 starch largely retains its RS through moderate processing, including typical baking conditions, while maintaining very good organoleptic and processing qualities. Hi-maize® starch has been used in foods since 1994 when it was added to a white bread in Australia, doubling the dietary fiber content of the bread from 2.9% to 5.6% (Brown et al. 1995). This starch has since been added to many different foods including baked goods, breakfast cereals, nutrition bars, and pasta, and has been successfully marketed as a functional dietary fiber for digestive health and glycemic management benefits. Hi-maize® flours and meals are prepared from high-amylose corn grain and represent a relatively new and promising class of natural functional nutritional ingredients that are particularly suited for low-moisture products such as batters and breadings. They were launched by National Starch and Chemical Co. in 2006, and provide the nutritional benefits of RS with the labeling and process capabilities of conventional flours and meals. Manufacturing is a relatively simple process, whereby high-amylose corn is dry milled into flours or meals, then further processed with a proprietary treatment. Physical characteristics of RS starch, flour, and meal ingredients are compared in Table 10.2. Commercially available sources and forms of traditional RS ingredients are summarized in Table 10.3. Note that not all RS ingredients are created equal. The selection of a natural RS depends on a variety of factors that include fiber content, physiochemical properties, compatibility with the food product (formulation and process), and most importantly validated claims that refer to specific health benefits. Commercially Available Non-Traditional RS: Soluble Dextrins, Chemically Modified Starch Chemically modified RS4 ingredients were first introduced into the market in 2003, followed by numerous subsequent introductions. Generally, granular starches are modified by known chemistries; however, recent patent publications have illustrated that pre-gelled starches can also be chemically modified to produce RS4 ingredients (Woo et al. 2006).
High amylose corn, tapioca
RS3
d
c
b
Varies
30–40
200–600a
100–300c
5–25
Particle Size (μm)
Varies
0.8
3
5
0.8
Fat Content (weight percent)d
Varies
0.8
9
9
0.8
Protein Content (weight percent)d
By source
Maltodextrin
Yellow corn meal
Corn starch or resistant corn starch Yellow corn flour
Label Declaration
National Starch & Chemical Co. National Starch & Chemical Co. National Starch & Chemical Co. National Starch & Chemical Co. Multiple
Key Suppliers
Per the standard of identity for yellow corn meal: not less than 95% passes through a No. 12 sieve, not less than 45% through a No. 25 sieve, but not more than 35% through a No. 72 grits gauze. Although RS3 is naturally occurring, National Starch does not promote NOVELOSE® 330 starch as natural. Per the standard of identity for yellow corn flour: not less than 98% passes through a No. 50 sieve and not less than 50% passes through No. 70 woven-wire cloth. Typical values for specific National Starch products listed above, information is not necessarily applicable to the entire category.
Varies
High amylose corn
RS1 & RS2
RS1 & RS2
High amylose corn
RS1 & RS2
Flours (Hi-maize® corn flour) Meals (Hi-maize® corn meal) Maltodextrinb (NOVELOSE® 330 starch) Whole grains
a
High amylose corn
Source
RS1 & RS2
RS Classification
Starch (Hi-maize® 260)
Commercial Form (product example)
Physical Comparisons of Commercial Natural RS
Table 10.2
Resistant Starch (RS) 211
Hi-maize® Meal 130
Hi-maize® Flour 150
RS1 (high amylose corn grain)
RS1 & RS2 (high amylose corn grain)
Commercial Name
Hi-maize® Flour 120
RS1 (high amylose corn grain)
Classification (grain source) Supplier
National Starch & Chem. Co., Bridgewater, NJ
National Starch & Chem. Co., Bridgewater, NJ
National Starch & Chem. Co., Bridgewater, NJ
59
75
59
RSa (% db)
50 c
39 c
27 c
TDFb (% db)
Commercial Sources and Forms of Traditional (Natural) RS1, RS2, and RS3
Table 10.3
Top Benefits High fiber content Increased bowl life in ready-to-eat (RTE) cereals Superior adhesion in breaded food “Natural” ingredient declaration Exhibits good process tolerance High fiber content Increased bowl life of RTE cereals Superior adhesion in breaded foods Crisp texture “Natural” ingredient declaration Good process tolerance High fiber content Increased bowl life of RTE cereals Superior adhesion in breaded foods Crisp texture “Natural” ingredient declaration Good process tolerance
Key Applications
Baked & fried snacks, battered & breaded foods, cereals, specialty bakery goods (English muffins, corn tortillas, and waffles, handheld bakery goods, and pizza crust)
Baked & fried snacks, battered & breaded foods, cereals, specialty bakery goods (English muffins, corn tortillas, and waffles, handheld bakery goods, and pizza crust) Baked & fried snacks, battered & breaded foods, cereals, specialty bakery goods (English muffins, corn tortillas, and waffles, handheld bakery goods, and pizza crust)
212 Fiber Ingredients: Food Applications and Health Benefits
Hi-maize® Meal 150
Hi-maize® Whole Grain Corn Flour
Barleyplus™ Flour
Hi-maize® 220 starch
RS1 & RS2 (high amylose corn grain)
RS1 (high amylose corn grain)
RS1 (high amylose barley flour)
RS2 granular starch (unmodified high amylose corn starch)
Ascentia Pty Ltd (CSIRO), Canberra, Australia National Starch & Chem. Co., Bridgewater, NJ
National Starch & Chem. Co., Bridgewater, NJ
National Starch & Chem. Co., Bridgewater, NJ
80
59
60
77
20 c
30 c
36 c
60 c
High fiber content Enables labeling of health benefits substantiated by Hi-maize® starch clinical data Imparts excellent textures without compromising eating quality Low water holding capacity (WHC) Small particle size Clean flavor
Provides health benefits to consumers: low glycemic index, high in β-glucan
High fiber content Increased bowl life of RTE cereals Superior adhesion in breaded foods Crisp texture “Natural” ingredient declaration Good process tolerance Provides increased TDF and RS while delivering whole grain benefits Provides textural benefits Good process tolerance
(continued)
Baked & fried snacks, battered & breaded foods, cereals, specialty bakery goods (English muffins, corn tortillas, and waffles, handheld bakery goods, and pizza crust) Extruded snacks, extruded breakfast cereal, rolled cereal, breads, and muffins RTE cereals, snacks, pasta/noodles, baked goods, and fried foods
Baked & fried snacks, battered & breaded foods, cereals, specialty bakery goods (English muffins, corn tortillas, and waffles, handheld bakery goods, and pizza crust)
Resistant Starch (RS) 213
National Starch & Chem. Co., Bridgewater, NJ
National Starch & Chem. Co., Bridgewater, NJ
SunOpta Inc., Bedford, MA
NOVELOSE® 330 starch
Crystalean®
RS3 (high amylose corn starch) retrograded crystalline amylose-nongranular
RS3 (high amylose corn starch); Crystalline amylose
Supplier
Hi-maize® 260 starch
Commercial Name
RS2 granular starch (high amylose corn starch)
Classification (grain source)
57
57
53
RSa (% db)
33 c
33 c
60 c
TDFb (% db)
Commercial Sources and Forms of Traditional (Natural) RS1, RS2, and RS3
Table 10.3 (Continued)
Top Benefits All natural Fewer calories than flour Proven health benefits Prebiotic fiber Improves digestive health Enhances mineral absorption Reduces glycemic response of foods Increases insulin sensitivity Provides sustained energy release Promotes digestive health Good expansion aid in extrusion; offers uniform cell size, excellent expansion, improved processing, improved overall good eating quality Low WHC, small particle size and clean flavor Provides concentrated source of RS Adds fiber, bulking agent, and enhances texture, low WHC Thermally stable Increases strength & crispness of cereals Improves cell structure and expansion in extruded products
Key Applications
Baked products (improved mouthfeel and volume), RTE cereal, extruded snacks, nutrition bars, low-glycemic & diabetic foods
Extruded foods (RTE cereals & snacks), pasta & noodles, some baked goods, and fried foods
Bakery products, other low-moisture baked goods, cookies/ biscuits, pasta & noodles, RTE cereals, snack foods (cheese curls and pretzels), soups, cereal drinks, yogurt, and selected dairy products
214 Fiber Ingredients: Food Applications and Health Benefits
d
c
b
Cargill, Minneapolis, MN; Cerestar, Cedar Rapids, IA
Cargill Texturizing Solutions, Minneapolis, MN
Min. 53% (Goni Method)
50 (AOAC 2002.02)
Does not analyze as fiber
2 c
All-natural Promotes digestive health Stable under high-heat & high-acid conditions Low glycemic and insulinemic response Good dispersibility Relatively low viscosity and water binding capacity Reduces intestinal pH Increases calcium and magnesium absorption Beverages, low-fat fermented milks, UHT flavored milk drinks
Baked goods, breakfast cereals, cereal bars, tortillas, snack foods, instant soups, powdered drinks & mixes, smoothies, yogurt, UHT milk drinks
Modified Englyst Assay: H. N. Englyst, S.M. Kingman, and J. H. Cummings: Classification and Measurement of Nutritionally Important Starch Fractions. Eur. J. Clin. Nutr. Suppl. 2, 46 (1992) 33–50. TDF Assay Utilized AOAC Method 991.43 Total, Soluble, and Insoluble Dietary Fiber in Foods (Enzymatic-Gravimetric Method, MES-TRIS Buffer) AOAC Method 2001.03 Total Dietary Fiber in Foods Containing Resistant Maltodextrin
C* Actistar
RS3 (tapioca, short chain amylose)
a
Actistar™ RM
RS3 (tapiocabased) nongranular resistant maltodextrin
Resistant Starch (RS) 215
216
Fiber Ingredients: Food Applications and Health Benefits
Resistant dextrins, which are soluble starches derived via pyrodextrinization, can also be considered RS4. Two commercial patented ingredient lines that are available include Nutriose® and FiberSol® (Ohkuma et al. 1994; Fouache et al. 2003). In a generalized process scheme, starch granules from a variety of sources are cooked out, hydrolyzed, and chemically re-arranged with heat and acid, then concentrated and dried as a finished ingredient. These materials tend to be highly soluble with fiber contents greater than 85%, and hence are very useful in ready-to-drink (RTD) beverages and dairy products. Table 10.4 summarizes the various commercial forms of non-traditional RS4, namely chemically modified starches and resistant dextrins. RS4 modifications represent a flexible approach to RS ingredients; however, there is comparatively little nutritional research on their physiological effects compared with 20 years of research for natural RS ingredients. New commercial RS4 ingredients should be subjected to extensive clinical evaluation to ensure safety, physiological benefit, and optimal product performance, including shelf stability. The potential for using such starches at macronutrient levels in foods is fairly new and warrants careful consideration and assessment.
Analysis of RS: AOAC and Non-AOAC Methodologies RS quantification by one simple in vitro method is technically challenging for many reasons. First and foremost is the obvious fact that multiple forms of RS exist. Compounding this issue is the observation that different methods are more suited to selected RSs. Today a variety of RS analytical methods are now available, each with their own respective strengths and weaknesses (Table 10.5). Additional complications arise from the fact that there is still no regulatory definition of RS in the United States. Also, many U.S. food manufacturers desire a fiber content claim when commercial RS ingredients are used for fiber enrichment. In the early 1980s, Englyst et al. (1982) observed that starches differ in their extent and rate of digestion. This was later associated with the source of starch, food-processing conditions, and the way in which foods were consumed (Englyst et al. 1992; Brown et al. 1995). Over the ensuing years several research groups advanced the analytical understanding of RS, with methods gradually incorporating improvements to a procedure originally developed for non-starch polysaccharide determination (Englyst et al. 1982). Generally, methods can be dissected into three consecutive steps:
Resistant Starch (RS)
217
1. Sample pretreatment (e.g., grinding, sieving, or chewing);
2. Controlled enzymatic hydrolysis (to mimic physiological digestion); and
3. Quantification of RS.
RS methods are categorized as “direct” or “indirect” based on the technique employed for RS quantification. Direct methodology was initially developed by Berry (1986) who recognized that in vitro digestion temperatures of 42oC, which are closer to physiological conditions, would be more appropriate for RS detection. Following digestion, RS was recovered by alcohol precipitation and centrifugation. Measurement of RS involved dispersion of the RS pellet in potassium hydroxide (KOH) followed by amyloglucosidase treatment and detection of glucose with a glucose oxidase kit. Goni et al. (1996) further developed Berry’s procedure by eliminating the alcohol precipitation step, recovering the RS by centrifugation only. Muir and O’Dea (1992) introduced a chewing step prior to enzymatic digestion. The RS residue was typically recovered using potassium hydroxide followed by amyloglucosidase (Berry 1986; Goni et al. 1996; Champ 1992), or dimethylsulfoxide (DMSO) and Termamyl (Muir and O’Dea 1992). Free glucose released from the RS fraction was typically quantified by a glucose oxidase kit. In 2002, McCleary and Monaghan published the first AOAC method to measure RS. To date, this is the only AOAC-approved RS method. Like the other direct methods, this method does not detect RS4 (McCleary et al. 2006) and resistant dextrins. All the aforementioned methodologies/variations are generally sufficient to quantify naturally occurring RS (RS1, RS2, and RS3), but underestimate RS4. Further information on direct RS methods is available in a review by Champ et al. (1999). Indirect methodologies date back to the work of Englyst et al. (1992). Their method involved digestion of a sample with enzymes and detection of released glucose using a glucose oxidase colorimetric procedure. The amount of glucose released as result of digestion was then reported as rapidly digested starch (RDS), slowly digested starch (SDS), and RS, calculated by difference. In contrast to the direct methods, RS was not recovered in the Englyst procedure and therefore no dispersion step was required. The method was later improved by introducing simulated stomach conditions (i.e., pepsin), and excluding pullulanase from the enzymatic digestion step (Englyst et al. 1996). Later, a chromatographic detection step was added to distinguish small molecular weight saccharides released during hydrolysis. This method has been correlated with the glycemic index (GI) (Englyst et al. 1999) and is the only procedure that allows detection of all four RS types, including RS4 and resistant dextrins, and hence has great value as an analytical tool for RS research.
FiberRite™ RW
Fibersym® 70
Fibersym® 80ST
Actistar™ RT
RS4 (wheat starch)
RS4 (potato)
RS4 (tapioca)
Commercial Name
RS4 (pregelatinized wheat starch)
Classification (Grain Source)
Cargill, Minneapolis, MN
MGP Ingredients, Atchison, KS
MGP Ingredients, Atchison, KS
MGP Ingredients, Atchison, KS
Supplier
Commercial Sources and Forms of Non-Traditional RS4
Table 10.4
54
97
82
16
RSa (% db)
82
82
76
72
TDFb (% db)
Low WHC Small particle size Bland flavor profile Replacement for flours in baked goods
Fat replacement properties (high WHC) Caloric reduction Smooth texture, white color, neutral flavor Excellent freeze-thaw stability Low WHC Smooth texture Neutral flavor & white color Low WHC Smooth texture Neutral flavor, white color
Key Benefits
Baked goods, breakfast cereals, cereal bars, snack foods, yogurt, powdered & drink mixes, instant soups, smoothies, low-fat fermented milks
Bakery products, pasta, snack foods, batters & breadings, RTE breakfast cereals Bakery products, pasta, snack foods, batters & breadings, RTE breakfast cereals
High moisture foods, bakery mixes and sweet goods, icings and crème fillings, sauces, yogurt and sour cream, confectionary products, salad dressings
Key Applications
218 Fiber Ingredients: Food Applications and Health Benefits
Nutriose® FB06
Nutriose® FB10
Fibersol-2
Resistant maltodextrin (wheat-based)
Resistant maltodextrin (wheat-based)
Resistant maltodextrin (corn starch)
b
90
~ 90
~ 90
~ 90
~ 90
Min. 90 b
70 b
85 b
70 b
85 b
Water soluble Easily dispersed in water Extended energy release Acid and heat stable Low viscosity Clean flavor Water soluble Easily dispersed in water Acid and heat stable Low viscosity Clean flavor Water soluble Easily dispersed in water Acid and heat stable Low viscosity Clean flavor Water soluble Easily dispersed in water Acid and heat stable Low viscosity Clean flavor Water soluble Easily dispersed in water No off flavors Very low viscosity Acid and heat retort stable Beverages, nutritional & functional foods, bars, cereal, dairy foods, dry mixes, cultured dairy products, frozen dairy desserts
Ideal for high moisture applications: beverages, dairy, fruit fillings (breakfast bars)
Ideal for high moisture applications: beverages, dairy, fruit fillings (breakfast bars)
RTD beverages, sweet baked goods, frozen dairy/desserts, sauces/gravies, pasta, meats, savory dips, cereals, snacks (sheeted/extruded, fried/ baked) Ready meals, soups, side dishes, dairy beverages, yogurts, yogurt beverages
Modified Englyst Assay: H. N. Englyst, S.M. Kingman, and J. H. Cummings: Classification and Measurement of Nutritionally Important Starch Fractions. Eur. J. Clin. Nutr. Suppl. 2 46 (1992) 33-50. TDF Assay Utilized: AOAC Method 991.43 Total, Soluble, and Insoluble Dietary Fiber in Foods (Enzymatic-Gravimetric Method, MES-TRIS Buffer) AOAC Method 2001.03 Total Dietary Fiber in Foods Containing Resistant Maltodextrin
National Starch, Bridgewater, NJ & Roquette America, Inc., Keokuk, IA National Starch, Bridgewater, NJ & Roquette America, Inc., Keokuk, IA National Starch, Bridgewater, NJ & Roquette America, Inc., Keokuk, IA Matsutani America, Inc., Decatur, IL
Nutriose® FM10
Resistant maltodextrin (maize-based)
a
National Starch, Bridgewater, NJ & Roquette America, Inc., Keokuk, IA
Nutriose® FM06
Resistant maltodextrin (maize-based)
Resistant Starch (RS) 219
Grinding
Grinding
Mincing
Chewing
Bjôrck et al. [1986]
Englyst et al. [1992, 1996]
Muir & O’Dea [1992]
Sample Pre-treatment
Berry [1986]
RS Methods
Method
37°C Pepsin Pancreatin Amyloglucosidase
100°C, 37°C Pepsin Heat stable α-amylase Pancreatin 37°C Pepsin Pancreatin Amyloglucosidase Invertase
42°C Pancreatic α-amylase Pullulanase
Digestion
Key Methods employed in the Detection of RS
Table 10.5
Centrifugation RS dispersion in DMSO followed by heat stable α-amylase
Alcohol precipitation RS dispersion: KOH & amyloglucosidase Alcohol precipitation Supernatant is used for further assays
Alcohol precipitation RS dispersion in KOH & amyloglucosidase
Recovery
Glucose Oxidase Assay
Glucose Oxidase Assay or chromatography
Glucose Oxidase Assay
Glucose Oxidase Assay
Detection
Humans
Humans
Rats
No
Validation in Vivo
Underestimation of RS2 and possibly RS3 May overestimate RS1 in absence of proteolytic digestion step No mechanism to detect RS4 Underestimation of RS1 if grinding is too fine Underestimation of RS1, RS2, and possibly RS3 No mechanism to detect RS4 Underestimation of RS1 if grinding is too fine Analyzes all RS types Detection of various digestion products only if HPLC is used Complicated and laborious Widely used in research labs Used primarily by the authors No means to detect RS4 or small MW indigestible components
Advantages/Disadvantages
220 Fiber Ingredients: Food Applications and Health Benefits
Grinding
McCleary & Monaghan [2002]
Grinding
As AOAC 991.43
AOAC 991.43
AOAC 2001.03
Dietary Fiber Methods
37°C Pancreatic α-amylase Amyloglucosidase
Grinding
Champ et al. [1999]
100°C, 60°C Heat stable α-amylase Protease (Subtilisin) Amyloglucosidase As AOAC 991.43
37°C Pancreatic α-amylase Amyloglucosidase
40°C, 37°C Pepsin Pancreatic α-amylase
Milling and sieving
Goni et al. [1996]
As AOAC 991.43
Alcohol precipitation
Alcohol precipitation RS dispersion: KOH & amyloglucosidase Alcohol precipitation RS dispersion: KOH & amyloglucosidase
Centrifugation RS dispersion in KOH followed by amyloglucosidase
Gravimetric & Chromatographic
Gravimetric
Glucose Oxidase Assay
Glucose Oxidase Assay
Glucose Oxidase Assay
Yes
No
Humans
Humans
Based on comparison to EURESTA 1994
Underestimation of RS2 and RS3
Underestimation of RS2 and RS3 No detection of resistant maltodextrin or other small MW fragments
No means to detect RS4 or resistant maltodextrin Underestimation of RS1 if grinding is too fine Robust The only AOAC method for detection of RS
No means to detect RS4 or small MW indigestible components Underestimation of RS1 if milling is too fine Use not recently reported No means to detect RS4 or small MW indigestible components
Resistant Starch (RS) 221
222
Fiber Ingredients: Food Applications and Health Benefits In Vitro Measurement of Resistant Starch Englyst Method Enzymatic Digestion Pepsin Incubation at 37°C
2 hr
Pancreatin Invertase Amyloglucosidase
Measure glucose released from digested fraction
Figure 10.1 Englyst RS method. (From Englyst et al., Euro J Clinical Nutr, 1999, 46 Suppl 2, S33–S50 & Englyst et al., Am J Clin Nutr 1999, 69, 448–54.
A more sophisticated and complex in vitro approach to estimating RS is a dynamic computer controlled system that simulates the mouth, stomach, and small intestine (Minekus et al. 1995; Fässler et al. 2006). The RS2 values obtained using this system are comparable with the indirect method; however, its complexity restricts its use for routine screening of ingredients and foods during the development process, nor is it useful for labeling purposes. The system is more suited for research. All in vitro RS methods should be interpreted cautiously. Currently they all share one common drawback—none employ human digestive enzymes. Animal and microbial enzyme sources are used, which could vary in specificity compared with human digestive enzymes. As research and development tools, however, such methodology can be quite useful. For example, National Starch has adopted two methods to support internal product development: Englyst et al. (1996) with glucose oxidase detection, and AOAC method 2002.02. Differences between the methods include the digestion and detection steps (Figures 10.1 and 10.2). The Englyst method simulates the stomach environment with pepsin digestion, followed by pancreatin digestion for 2 hr at 37oC. The AOAC (McCleary) method 2002.02 does not simulate the stomach, and pancreatin digestion is conducted for 16 hr at 37oC. Although both methods were reported to be validated against in vivo data, they still show differences in RS content when used to compare a variety of commercial RS ingredients (Table 10.6), thus underscoring the need to fully understand the strengths and weaknesses of each method. Since the Englyst method allows for the detection of all RS types, it is preferred by some in spite of its complexity (Champ et al. 1999). Fiber methods have also been used to measure RS, principally due to labeling regulations. A comprehensive review of fiber determination methodologies was prepared by DeVries (2004). The fiber methods most com-
223
Resistant Starch (RS) In Vitro Measurement of Resistant Starch AOAC 2002.02 Enzymatic Digestion
Incubation at 37°C
16 hr
Pancreatic α-amylase Amyloglucosidase
Isolate undigested components
Dissolve undigested components
Quantify RS as glucose from solubilized undigested components
Figure 10.2 McCleary RS method. (From McCleary & Monaghan, J. AOAC Int., 2002, 85 (3): 665–675.
monly used in the United States include AOAC 985.29 and AOAC 991.43 (Prosky et al. 1985, 1988, 1994; Lee et al. 1992). These methods are gravimetric and employ an enzymatic digestion step at 100oC, which was originally designed to remove any starch by gelatinization (Figure 10.3). AOAC method 991.43 (Lee et al. 1992) is a newer procedure with an improved buffer system. More recently, Gordon and Okuma (2002) introduced AOAC method 2001.03 for quantification of resistant (malto) dextrins. In this method the first steps are the same as in AOAC 985.29, but are followed by a chromatographic detection of small molecular weight indigestible components from a supernatant that is normally discarded in AOAC 985.29 (Figure 10.4). The final dietary fiber value in AOAC 2001.03 includes insoluble fiber and two fractions of soluble fiber; the high molecular weight component that can be precipitated by alcohol and the small molecular weight component detected by HPLC. Additional analytical complexity is introduced when AOAC fiber methods are implemented for RS-containing ingredients. The 100oC digestion step can result in loss of RS (which is actually defined by a physiological process occurring at 37oC). Therefore, as presented in Table 10.6, in vitro estimation of the RS content of commercial ingredients is dependent upon the method chosen for analysis. Most RS1, RS2, and RS3 have lower TDF than RS contents. Only naturally inhibited RS2 and cross-linked RS4 ingredients have TDF values comparable to RS values. These reported differences are concerning and indicate a need for development of a comprehensive in vitro method that would allow accurate detection of RS, to enable consumers to make educated high-RS choices.
224
Fiber Ingredients: Food Applications and Health Benefits
Table 10.6 Dietary fiber and RS contents of commercial products by different methods
RS Type RS1
RS2 RS3
RS4
a
b
Product Hi-maize Flour 120 Hi-maize® Flour 150 Hi-maize® Meal 130 Hi-maize® Meal 150 Hi-maize® Whole Grain Corn Flour Barleyplus™ Flour Hi-maize® 220 starch Hi-maize® 260 starch NOVELOSE® 330 starch CrystaLean® Actistar™ RM C* Actistar Nutriose® FM10 Nutriose® FM06 Fibersol-2® Fibersym® 70 Fibersym® 80 FiberRite™ RW Actistar™ RT ®
TDF (% db) AOAC 991.43 25 58 38 62 36 30 17 60 37 33 2 0 75 b 92 b 98 b 80 97 72 82
RS (% db) AOAC Englyst a 2002.02 67 66 68 75 60 59 76 51 56 57 65 65 79 81 92 82 97 16 54
31 37 37 45 22 3 48 46 48 48 50 56 0 0 0 0 3 0 1
RS values based on carbohydrate content which is 80–90% for evaluated flours and meals [Englyst et al. 1996] Measured by AOAC 2001.03 method
Food Applications: Key Functional Properties in Low- and High-Moisture Systems RS ingredient selection is a function of a variety of factors, many of which have already been discussed above. Food matrix compatibility is critically important, as well as food processing conditions, organoleptics, fiber retention, nutritional impact, shelf stability, and clinical validation. Table 10.7 summarizes the key functional attributes to consider when deciding on which type of RS to use in the developmental process. Today’s formulators have a diverse selection of RS ingredients to choose from, ranging from crystalline amylose to soluble dextrins. In baked goods, RS2 from high-amylose corn starch improves loaf volume, texture, and cell structure, and in breakfast cereals it extends bowl-life and crispiness. Unlike traditional dietary fibers, RS2 does not lower volume, does not typically alter the texture of baked goods, or hold significant amounts of water, which can negatively impact the processing and manufacturability of high-fiber foods.
225
Resistant Starch (RS) Total Dietary Fiber Methods AOAC 985.29 & 991.43
Enzymatic Digestion Incubation at 95°C
Filtration Filtrate
Amylase Protease Amyloglucosidase
Insoluble DF
Alcohol Precipitation
Supernatant
+
Soluble DF
TDF
Waste AOAC Official Methods of Analysis, 1997, 16th Ed.
Figure 10.3 Total dietray fiber methods AOAC 985.29 & 991.43.
Total Dietary Fiber Methods AOAC 2001.03 985.29
DF
2001.03
Insoluble Soluble
Supernatant
Chromatography
Small MW Non Digestible Fraction Godon & Okuma, J. AOAC Int., 2002, 85 (2): 435
Figure 10.4 Total dietray fiber methods AOAC 2001.03.
TDF & RMD
Products Fibersol Nutriose
226
Fiber Ingredients: Food Applications and Health Benefits
Table 10.7 Key Product Attributes of Commercial RSs
Classification RS1
RS2 RS3 RS4 Resistant Maltodextrin a
b
Key Physical Form Physically inaccessible starch (granular starch as starch, flour, or meal) Raw granular starch Retrograded amylose Chemically modified starch Low molecular weight starch fractions
Solubility
Particle Size of Resistant Material (microns)
RSa (% db)
TDFb (% db)
Insoluble
Flours 150–250 WGCF 175–420 Meals 300–850
55–80
25–60 b
Insoluble
75–150
50–80
20–60 b
Insoluble
40–150
50–60
0–35 b
Insoluble
50–100
15–100
60–90 b
Soluble
40–500
~ 90
70–90 b
Modified Englyst Assay: H. N. Englyst, S.M. Kingman, and J. H. Cummings: Classification and Measurement of Nutritionally Important Starch Fractions. Eur. J. Clin. Nutr. Suppl. 2 46 (1992) 33–50. TDF Assay Utilized: AOAC Method 991.43 Total, Soluble, and Insoluble Dietary Fiber in Foods (Enzymatic-Gravimetric Method, MES-TRIS Buffer) OAC Method 2001.03 Total Dietary Fiber in Foods Containing Resistant Maltodextrin
Overview of Health Benefits Introduction Resistant starch has been the subject of nutritional research for almost 30 years. Early research focused on the digestibility of RS (e.g., using ileostomates, in vitro methodologies, and animal models) to confirm that RS indeed resisted digestion, and increased fermentation. Animal models have often been used for sampling and measurements more difficult to conduct in human subjects, to enhance understanding of the rate, site, and extent of RS fermentation. More recently research has addressed the physiological importance of reduced digestibility and increased fermentability, as researchers learn about the relationship between the large intestine and integrated systemic function. High-RS diets can be designed by increasing intake of high-RS foods, or by incorporating high-RS ingredients in place of digestible starch. The latter has proven quite successful in nutritional research, and is a differentiating feature of RS compared with many other fibers in terms of food quality, so
Resistant Starch (RS)
227
most studies have used high-RS ingredients. In particular RS2 from highamylose corn starch has frequently replaced regular or low-amylose corn starch and wheat flour, so will be discussed in more detail in this section. At the time of writing this chapter, more than 200 studies had reported on the nutritional effects of this RS source: 31% were in human subjects, 53% were in animal models, and 16% were in vitro studies. Most of these studies (76%) used granular starch, with the remaining studies using non-granular derivatives. Table 10.8 shows that a broad range of health effects have now been attributed to RS2 from high-amylose corn starch, based collectively on human, animal, and in vitro research. They generally fall into three categories: digestive health (including prebiotic effects), glycemic management, and weight management. Human studies tend to indicate that RS is well tolerated, which is an important feature of functional ingredients for consumer acceptance and market sustainability. This is demonstrated in Table 10.9 where diets fed for multiple weeks contained between 22 to 60 g of RS2 from high-amylose corn starch each day. One study by Kendall et al. (2003), which was designed specifically to observe RS tolerance, reported that up to 100 g of RS2 high-amylose corn starch consumed each day in typical foods was well tolerated. RS has been a natural part of the diet since our ancestors began eating cereals and grains, and animal studies show that RS is well fermented along the entire length of the large intestine (Morita et al. 1999). Together this could contribute to high tolerance. In summary, RS, which functions as a dietary fiber within the body and is well tolerated, represents a practical solution for meeting dietary fiber recommendations. Digestive Health Fermentation With the exception of a direct impact on glycemic response (see next section) most health effects of RS can be attributed either directly or indirectly to fermentation of the starch by the colonic microflora (Table 10.8). Fermentation is the process whereby the colonic microflora utilize available substrates to generate energy for maintenance and growth. RS readily serves as a fermentable substrate, as demonstrated by increased breath hydrogen production following consumption of high-RS diets (Robertson et al. 2003). Under the anaerobic conditions in the colon a range of metabolic end products are produced that include short-chain fatty acids (SCFAs), gases, and water. SCFAs are important for colonic function (Bird et al. 2000): They lower pH, inhibiting growth of pathogens; they stimulate colonic blood flow and promote colonic muscular contraction, enhancing tone and nutrient flow; and they promote colonocyte proliferation to reverse atrophy associated with low-fiber diets. As a consequence of fermentation, bacterial biomass is increased, contributing to increased fecal weight and cecal content weight; laxation is enhanced; and changes in bacterial activity occur, resulting in lower production with
228
Fiber Ingredients: Food Applications and Health Benefits
Table 10.8 Health Effects Attributed to Resistant Starch from High Amylose Corn Rs2 Ingredients (Byrnes et al. 1995; Noakes et al. 1996; Brown 2004; Higgins et al. 2004, 2006; Morita et al. 2004A, 2004B; Robertson et al. 2005; Keenan et al. 2006; Toden et al. 2006) Health Opportunity Glycemic Management
Weight Management
General Physiological Effect Improved glucose response
Lower postprandial glucose response.
Improved insulin response
Lower postprandial insulin response; Increased insulin sensitivity; Delayed onset of insulin resistance. Non-digested; Fewer available calories; Increased excreted energy. Increased GLP-1 and PYY.
Reduced energy
Increased satiety hormone production Modified body composition profile
Digestive Health
Detailed Physiological Effect
Modified energy partitioning Modified intestinal environment
Improved intestinal health Improved intestinal function
Prebiotic
Culture protagonist
Tolerance
Decreased total body fat and regional fat; Decreased adipose lipogenesis. Increased lipid oxidation. Fermentable substrate; Cecal and fecal bulking; Increased production of short chain fatty acids, including butyrate; Reduced pH; Decreased levels of cytotoxic compounds, e.g., ammonia, phenols & secondary bile acids. Increased apoptotic index; Decreased DNA damage. Increased mineral absorption (calcium, magnesium); Reduced symptoms of diarrhea; Increased fecal frequency; Increased mucosal barrier strength; Improved immune response. Selectively utilized by Bifidobacteria; Promotes growth of beneficial indigenous bacteria (Lactobacilli & bifidobacteria); Promotes probiotic growth and activity (Bifidobacteria); Reduced pathogenic bacteria levels; Increased butyrate production. Improves yield of probiotic cultures during growth; Improves survival of probiotic cultures during processing, in foods, in vivo. Well tolerated at high levels.
O
↑ ↑ O ↑ ↑ ↑
39 g RS 55 g RS 22 g RS 20 g RS ingredient
39 g RS 37 g RS 45 g RS ingredient
51-60 g RS
Healthy; 4 wk
Note: (↓ = decreased; ↑ = increased; O = no effect)
↑
↑
O
Fecal Weight
29 g RS
Amount of RS Fed
Fecal Frequency
Healthy & hyperinsulinemic; 14 wk Healthy; 3 wk Healthy; 4 wk Healthy; 3 wk Metabolic syndrome predisposed; 4 wk Healthy; 3 wk Healthy; 19 d Healthy; 2 wk
Subject Type & Duration
↑ ↑
↑ ↑
↑ ↑
↑
Fecal SCFA
O
Fecal Butyrate
O
Fecal pH ↓ ↓ O
↓ ↓
O
Fecal Ammonia O
↓
↓
Fecal Phenols ↓
↓
↓
Fecal Secondary Bile Acids
Phillips et al. 1995 Silvester et al. 1997 van Munster et al. 1994 Wacker et al. 2002
Birkett et al. 1996 Hylla et al. 1998 Muir et al. 2004 Noakes et al. 1996
Behall et al. 2002
Reference
Effect of RS on Digestive Health Biomarkers in Human Subjects with Normal Functioning Gastrointestinal Tracts. RS2 High Amylose Corn Starch Meals Compared with Control Meals Containing Digestible Carbohydrates.
Table 10.9
Resistant Starch (RS) 229
230
Fiber Ingredients: Food Applications and Health Benefits
lower concentrations of potentially toxic substances such as ammonia, phenols, and secondary bile acids. These changes have been observed across many studies, for varying RS sources, as reviewed by Nugent (2005). In Table 10.9 human intervention studies are summarized where RS2 was incorporated into diets as a replacement for digestible starch, and fed for a period of at least two weeks. There was good consistency in fecal observations across the studies, particularly increased fecal weight – six of eight studies; increased total SCFAs – three of four studies; increased butyrate – four of five studies; decreased pH – four of six studies; decreased ammonia – two of three studies; and decreased phenols – two of two studies. The fecal bulking effect of RS is less than for other non-fermented fibers such as wheat bran, owing to the fact that RS is fermented; hence its colonic benefits arise from fermentation and not simple bulking effects. The fecal bulking index for the studies in Table 10.9 average a 1.3 g increase in fecal weight for each additional gram of RS. This is similar to that reported for inulin at 1.5, which is another fermented fiber (Den Hond et al. 2000). Prebiotic Colonic microflora composition and activity reflect the supply and utilization of fermentable substrate. This is substrate and bacteria specific. Several bacterial groups have the capacity to utilize starch including Eubacteria, Bacteroides, Bifidobacteria, and Escherichia (Bird et al. 2000); however only selected groups utilize RS2 from high-amylose corn starch in vitro, including Bifidobacteria and Clostridium butyricum, but not Escherichia coli, Staphylococcus aureus, Streptococcus, and Lactobacilli (Wang et al. 1999A). In vivo studies also indicate that RS can selectively promote the growth and/or activity of the colonic microflora. In rat studies, RS2 diets containing high-amylose corn starch increased fecal/cecal levels of Bifidobacteria (Wang et al. 2002; Le Leu et al. 2005). Lactobacilli also increased indicating co-utilization of starch and its metabolites with other bacteria because Lactobacilli could not utilize RS2 directly as mentioned above. In human studies, consumption of RS2 from high-amylose corn results in selective colonic microflora activity, as demonstrated by increased fecal butyrate (Table 10.9), because not all bacteria produce this metabolic by-product. Butyrate is important for colonic health because it is the preferred metabolic fuel for colonocytes; it enhances growth of normal colon cells while inhibiting growth of malignant ones; it promotes DNA repair and tumor cell differentiation; and it is linked with apoptosis of malignant cells (Bird et al. 2000). Brown et al. (2006) described one human study where fecal Bifidobacteria measurements increased when RS2 was fed; however additional human studies are required. RS2 from high-amylose corn also functions as an effective synbiotic, improving probiotic viability in food products and protecting probiotics under harsh physiological conditions. For food manufacturers, this characteristic could be usefully employed to reduce probiotic inclusion levels in
Resistant Starch (RS)
231
food formulations which would be necessary to achieve desired viable bacterial counts in the food when eaten. Bifidobacteria bind to high-amylose corn starch granules, which affords protection and increases survival at pH 6.5, pH 3.5, and under bile salt conditions for up to six hours (Wang et al. 1999B). Probiotic protection was provided in vivo through the gastrointestinal tract of mice, pigs, and rats (Brown et al. 1997; Wang et al. 2002; Le Leu et al. 2005) and during food preparation and storage (Brown et al. 1998). Colonic Cell Health The colonic mucosa functions as a barrier, protecting the body from harmful agents in the colon. Colonic RS can improve colonic cell health, which therefore contributes to stronger barrier function. Two biomarkers of colonic cell health, in particular, have been used to measure the protective benefits of high-RS diets on colonocytes in animal models, namely apoptosis and DNA damage. Apoptosis is a marker of the body’s ability to remove damaged cells, with a higher relative index score preferred. Feeding rats RS2 from high-amylose corn increased the apoptotic index by more than 30% in a dose-dependent manner, after the rats were exposed to the colon-specific genotoxin azoxymethane (Le Leu et al. 2003). Apoptosis correlated with SCFA and butyrate levels, indicating that RS fermentation markers could also be good indicators of colonic cell health. DNA damage is an early step in cancer initiation. Rats fed high-RS2 diets had less DNA damage when rats were simultaneously fed high-protein diets, a macronutrient linked with higher risk for colorectal cancer (Toden et al. 2006). This suggests that RS may offer protection for the colon against diet-induced assaults. These biomarkers are indicative of colorectal cancer risk. Le Leu et al. (2006) have extended their apoptosis model to show that rats fed RS2 from high-amylose corn had reduced incidence of neoplasms in the colon and small intestine. Mucin serves as a protective layer for the mucosa, restricting the adhesion and invasion of pathogenic bacteria. RS is associated with a stronger mucus layer. Healthy rats fed high-RS2 diets had a thicker mucus layer with reduced colonic permeability (Morita et al. 2004B). Incorporating RS2 into high-protein diets prevented mucosal thinning typically observed when a high-protein diet is fed (Toden et al. 2006). In rats exposed to liver injury via a gut-derived endotoxin, mucin weight was higher, with improved mucosal barrier function shown by lower endotoxin translocation (Morita et al. 2004A). Intestinal Function The large intestine not only functions as a physical barrier, but also functions to salvage water and minerals. The gastrointestinal tract also accounts for approximately two-thirds of the body’s immune system. RS2 ingredients are useful for inclusion in foods and preparations designed for alleviating symptoms of diarrhea. In two studies in India, RS2 high-
232
Fiber Ingredients: Food Applications and Health Benefits
amylose corn starch enhanced water salvage for children and adults suffering chronic diarrhea, with decreased time to first stool (Ramakrishna et al. 2000; Raghupathy et al. 2006). This is SCFA-mediated, similar to the mechanism proposed for the increase in calcium, magnesium, zinc, iron, and copper absorption observed when rats were fed high-RS2 diets (Lopez et al. 2001). SCFAs produced during fermentation lower the colonic pH, making the minerals more soluble and more readily absorbed. In addition, SCFAs promote colonic tissue growth increasing the absorptive area, and promote colonic blood flow. New research is investigating the effect of high-RS diets on intestinal immune potential. Morita et al. (2004A; 2004B) reported that rats fed high-RS2 diets containing high-amylose corn starch had higher intestinal and fecal IgA. Further studies are required to see if this benefit translates to humans. Nutrient Interactions Various carbohydrate and non-carbohydrate endogenous and exogenous substrates pass into the large intestine, of which RS is but one. It is therefore important to understand how RS interacts with other colonic substrates, to influence the colonic environment and cell health. Table 10.10 summarizes evidence for the additive impact of RS in selected nutrient combinations, categorized as carbohydrate and non-carbohydrate, with studies spanning both human and animal models. Carbohydrate nutrients included wheat bran, cellulose, psyllium, and fructooligosaccharide (FOS). For all these non-digested carbohydrates, combining RS with the nutrient improved the digestive health effects above that of the nutrient alone. For example, in human subjects, rats, and pigs, combining RS with wheat bran further improved markers of fermentation typically attributed to wheat bran, including fecal and cecal content weight, pH, and SCFA production. This property of RS could be useful for formulators because RS is organoleptically more appealing to consumers than many other fiber ingredients (i.e., RS could replace some of the traditional fiber and still obtain the same health benefit, but with improved food quality). For the non-carbohydrate nutrients (protein and probiotics), combining with RS also further improved markers for digestive health. Thus RS-containing diets provide improved opportunity for digestive health as part of multi-component diets. Glycemic Management Glucose management is of topical interest because prolonged extreme glucose and/or insulin responses are associated with onset of insulin resistance and development of chronic diseases such as type 2 diabetes and coronary heart disease (Higgins 2004). RS is defined by its indigestibility within the small intestine; therefore by its very nature RS will not contribute directly to blood glucose. Methodology is an important factor in considering glycemic impact of RS. Standard GI (glycemic index) tests only compare the avail-
↑
Rat Rat Rat ↑
↑ ↑ ↑
↑ ↑ ↑
↑
↓
↑
↑ O
↓
↓
↓ ↓ ↓
↓
pH
↑
Fecal Weight, Cecal Contents
Rat Rat
Healthy Humans (22 g RS fed) Rat Rat Pig Rat Rat Pig
Model
Tissue Weight
Notes: (↓ = decreased; ↑ = increased; O = no effect)
RS + probiotic RS + resistant potato protein RS + whey RS + casein RS + red meat
Non-Carbohydrates
RS + wheat bran RS + wheat bran RS + wheat bran RS + cellulose RS + psyllium RS + FOS
RS + wheat bran
Carbohydrates
Co-Nutrients
SCFA ↑ ↑ ↑ ↑ ↑
↑ ↑ ↑
↑ ↑ ↑
↑ O
↑
Butyrate
↑ ↑
↑ ↑ ↑ ↑ ↑
↑
Ammonia ↓
↓
Phenols ↓
↓
↓
Bifidobacteria ↑
↑
Apoptosis ↑
O
O
Neoplasm ↓
DNA Damage ↓ ↓ ↓
↑ ↑ ↑
Mucus Thickness
Toden et al. 2005A Toden et al. 2005B Toden et al. 2006
Le Leu et al. 2005 Le Leu et al. 2006
Le Leu et al. 2002 Henningsson et al. 2002 Govers et al. 1999 Le Leu et al. 2002 Morita et al. 1999 Brown et al. 1998
Muir et al. 2004
Reference
Additive Effect of Nutrient Combinations with RS2 High Amylose Corn Ingredients on GI tract Related Events, Relative to the Non-RS Ingredient Alone
Table 10.10
Resistant Starch (RS) 233
234
Fiber Ingredients: Food Applications and Health Benefits
able carbohydrate component of a food, so are not relevant to testing the impact of RS. However when these tests are adapted to compare the glycemic impact of total carbohydrate present a true indication of the effect on glycemic response is revealed. Table 10.11 shows that RS2 can play an important role in foods across various populations including healthy people, people with type 2 diabetes, and people predisposed to metabolic syndrome. Figure 10.5 shows the glycemic response for two slices of bread (70 g serving, 36 g total carbohydrate) with or without a high-RS ingredient. In this study glycemic response was assessed according to the standard WHO protocol, modified for serving size and with a total carbohydrate comparison. Substituting part of the flour with the high-RS ingredient increased the dietary fiber content from 2 to 9 g per serving, resulting in a lower integrated two-hour area under the curve (AUC), and lower peak response (p < 0.05). This is consistent with other acute studies comparing low-RS with high-RS meals (Table 10.11). Figure 10.5 also shows that insulin response is beneficially influenced by RS inclusion. Due to the reduced contribution of RS to blood glucose, a lower insulin peak response and insulin AUC was observed (p < 0.05). This is also consistent with most of the studies listed in Table 10.11. Attenuation of insulin to a high-RS meal is typically more pronounced than the attenuation of glucose (Higgins et al. 2004), indicating that it is important to measure both glucose and insulin in these types of studies. For example, in Table 10.11 no difference in glucose AUC was observed in several studies even though insulin AUC and time-point response was decreased. The magnitude of the effect of RS on glucose and insulin response is dependent upon the amount of RS present relative to the amount and type of other carbohydrates present. Replacing more flour with RS will sequentially lower the glucose and insulin response. For example, Brown et al. (1995) reported that white bread containing 20% Hi-maize® starch had a 47% lower glucose AUC relative to a commercial white bread, almost twice the reduction of a bread containing 10% Hi-maize® starch, which had a 26% lower glucose AUC. Behall et al. (2002; 2006) reported that 13 g RS but not 6.5 g RS decreased both glucose and insulin AUC. Figure 10.6 compares the glucose peak for a series of breads made with increasing levels of RS2; from 0 to 40% flour replacement (70 g serving, 36 g total carbohydrate). The glucose peak (horizontal axis) was sequentially lowered with increasing flour replacement. Of note, the insulin peak response was well correlated, and can also be manipulated by replacing digestible starch with RS. Replacing digestible starch with RS will lower glucose and insulin response (Table 10.11). Other studies have looked at the effect of RS itself on glycemic management (e.g., RS was added to the diet not just substituted for digestible starch, and found that RS (by addition not substitution) can influence how well the body responds to the insulin that is produced). In a series of acute and longer term studies, RS2 from high-amylose corn increased insulin sensitivity, and higher glucose clearance was observed in both adipose and muscle tissue (Robertson et al. 2003; 2005). RS fermentation has been
Food
Bread Cracker Bread Muffin
Bread Muffins Cracker Sponge cake Bread Arepas Bread Pasta Hot mixed meal of meat, veg., rice Bread Cheesecake Muffin
Notes: (↓ = decreased; O = no effect).
Healthy Type 2 diabetics Type 2 diabetics Chronic Studies Healthy and hyperinsulinemic Healthy Healthy and hyperinsulinemic Metabolic syndrome predisposed
Healthy Healthy Healthy Healthy Healthy Healthy Healthy Healthy Healthy
Acute Studies
Subject Type
20g RS ingredient
1g RS ingredient / kg bw
10 g RS 16 g RS ingredient 50 g RS ingredient
13 or 22 g RS 6.5 g RS 1 g RS ingredient/kg bw 60 g RS ingredient 5%, 10%, 20% 45 g RS ingredient 16.5 g RS 20% flour replacement 41 g RS ingredient
Amount of RS Fed
Glucose Response (AUC) (Timepoint) O O ↓ O
↓ ↓
↓ ↓ ↓ ↓
↓ O O
Glucose Response ↓ ↓ ↓
↓ ↓
↓ ↓ ↓ ↓
↓ ↓ ↓ ↓
Insulin Response (AUC) O O ↓ ↓ ↓ ↓
↓ ↓ ↓ ↓
↓ ↓ ↓ ↓
↓ ↓ ↓ ↓
O
O
↓ ↓ ↓ ↓
↓ ↓ ↓
Insulin Response (Timepoint)
Behall et al. 1995 Behall et al. 1989 Howe et al. 1996 Noakes et al. 1996
Behall et al. 2002 Behall et al. 2006 Behall et al. 1988 Brighenti et al. 2006 Brown et al. 1995 Granfeldt et al. 1995 Hoebler et al. 1999 Hospers et al. 1994 van Amelsvoort et al. 1992 Weickert et al. 2005 Giacco et al. 1998 Krezowski et al. 1987
Reference
Effect of RS Meal Tolerance Tests on early Postprandial Glucose and Insulin Response in Human Subjects; RS2 High Amylose Corn Starch Meals Compared with control Meals Containing Digestible Carbohydrates of Similar Composition.
Table 10.11
Resistant Starch (RS) 235
236
Fiber Ingredients: Food Applications and Health Benefits Control bread
7
High amylose corn starch bread
Glucose (mmol/L)
6.5 6 5.5 5 4.5 4 3.5
0
20
40
60 80 Time (min)
100
120
0
20
40
60 80 Time (min)
100
120
400
Insulin (pmol/L)
350 300 250 200 150 100 50 0
Figure 10.5 Glucose and insulin response of bread with and without RS2 high amylose corn starch. Mean ± SEM.
postulated as a contributing factor as higher circulating SCFA, higher adipose SCFA uptake, and lower adipose free fatty acid output were reported. Future work is required to further understand the metabolic role of SCFAs in liver, muscle, and adipose tissue, and the relative importance of the ratio of individual SCFAs. Future studies could also explore longer term benefits of RS for glycemic management, to translate benefits observed in rat studies. Byrnes et al. (1995) fed rats diets containing digestible starch or RS2 and observed that the rats fed the digestible starch diets developed insulin resistance earlier, within eight weeks. By 12 weeks their insulin response to an in vivo glucose tolerance test was double that of the RS2 fed rats. If translated to humans, this could potentially delay the onset of diabetes.
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Insulin Peak (∆ from baseline)
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r = 0.91
300 280 260 240 220 200 180 160
1.2
1.4
1.6
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2
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Glucose Peak (∆ from baseline) Figure 10.6 Relationship between glucose peak (mmol/L) and insulin peak (pmol/L) for breads containing RS2 high amylose corn starch.
Weight Management RS is relevant to weight management in at least four ways: • • • •
Reduced available calories Increased satiety hormone production Modified body composition profile Modified energy partitioning
Available Calories Foods containing RS have a lower caloric contribution because RS does not contribute to available glucose. SCFAs generated by colonic RS fermentation do contribute some energy to the body. SCFAs can either be utilized by the colonic microflora (providing no energy to the body), utilized by the mucosa, or absorbed (providing some energy to the body). This is less metabolically efficient than metabolism of digestible starch. Typically the energy contribution of RS is one-third less than for digestible starches. Behall et al. (1996) reported a partial digestible energy value measured in humans of 11.7 kJ/g, and Keenan et al. (2006) reported a metabolizable energy value of 11.7kJ/g measured in rats. RS also contributes to increased energy wastage (excretion). For example, Behall and Howe (1996) reported in their human study that fecal energy was increased. In other human studies fecal excretion of fat, starch, fiber, and nitrogen/protein was increased (Behall and Howe 1996; Cummings et al. 1996; Alles et al. 1997; Heijnen et al. 1998; Hylla et al. 1998; Jenkins et al. 1999; Muir et al. 2004).
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Satiety Hormone Production Research into long- and short-term mechanisms of satiety and satiation is an emerging field. Recent research indicates that diets containing RS2 from high-amylose corn can influence intestinal production of the satiety hormones peptide YY (PYY) and glucagon-like peptide-1 (GLP-1). These hormones have a regulatory role in the ileal break to control stomach emptying and food intake (Zhou et al. 2006). In one study, Keenan et al. (2006) fed rats a low-RS digestible starch or high-RS diet, and observed increased serum PYY with higher cecal and large intestine PYY gene expression in the highRS-fed rats. GLP-1 was increased, with greater proglucagon gene (i.e., gene for GLP-1) expression in the cecum and large intestine. In a second study, Keenan et al. (2006) fed rats a high-RS or high-non-fermentable fiber diet. The RS-fed rats had greater plasma PYY and gene expression of PYY and proglucagon, indicating that fermentable RS is more efficacious due to its fermentation characteristics. Further clinical research is required to assess whether this benefit translates to human subjects and is applicable for weight loss or weight maintenance regimes. Body Composition Regional fat deposition is an important indicator of chronic disease. High-RS diets could help shift the body composition profile, which could be important for insulin resistance and metabolic syndrome development. Pawlak et al. (2004) fed rats high-RS diets by replacing digestible starch with RS2 from high-amylose corn and noted decreased total body fat and % adiposity, with increased lean mass. Importantly, regional body fat has been consistently decreased by high-RS diets across a number of animal studies, reported as: abdominal fat, epididymal fat, perirenal fat, mesenteric fat, gonadal fat, brown fat, peritoneal fat, and retroperitoneal fat (Keenan et al. 2006; Morita et al. 2005; Pawlak et al. 2001, 2004; Zhou et al. 1997). Energy Partitioning In the case for RS, changes in fat storage could be related to glucose and insulin response, insulin sensitivity, or lipid metabolism. A link is also being established between colonic fermentation and lipid metabolism, with acetate and propionate in particular being implicated. When high-RS diets are fed to rats, lipogenesis is lower in adipocytes, and adipocytes are smaller (Kabir et al. 1998A; Kabir et al. 1998B; Higgins et al. 2006;\). Changes in metabolic substrate selection have also been noted for high-RS diets. In an acute study Higgins et al. (2004) fed human subjects a low- or high-RS diet, with macronutrients and total fiber content controlled. Lipid oxidation was measured by respiratory quotient (RQ), which represents the balance between carbohydrate and lipid oxidation. Within two hours of consuming the meal 5.4 g of RS2 high-amylose corn starch reduced RQ, which continued to be lower than
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the control diet for up to six hours. This was associated with increased total and meal lipid oxidation, with a 23% increase in meal lipid oxidation during the following 24-hour period. Further studies are required to validate these observations over a longer time period, to demonstrate a benefit for weight reduction or maintenance regime.
Conclusion Dietary RS is a naturally occurring food polymer that is able to resist digestion in the small intestine and pass to the large intestine where it is fermented and can act as a fiber in the body. Although natural RS has been in the diet for centuries in relatively unprocessed foods, recent technological advancements have enabled food manufacturers to enrich and stabilize the RS content of many processed foods. RS is generally classified into four distinct categories: RS1, RS2, RS3, and RS4. First generations of commercial RS ingredients were based largely on crystalline amylose (RS3) with inherent organoleptic and cost limitations. These were followed with more user friendly granular ingredients (RS2s), which addressed many of the challenges of the earlier RS3s. Although recent commercial introductions expanded the use of commercial RS ingredients and have centered on the RS4 category of chemically modified materials including the soluble resistant dextrin types, more clinical research is needed to fully understand the differences and similarities among the various forms of RS. The analytical determination of RS is somewhat confusing as differing methodologies will give varying quantitative data based on the specific category of RS in the food itself. Further complications arise from the fact that there still is no regulatory definition of RS in the United States, and worldwide regulatory definitions do not necessarily agree with each other. Care must be taken when choosing which analytical method to use, and a solid understanding of fiber analytical techniques would be advised. RS has been the subject of nutritional research for almost 30 years. A large body of scientific evidence has validated the nutritional properties of RS2 from high-amylose corn. Recent discoveries have addressed the physiological importance of reduced digestibility and increased fermentability as researchers learn more about the relationship between the large intestine and integrated systemic functions. Moreover, human studies tend to indicate RS is well tolerated, an important feature of functional macronutrients. The major health benefits of dietary RS can be classified into three main areas that encompass digestive health, glycemic management, and weight control. Emerging research is expected to further validate the many health benefits of dietary RS.
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Acknowledgments The authors wish to acknowledge and thank Matthew R. Park and Wendy Dalidowicz at National Starch Food Innovation for their technical contributions.
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Toden, S., A.R. Bird, D.L. Topping, M.A. Conlon, Differential effects of dietary whey and casein on colonic DNA damage in rats, Australian Journal of Dairy Technology 60:44–46 (2005A). Toden, S., A.R. Bird, D.L. Topping, M.A. Conlon, Resistant starch attenuates colonic DNA damage induced by higher dietary protein in rats, Nutrition and Cancer 51:45–51 (2005B). Toden, S., A.R. Bird, D.L. Topping, M.A. Conlon, Resistant starch prevents colonic DNA damage induced by high dietary cooked red meat or casein in rats, Cancer Biology & Therapy 5:267–272 (2006). Tovar, J., Bioavailability of carbohydrates in legumes: digestible and indigestible fractions, Archivos Latino-americanos De Nutricion 44(4 Suppl 1):36S–40S (1996). van Amelsvoort, J.M.M., J.A. Weststrate, Amylose-amylopectin ratio in a meal affects postprandial variables in male volunteers, American Journal of Clinical Nutrition 55:712–718 (1992). van Munster, I.P., A. Tangerman, F.M. Nagengast, Effect of resistant starch on colonic fermentation, bile acid metabolism, and mucosal proliferation, Digestive Diseases and Sciences 39:834–842 (1994). Wacker, M., P. Wanek, E. Eder, S. Hylla, A. Gostner, W. Scheppach, Effect of enzymeresistant starch on formation of 1,N2-propanodeoxyguanosine adducts of trans4-hydroxy-2-nonenal and cell proliferation in the colonic mucosa of healthy volunteers, Cancer Epidemiology, Biomarkers and Prevention 11:915–920 (2002). Wang, X., I.L. Brown, A.J. Evans, P.L. Conway, The protective effects of high amylose maize (amylomaize) starch granules on the survival of Bifidobacterium spp. in the mouse intestinal tract, Journal of Applied Microbiology 87:631–639 (1999B). Wang, X., I.L. Brown, D. Khaled, M.C. Mahoney, A.J. Evans, P.L. Conway, Manipulation of colonic bacteria and volatile fatty acid production by dietary high amylose maize (amylomaize) starch granules, Journal of Applied Microbiology 93:390–397 (2002). Wang, X., P.L. Conway, I.L. Brown, A.J. Evans, In vitro utilization of amylopectin and high-amylose maize (amylomaize) starch granules by human colonic bacteria, Applied and Environmental Microbiology 65:4848–4854 (1999A). Weickert, M.O., M. Mohlig, C. Koebnick, J.J. Holst, P. Namsolleck, M. Ristow, M. Osterhoff, H. Rochlitz, N. Rudovich, J. Spranger, A.F.H. Pfeiffer, Impact of cereal fibre on glucose-regulating factors, Diabetologia 48:2343–2353 (2005). Wolf, B.W., L.L. Bauer, G.C. Fahey Jr, Effects of chemical modification on in vitro rate and extent of food starch digestion: an attempt to discover a slowly digested starch, Journal of Agricultural and Food Chemistry 47:4178–83 (1999). Woo, K., S.D. Bassi, C.C. Maningat, L. Zhao, E.E. Trompeter, G.A. Kelly, S. Ranjan, J. Gaul, C.T. Dohl, G.K. DeMeritt, G.J. Stempien, K.D. Krebbiel (inventors), Pregelatinized chemically modified resistant starch products and uses thereof, US patent application US 2006/0188631 (2006). Zhou, J., M. Hegsted, K.L. McCutcheon, M.J. Keenan, X. Xi, A.M. Raggio, R.J. Martin, Peptide YY and proglucagon mRNA expression patterns and regulation in the gut, Obesity 14:683–689 (2006). Zhou, X., M.L. Kaplan, Soluble amylose cornstarch is more digestible than soluble amylopectin potato starch in rats, Journal of Nutrition 127:1349–1356 (1997).
Section III
Conventional Fibers
11 Oat Fiber from Oat Hull J. Bodner and Susan S. Cho
Contents Introduction.......................................................................................................... 249 Production of Oat Fiber....................................................................................... 250 Characteristics...................................................................................................... 252 Application of Oat Fiber to Bakery Products and Pasta Shells..................... 252 Application of Oat Fiber to Light Bologna, Fat-Free Frankfurters, and Pork Products.............................................................................................. 253 Application of Oat Fiber to Yogurt and Frozen Desserts...............................254 Oat Fiber and Glycemic Control........................................................................254 Oat Fiber and Intestinal Regularity.................................................................. 255 Oat Fiber and Body Weight................................................................................ 256 Oat Fiber and Serum Lipids............................................................................... 257 Digestibility of Oat Fiber..................................................................................... 257 Fermentability...................................................................................................... 258 Effect of Oat Fiber on Nitrogen Metabolism.................................................... 258 Morphology of Large Intestine.......................................................................... 259 References............................................................................................................. 259
Introduction Oat hulls comprise approximately 30% by weight of the grain. Traditionally, oat hulls were discarded during processing or used as animal feeds (Dougherty et al. 1988). Recently it has become an important ingredient that can be incorporated in several food formulations due to its high fiber content (about 90%), higher than wheat (42% to 47%) or corn bran (62%). However, gritty texture and degradation of dough properties are frequently associated with high fiber addition, because these brans and fibers tend to hydrate superficially, reducing the particles’ swelling in the dough matrix (Gould et al. 1989). These physical properties of oat fiber have been improved by physico249
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chemical treatments, such as hydrogen peroxide treatments in combination with heating. In meat products, oat fibers act as an extender. Since fat gives a lubricating mouthfeel, some products tend to feel dry and a bit rubbery when fat is removed. Oat fiber can minimize that effect and make the texture soft. Oat fiber can also be successfully used in formulations of high-fiber bakery products, yogurts, and frozen desserts. Oat fibers have shown various health benefits. Numerous studies indicated that oat fiber was effective in controlling glycemic responses (Anderson et al. 1991; Weickert et al. 2005) and improving intestinal regularity (Stephen et al. 1997). Also studies (Cameron et al., 1991; Younes et al., 1995) showed that the addition of oat fiber to the diet induced a decrease in blood urea and renal nitrogen excretion relative to the control, indicating a potential for oat fiber diet therapy in chronic renal disease. A pig study (Thomsen et al., 2006) suggests that oat fiber may play a role in the susceptibility to intestinal helminth infections and intestinal morphology.
Production of Oat Fiber Ground oat hulls have been used in animal feed for some time, and largescale production of oat fiber for human consumption began in the 1980s. One of the first commercial production plants for oat fiber utilized the processes outlined by Gould (1987 and 1988) in patents 4,649,113 and 4,774,098. These patents describe the use of an alkaline peroxide solution for bleaching and partial delignification of the oat hulls to produce an edible oat fiber. The resultant fiber had an increased water retention capacity that improved textural properties. Another process method that has been commercially implemented for oat fiber production was described by Ramaswamy (1988) in the patent 5,023,103. As noted in this patent, the lignin portions of the oat hulls contain silica, which results in a gritty texture. This method uses a sodium hydroxide solution under high temperature and high pressure to dissolve the lignin and silica structures. The resulting fiber has a significantly improved texture and greatly increased water retention capacity. These processes solubilize a portion of the lignin, originally present in the lignocellulosic matrix. Thus processed oat fiber can have increased water holding capacity, which contributes to improved sensory and functional properties of food products containing oat fiber (Gould et al. 1989). In addition, several researchers have developed laboratory scale processes to improve functionality of oat fiber. In a study of Dougherty et al. (1988), bleached oat fiber was prepared by water washing oat hulls to remove impurities and adding food-grade hydrogen peroxide in an alkaline environment (pH 10 to 12) for 1-2 hr at an elevated temperature (50°C–100°C). The hulls were washed with water, neutralized with hydrochloric acid, and washed
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again to remove any residual acid. The bleached product was then dried at 330°F (165°C) air, and ground in a hammer mill. Inglett (1995) processed oat hulls in multistep shear process and long time of digestion (up to 72 h) with alkaline hydrogen peroxide. Larrea et al. (1997) pretreated rice hulls with alkaline solution of hydrogen peroxide followed by extrusion. However, these procedures are time consuming and have the disadvantage of generating a great volume of effluents. To overcome these problems, Galdeano and Grossmann (2005) developed a one-step process with short time of reaction to improve hydration capacity of oat hull fibers. Most of the various oat fiber production techniques previously described involve an extraction process. In these processes the starting oat hulls are exposed to varying levels of chemicals and heat in order to remove certain fractions while preserving others. Typically the majority of the starch, protein, and fat portions of the oat hulls are removed in even the most minimally extracted fiber, while the lignin, hemicellulose, cellulose, and silica portions of the oat hull are preserved. As the extraction process is intensified (through the use of higher chemical loads or increased temperature/pressure) more of the lignin structure starts to be degraded. As the lignin is removed, there is also a decrease in the ash/silica content of the oat hulls and a reduction in the gritty texture of the fiber. The removal of the lignin also allows the fiber bundles to separate into individual fiber strands (defibrillation). These individual fiber strands have much more surface area and are able to freely swell and absorb liquids. The photos in Figure 11.1 and Figure 11.2 show two examples of oat fiber at opposite ends of the extraction spectrum. The minimally extracted oat fiber (Figure 11.1) consists primarily of milled fiber bundles with only a small amount of individual defibrillated fibers. The water absorption properties of this type of fiber would be relatively low. This oat fiber would be useful as an economical source of dietary fiber for items such as cereal, granola bars, cookies, and other low-moisture, high-texture applications. Contrasted with the minimally extracted oat fiber, the highly extracted fiber (Figure 11.2) con-
Figure 11.1 Minimally extracted oat fiber.
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Figure 11.2 Highly extracted oat fiber.
sists almost entirely of small defibrillated strands. This results in a fiber with extremely high water and oil absorption and a low density. This type of fiber would be appropriate for use as a binder/extender in processed meats. It also could be used as carrier for oil-based flavors/colors. Another interesting use for this type of fiber is for structural enhancement of fragile products. When incorporated at low levels (2% to 3%), these long-stranded fibers act like reinforcing rods in items like ice cream cones, pretzels, and other crisp snacks to reduce breakage.
Characteristics • 90% total dietary fiber • Water binding up to 800%
Application of Oat Fiber to Bakery Products and Pasta Shells In Western countries, it is essential to increase the fiber intake levels. Fortification of various foods with oat fiber can help improve the fiber intake status of the population. Manufacturers of low-carbohydrate bakery products need to replace flour with fiber ingredients in the formulation. Oat fiber has desirable water-holding capacity, mixes easily into doughs, and does not affect color and flavor. A minimally extracted oat fiber with improved waterbinding capacity would be desirable for manufacturing of crackers, cookies, and ice cream cones. In these products, too much water binding could
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damage product integrity since too much water causes structural problems and changes sensory properties. Food products can become bland because the flavor components are diluted with water. Excess water also decreases strength in baked products by preventing dough from rising. Addition of oat fiber made it possible to produce high-fiber cookies without sacrificing sensory properties (Dougherty et al. 1988; Galdeano and Grossman 2005). In a study of Galdeano et al. (2006), cookies were prepared with the replacement of 20% of wheat flour by physicochemically (extrusion and alkaline hydrogen peroxide) treated oat hulls. Cookies elaborated with the untreated hulls were used as control. Cookies were evaluated for their physical (spread ratio, specific volume, and color) and sensory characteristics, and no difference was detected (p < 0.05) among the cookies in relation to the physical properties. Oat fiber cookies contained 10.6% of fiber and obtained 91% acceptance when evaluated by potential consumers of the product. Oat hull fiber was also used as a fiber source for bread (14.4% to 15.5% fiber vs. 1.5% in white bread) and soft cookies (9.8% to 12.0% fiber; Dougherty et al. 1988). The bread loaf containing bleached oat fiber had an appealing creamy white interior without any objectionable flavor or aroma. Also addition of oat fiber to pasta shell (2.4% fiber vs. 0.8% in conventional pasta shell) did not affect cooking quality (Dougherty et al. 1988). Longer-strand fibers generally hold more water and reinforce a rod-type structural component. High-water-absorption fibers also tend to deter susceptibility to breakage. Longer-strand fibers are used to prevent bagel chips from deteriorating and resulting in a fine dust at the bottom of the bag.
Application of Oat Fiber to Light Bologna, FatFree Frankfurters, and Pork Products Reducing fat in processed meat products can be accomplished by using leaner meats and by dilution of the fat with added water and other nonmeat ingredients (Steenblock et al. 2001). In developing low-fat products, it is essential to find ingredients that can hold water since adding water to meat products increases cooking losses and purge. Oat fiber has high waterholding capacity (Zarling 1994), thus it can be successfully used in the formulations of various meat products. The USDA has allowed the addition of oat fiber (which can be labeled as isolated oat product) up to 3.5% in meat and poultry products including sausages and franks. Steenblock et al. (2001) reported that addition of both types of oat fiber at 3% produced greater processing yield for both bologna and frankfurters. Two varieties of oat fiber, bleached and high absorption oat fibers (each at three levels ranging from 1% to 3%), were studied to determine effects of the oat fiber on quality characteristics of light bologna and fat-free frank-
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furters. Results indicated that addition of both types of oat fiber produced greater yields, and lighter, less red color. Purge was reduced with oat fiber at 3%. Product hardness increased for bologna with both fiber types. Results indicated that addition of both types of oat fiber at 3% produced greater processing yield for both bologna and frankfurters. Product moistness assessed by the sensory panel was also reduced as oat fiber was increased. A similar positive effect of oat fiber was reported in processing of pork products (Lee et al. 1990) and beef patties (Berry 1997).
Application of Oat Fiber to Yogurt and Frozen Desserts Fernandez-Garcia et al. (1988) found that oat fiber addition improved the body and texture of unsweetened yogurts. In their study, calorie-reduced yogurts that were fortified with 1.32% oat fiber were prepared from lactosehydrolyzed milk, alone and supplemented with 2% to 4% sucrose or with 1.6% to 5.5% fructose. Fiber addition led to increases in concentrations of acetic and propionic acid. After 28 days of storage, Lactobacilli counts were consistently higher in fiber-fortified yogurts, but total bacteria counts were lower. Apparent viscosity increased with the addition of sweetener and oat fiber. This study indicated that oat fiber addition improved the body and texture of unsweetened yogurts but lowered overall scores for body and texture in yogurts sweetened with sucrose.
Oat Fiber and Glycemic Control Insoluble fibers can reduce blood glucose levels in people with and without diabetes. A couple of human studies (Anderson et al. 1991; Weickert et al. 2005) indicated that oat fiber can modulate glycemic responses. Anderson et al. (1991) reported that oat fiber diet decreased fasting blood glucose levels by 13% (p < 0.05), although significant decreases in blood glucose levels were not maintained during the ambulatory phase. In this study, eight lean men with type 2 diabetes consumed a traditional diabetes diet for one week, followed by a control diet plus 30 g/day of insoluble oat fiber for two weeks in a hospital metabolic ward. The oat fiber was well accepted and produced no serious side effects. The authors concluded that oat fiber may have beneficial metabolic effects in persons with type 2 diabetes. In a study of Weickert et al. (2005), 14 healthy women consumed three matched portions of control or fiber-enriched bread (10.4 to 10.6 g/portion; wheat fiber, oat fiber). Fiber enrichment accelerated the early insulin response (p < 0.001 for oat fiber). It was also associated with an earlier postprandial
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glucose dependent insulinotropic polypeptide (GIP )response after oat fiber. A reduced postprandial glucose response occurred on the following day subsequent to ingestion of a control meal. No differences in insulin responses were observed after the fiber-enriched diets compared with control (p>0.15). The authors concluded that only 30 g of insoluble dietary fiber from wheat or oats reduce blood sugar levels without raising the insulin response, and contribute to a significant improvement in the glucose metabolism.
Oat Fiber and Intestinal Regularity Four out of five animal studies (Lopez-Guisa et al. 1988; Wang et al. 1994; Hetland et al. 2001; Mateos et al. 2006) and three out of four human studies (Zarling et al. 1994; Sunvold et al. 1995; Stephen et al. 1997)reported that oat fiber was effective in improving intestinal regularity, indicating that oat fiber has a role in relieving constipation and/or diarrhea. In a pig study of Mateos et al. (2006), it was reported that the inclusion of moderate levels of fiber as oat hulls reduces the incidence of diarrhea. This experiment was conducted to investigate the influence of the main cereal (cooked maize or cooked rice) and the inclusion of cooked and expanded oat hulls (0, 20, or 40 g/kg) in the diet on total tract apparent nutrient digestibility and productive performance of piglets weaned at 21 days. Each of the six treatments was replicated eight times (five piglets penned together), and the trial lasted for 33 days. From 21 to 41 days of age piglets were given their respective experimental complex diets that contained 530 g/kg cooked cereal, and from 41 to 54 days they received a common starter diet based on maize, barley, and soya-bean meal. The inclusion of oat hulls in the diet tended to reduce the incidence of diarrhea from 21 to 41 days of age (p < 0.01). In a young broiler chicken study of Hetland and Svihus (2001), there was a tendency (p = 0.08) for faster feed passage with inclusion of coarsely ground oat hulls. But no effect of finely ground oat hulls was found (wheat or naked oats base was mixed with 0, 40, or 100 g/kg oat hulls, which replaced a maize starch/soy isolate mixture). In a rat study of Lopez-Guisa et al. (1988), addition of 5% to 15% oat hulls (processed oat hulls, bleached oat hulls, and processed oat hulls coated with starch) in the diet increased fecal weights, and fresh and dry fecal weights increased linearly as the concentration of oat hulls increased. Table 11.1 summarizes various studies related to the effects of oat fiber on intestinal regularity. In a study with 10 healthy males (aged 20 to 37 years, who ate, for two- to three-week periods), Stephen et al. (1997) reported that the diet with 25 g providing oat hull fiber per day (17 g of NSP/day) increased fecal weight from 113 +/– 10.4 to 155 +/– 10.8 g/day (P < 0.001) with no change in transit time. A controlled low-fiber diet contained 13.1 g of non-starch polysaccharide per day. In a crossover study (10 days for each period with a 10-day
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Table 11.1 Oat Fiber and Intestinal Regularity Positive effects Broiler chickens (Hetland and Svihus. 2001) Rats (Lopez-Guisa et al. 1988) Pigs (Mateos et al. 2006) Rats (Wang et al. 1994) Human (Sunvold et al. 1995) Human (Stephen et al. 1997) Human (Zarling et al. 1994)
No effect Broiler breeders (Hocking et al. 2004) Human (Kapadia et al. 1995)
washout period) of Zarling et al. (1994), the effect of 28.8 g/day of a 50% soy and 50% oat fiber combination was investigated in 10 medically stable residents of a chronic care facility. Oat fiber (14.4 g/L of fiber) significantly increased the number of bowel movements per day (0.9 +/– 0.4 vs. 0.5 +/– 0.2, p < 0.05) and fecal weights (57 +/– 31 vs. 32 +/– 25 g/day, p < 0.05). Fiber also caused a significant increase in fecal nitrogen output (110 +/– 65 vs. 75 +/– 74 mg/day, p < 0.05) and fecal energy (141 +/– 73 vs. 76 +/– 62 kcal/day, p < 0.05). Fiber did not affect fecal moisture, gastric emptying, or intestinal transit time. The authors conclude that the addition of a combination of soy and oat fiber to tube-feeding material is well tolerated, and promotes regular bowel movements without altering the rate of gastric emptying or intestinal transit time. In a healthy human subject study of Sunvold et al. (1995), it was reported that consumption of diet containing 3.4% oat fiber resulted in slightly firmer stools and provided the greatest amount of fecal output per unit fiber intake.
Oat Fiber and Body Weight A human study indicates that oat fiber may not have any effect on body weight control when eaten ad libitum (Wang et al. 1994). Hetland and Svihus (2001) reported that inclusion of oat hulls in wheat-based broiler diets did not affect weight gain. Feed consumption increased significantly when oat hulls were included in the diet, and relative gut weight increased correspondingly (P<0.05). In this study, wheat- or naked-oats-based diets with or without NSP-degrading enzymes were mixed with 0, 40, or 100 g/kg oat hulls, which replaced a maize starch/soy isolate mixture, and the diets were fed to broiler chickens from 7 to 21 days of age. In grower pigs, the addition of oat hulls (high, 5.0%; low, 3.6% crude fiber) did not affect average daily gain or feed efficiency (P > 0.10; Zervas and Zijlstra 2002).
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Oat Fiber and Serum Lipids Anderson et al. (1991) reported that an oat fiber diet decreased low-density lipoprotein cholesterol by 8.9% (p < 0.05) and apolipoprotein B-100 by 17% (p < 0.01). Other serum lipid levels did not change significantly, and values returned to pretreatment levels during the ambulatory phase. In this study, eight lean men with type 2 diabetes consumed a traditional diabetes diet for one week, followed by a control diet plus 30 g/day of insoluble oat fiber for two weeks in a hospital metabolic ward. However, animal studies (LopezGuisa et al. 1988; Sunvold et al. 1995) indicated that oat hull fiber did not affect serum lipid levels.
Digestibility of Oat Fiber Oat hulls contain a relatively high amount of ferulic acid (4-hydroxy-3-methoxycinnamic acid), which is known to have inhibitory effects on oat hull biodegradability by rumen microorganisms (Yu et al. 2002). Removing ferulic acid from oat hulls could improve rumen biodegradability and nutritional values of oat hulls (Garleb et al. 1991). It was reported that men fed diets containing oat fiber had lower digestibility of total dietary fiber as compared to a soy fiber diet (Sunvold et al. 1995). In this study, 18 healthy males with a body weight of 70.0 +/– 3.1 kg consumed three defined-formula diets that varied only in their fiber and/or lipid components: (1) 6.4% fiber (100% soy polysaccharides) and 13.1% lipid (50% medium-chain triacylglycerols, 40% corn oil, and 10% soy oil); (2) 3.4% fiber (75% oat fiber, 17.5% gum arabic, and 7.5% carboxymethylcellulose) and 15.6% lipid (20% medium-chain triacylglycerols, 50% canola oil, and 30% high oleic acid safflower oil); and (3) 4.4% fiber (same as diet 2) and 14.5% lipid (same as diet 1). Hetland and Svihus (2001) studied the effects of inclusion of oat hulls in diets based on digestibility of whole or ground wheat for broilers. Starch digestibility was significantly increased by inclusion of oat hulls for broilers. Heifers fed diets containing treated oat hulls had higher digestible dry matter and fiber intakes than controls. Lopez-Guisa et al. (1988) evaluated processed oat hulls as potential dietary fiber sources. Three levels (5%, 10%, and 15%) of processed oat hulls, bleached oat hulls, or oat hulls coated with starch, were added to purified diets and fed to rats for six weeks. Control diets consisted of 5% to 15% alpha-cellulose or commercial nonpurified diet. Apparent digestibility of fiber in all diets was low (Lopez-Guisa et al. 1988). However, Mateos et al. (2006) reported that inclusion of oat hulls in diets for young pigs did not affect nutrient digestibility. Overall, appears that treated oat hulls are promising ingredients in diets of growing ruminants (Cameron et al. 1991).
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Fermentability It is known that the physicochemical characteristics of fiber modify their fermentation characteristics in the colon. Various studies (Titgemeyer et al. 1991; Bourquin et al. 1993; Roland et al. 1995) indicated that oat fiber does not readily produce short-chain fatty acids (SCFAs) during anaerobic fermentation in the colon. Titgemeyer et al. (1991) conducted two studies with human fecal bacteria as inoculum to assess fermentation of various fiber sources and to quantify the SCFAs produced. Substrate fermentability based on total SCFA production ranked as follows: citrus pectin > soy fiber > sugar beet fiber > pea fiber > oat fiber. Bourquin et al. (1993) also studied in vitro fermentability of various fiber sources with human colonic bacteria obtained from each of three adult male subjects. Substrates tested were two varieties of oat hull fiber, gum arabic, carboxymethylcellulose (CMC), soy fiber, psyllium, and six blends containing oat fiber, gum arabic, and CMC in various proportions. All substrates contained greater than 900 g/kg of total dietary fiber except for CMC (816 g) and soy fiber (778 g). In vitro organic matter disappearance during fermentation was less than 20% for the two oat fibers, CMC, and psyllium; intermediate for soy fiber (56.4%); and the greatest for gum arabic (69.5%). Averaged across substrates, acetate, propionate, and butyrate were produced in the molar proportion of 64:24:12. Roland et al. (1995) also confirmed that the lowest amounts of gases and SCFA were found in rats fed on wheat bran, pea, and oat fiber. Cameron et al. (1991) reported that heifers fed larger amounts of treated oat hulls had higher molar percentage acetate, and greater acetate:propionate ratios than controls.
Effect of Oat Fiber on Nitrogen Metabolism The availability of fermentable carbohydrates could influence the digestive degradation and urea excretion (Cameron et al. 1991; Roland et al. 1995; Younes et al. 1995). Cameron et al. (1991) reported that heifers fed larger amounts of treated oat hulls had lower ruminal pH and ammonia N concentrations than controls. Roland et al. (1995) compared the effects of a poorly fermented cellulosic oat fiber, a soluble fermentable fiber (gum arabic) or one of two oligosaccharides (fructooligosaccharide or xylooligosaccharide) on nitrogen excretion in male Wistar rats (control: a wheat starch-based diet). The fibers and oligosaccharides were added to the semipurified diets at 7.5 g/100 g in place of wheat starch. Compared with rats fed the oat-fiber-based diet, urea flux from blood to cecum was nearly 50% greater and more than 120% greater in those fed the gum arabic and oligosaccharide diets, respectively. A rat study of Younes et al. (1995) also indicated that as a percentage of total excreted nitrogen, fecal nitrogen was 20% in the oat fiber group,
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compared with only 10% in fiber-free controls. However, in grower pigs, the addition of oat hulls (3.6% to 5.0% crude fiber) did not affect N excretion patterns and plasma urea (p > 0.10; Zervas and Zijlstra 2002). Overall results indicate that the addition of oat fiber to the diet induced a decrease in blood urea and renal and renal nitrogen excretion relative to the control, indicating a potential for oat fiber diet therapy in chronic renal disease.
Morphology of Large Intestine Thomsen et al. (2006) reported that both T. suis infection and dietary carbohydrates significantly influence the morphological architecture and the production and composition of mucins in the large intestine of pigs. An experiment was performed to study the influence of Trichuris suis infection and type of dietary carbohydrates on large intestine morphology, epithelial cell proliferation, and mucin characteristics. Two experimental diets were based on barley flour; oat hull meal was supplemented with oat hull meal, while sugar beet fiber/inulin meal was supplemented with sugar beet fiber and inulin. In this experiment, 32 pigs were allocated randomly into four groups. Two groups were fed oat hull meal and two groups sugar beet fiber/ inulin meal. Pigs from one of each diet group were inoculated with a single dose of 2000 infective T. suis eggs and the other two groups remained uninfected controls. All the pigs were slaughtered eight weeks post-inoculation (p.i.). Pigs fed oat hull meal had larger crypts both in terms of area and height than pigs fed sugar beet fiber and inulin, and T. suis infected pigs on both diets in Experiment 1 had larger crypts than their respective control groups. The area of the mucin granules in the crypts constituted 22% to 53% of the total crypt area and was greatest in the T. suis infected pigs fed oat hull meal. Epithelial cell proliferation was affected neither by diet nor infection in any of the experiments. The study suggests that both diet and infection factors are important in large intestine function and that fibers may play a role in the susceptibility to intestinal helminth infections.
References Anderson JW, Hamilton CC, Horn JL, Spencer DB, Dillon DW, Zeigler JA. 1991. Metabolic effects of insoluble oat fiber on lean men with type II diabetes. Cereal Chem. 68: 291–294. Berry BW. 1997. Effects of formulation and cooking method on properties of low-fat beef patties. J Food Serv Sys. 9: 211–228.
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Bollinger H & Noll B. 1999. Oat fiber — second generation dietary fiber Food Marketing Technol. 13:2, 5–6,8. Bourquin LD, Titgemeyer EC, Fahey GC Jr, Garleb KA. 1993. Fermentation of dietary fiber by human colonic bacteria: disappearance of short-chain fatty acid production from, and potential water-holding capacity of, various substrates. Scand J Gastroenterol. 28(3):249–255. Cameron MG, Cremin JD Jr, Fahey GC Jr., Clark JH, Berger LL, Merchen NR. 1991. Chemically treated oat hulls in diets for dairy heifers and wethers: effects on intake and digestion. J Dairy Sci. 74:190–201. Cherney DJ, Siciliano-Jones J, Pell AN. 1993. Technical note: forage in vitro dry matter digestibility as influenced by fiber source in the donor cow diet. J Anim Sci. 71:1335–1338. Dougherty M, Sombke R, Irvine J, Rao CS. 1988. Oat fibers in low calorie breads, soft type cookies, and pasta. Cereal Foods World 33:424–427. Fernandez-Garcia E, McGregor JU, Traylor S. 1988. The addition of oat fiber and natural alternative sweeteners in the manufacture of plain yogurt. J Dairy Sci. 81: 655–663. Galdeano MC, Grossmann MVE. 2005. Effect of treatment with alkaline hydrogen peroxide associated with extrusion on color and hydration properties of oat hulls, Brazilian Arch Biol Technol. 48: 63–72. Garleb A., Bourquin LD, Hsu JT, Wagner GW, Schmidt SJ, Fahey GC Jr. 1991. Isolation and chemical analyses of nonfermented fiber fractions of oat hulls and cottonseed hulls. J Anim Sci. 69:1255–1271. Gould JM, Jasberg BK, Dexter LB, Hsu JT, Lewis SM, Fahey GC Jr. 1989. High-fiber, noncaloric flour substitute for baked foods. Properties of alkaline peroxidetreated lignocellulose, Cereal Chem. 66: 201–205. Hetland H, Svihus B. 2001. Effect of oat hulls on performance, gut capacity and feed passage time in broiler chickens. Br Poult Sci. 42:354–361. Hocking PM, Zaczek V, Jones EK, Macleod MG. 2004. Different concentrations and sources of dietary fiber may improve the welfare of female broiler breeders. Br Poult Sci. 45:9–19. Inglett GE. 1995. Dietary fiber gels for preparing calorie reduced foods, U.S. Patent application serial number 08/563,834, November 28, 1995. Kapadia SA, Raimundo AH, Grimble GK, Aimer P, Silk DB. 1995. Influence of three different fiber-supplemented enteral diets on bowel function and short-chain fatty acid production. J Parenter Enteral Nutr. 19:63–68. Larrea MA, Grossmann MVE, Beleia AP. 1997. Changes in water absorption and swollen volume in extruded alkaline peroxide pretreated rice hulls, Cereal Chem. 74: 98–101. Lee S-F. 1990. The utilization of oat fiber and sodium erythorbate for the improvement of PSE pork quality. Thesis (M.S.), Iowa State University. Lopez-Guisa JM, Harned MC, Dubielzig R, Rao SC, Marlett JA. 1988. Processed oat hulls as potential dietary fiber sources in rats. J Nutr. 118:953–962. Mateos GG, Martin F, Latorre MA, Vicente B, Lazaro R. 2006. Inclusion of oat hulls in diets for young pigs based on cooked maize or cooked rice. Animal Sci Intl J Fund Appl. Res. 82:57–63. McPherson-Kay R. 1987. Fiber, stool bulk, and bile acid output: implications for colon cancer risk. Prev Med. 16:540–544. Ramaswamy SR. 1988. Fiber and method of making. 07/285,356, December 14, 1988.
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Roland N, Nugon-Baudon L, Andrieux C, Szylit O. 1995. Comparative study of the fermentative characteristics of inulin and different types of fiber in rats inoculated with a human whole faecal flora. Br J Nutr. 74:239–249. Steenblock RL, Sebranek JG, Olson DG, Love JA. 2001. The effects of oat fiber on the properties of light bologna and fat-free frankfurters. J Food Sci. 66:1409–1415. Stephen AM, Dahl WJ, Johns DM, Englyst HN. 1987. Effect of oat hull fiber on human colonic function and serum lipids. Cereal Chem. 74: 379–383. Sunvold GD, Titgemeyer EC, Bourquin LD, Fahey GC, Garleb KA. 1995. Alteration of the fiber and lipid components of a defined-formula diet: effects on stool characteristics, nutrient digestibility, mineral balance, and energy metabolism in humans. Am J Clin Nutr. 62:1252–1260. Thomsen LE, Knudsen KE, Hedemann MS, Roepstorff A. 2006. The effect of dietary carbohydrates and Trichuris suis infection on pig large intestine tissue structure, epithelial cell proliferation and mucin characteristics. Vet Parasitol. 142:112–122. Titgemeyer EC, Bourquin LD, Fahey GC, Garleb KA. 1991. Fermentability of various fiber sources by human fecal bacteria in vitro. Am J Clin Nutr. 53:1418–1424. Wang Y, Funk MA, Garleb KA, Chevreau N. 1994. The effect of fiber source in enteral products on fecal weight, mineral balance, and growth rate in rats. JPEN J Parenter Enteral Nutr. 18:340–345. Weber CW, Kohlhepp EA, Idouraine A, Ochoa LJ. 1993. Binding capacity of 18 fiber sources of calcium. J Agric Food Chem. 41:1931–1935. Weickert MO, Mohlig M, Koebnick C, Holst JJ, Namsolleck P, Ristow M, Osterhoff M, Rochlitz H, Rudovich N, Spranger J, Pfeiffer AFH. 2005. Impact of cereal fiber on glucose-relating factors. Diabetologia 48: 2343–2353. Younes H, Garleb K, Behr S, Rémésy C, Demigné C. 1995. Fermentable fibers or oligosaccharides reduce urinary nitrogen excretion by increasing urea disposal in the rat cecum. J Nutr. 125:1010–1016. Yu P, Maenz DD, McKinnon JJ, Racz VJ, Christensen DA. 2002. Release of ferulic acid from oat hulls by Aspergillus ferulic acid esterase and trichoderma xylanase. J Agric Food Chem. 50(6):1625–1630. Zarling EJ, Edison T, Berger S, Leya J, DeMeo M. 1994. Effect of dietary oat and soy fiber on bowel function and clinical tolerance in a tube feeding dependent population. J Am Coll. Nutr. 13:565–568. Zervas S, Zijlstra RT. 2002. Effects of dietary protein and oat hull fiber on nitrogen excretion patterns and postprandial plasma urea profiles in grower pigs. J Ani Sci. 80:3238–3246.
12 Cellulose Toru Takahashi
Contents Characteristics...................................................................................................... 263 Functionality and Food Applications............................................................... 264 Functionality............................................................................................... 264 Effects of Cellulose on Stool Output and Constipation............. 264 Fermentation in the Large Intestine............................................. 265 Dilution Effect................................................................................. 266 Effects on Carcinogenesis and Cell Proliferation....................... 266 Effects on Fats.................................................................................. 267 Effects on Carbohydrates............................................................... 267 Effect on Water Absorption in the Intestine............................... 269 Effects on Proteins.......................................................................... 270 Physiological Benefits of Hydroxypropylmethylcellulose........ 270 Food Applications....................................................................................... 271 Physiological Benefits.......................................................................................... 272 Significance of Mixing-In Behavior of Nutrients in the Lumen.......... 272 Flow Behavior in the Lumen of the Intestine Produced by Peristalsis......................................................................................... 275 Flow Behavior of the Intestinal Contents with Segmentation............. 276 Interrelationship between the Behavior of Nutrients and Cellulose.. 276 Safety and Technology........................................................................................ 277 References............................................................................................................. 277
Characteristics Cellulose is a linear polymer of β-1,4-d‑glucopyranose units. Natural cellulose can be divided into two groups: crystalline and amorphous. The overall structure of natural cellulose is crystallized. Cellulose is one of the most common biopolymers on earth because it forms the primary structural component of all green plants, including vegetables.1 Accordingly, cellulose is a common component of our diet. 263
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Modified celluloses and cellulose derivatives are also used as food ingredients. Cellulose and its derivatives include physically modified celluloses such as powdered and microcrystalline cellulose and chemically modified cellulose derivatives such as hydroxypropylmethyl, methyl, and carboxymethyl celluloses.2 The difference between cellulose and its derivatives is the extent of crystallization with crystal-forming hydrogen bonds. The water insolubility of cellulose is caused by its crystalline structure, which is tightly packed with intra- and intermolecular hydrogen bonds. To convert cellulose into its derivatives, which are water soluble, it is necessary to break hydrogen bonds and disturb the crystalline structure of cellulose.3 Cellulose derivatives have high solubility, and their solutions are viscous.3 Although powdered and microcrystalline celluloses have high crystallization, their suspensions in water, dough, and intestinal contents can change their rheological properties.3–5 The shape, particle size, surface activity, and water-holding capacity of such celluloses are important factors determining their properties and functionality.3, 5–7 Powdered and microcrystalline cellulose are thought to be relatively inert, with the exception of effects caused by adsorption and dilution. In this chapter, I discuss the functionality and application of celluloses and cellulose derivatives. I also describe the properties of microcrystalline cellulose in the gastrointestinal tract.
Functionality and Food Applications Functionality Effects of Cellulose on Stool Output and Constipation Epidemiologically, a lack of fiber (cellulose and pentose) may play an important role in the etiology of chronic idiopathic constipation in children.8 Cellulose is difficult for human enzymes to digest. Since large amounts of cellulose are not degraded in the gastrointestinal tract, the intestinal content and feces volume increase with cellulose intake. This may lead to increasing stool output with a shorter transit time and decreased stool pH in humans ingesting crystalline cellulose.9,10 In 80% to 90% of obese patients, the administration of 2.4 or 3.6 g of microcrystalline cellulose leads to defecation improvement.11 Daily consumption of 16 g of cellulose for one month significantly increased daily wet stool weight and frequency of defecation in healthy women.12 Consequently, cellulose can be used to improve defecation.13 Transit time in the gastrointestinal tract, the time to the first appearance of indigestible markers in feces, may be independent of microcrystalline cellulose ingestion. Studies have indicated that a single 5-g dose or a daily 16-g dose of microcrystalline cellulose for one month does not affect transit time, but improves defecation in healthy men14 and women,12 respectively.
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The frequency of defecation and weight of feces are associated with mean retention time in the digestive tract in dogs.15 Theoretically, increased feces weight should be more closely associated with a longer mean retention time than with transit time.16 In dogs, feces quality depends on the fiber length of cellulose, which might be related to water-holding capacity.17 Fiber length6 and water-holding capacity of insoluble fiber (Takahashi et al. unpublished data) are important factors affecting the physical properties of intestinal contents. Crystalline cellulose longer than 120 µm has a higher water-holding capacity than fibers shorter than 100 µm in vitro.4 Increased length and water-holding capacity of cellulose might be important to feces quality by improving the physical properties of feces. The addition of microcrystalline cellulose increases the viscosity and water content of rat intestinal contents,5 water content of rat feces,18 and human masticatory substances (Takahashi et al. unpublished data). The relationship between the alteration of the physical properties of the intestinal contents or masticatory substances by adding microcrystalline cellulose and the improvement of defecation is still unknown. Chemically modified cellulose derivatives also control constipation. Methylcellulose improves occasional constipation among patients using fiber therapy.19 Methylcellulose, in a daily 1-g dose, can be used as an effective laxative.20 Fermentation in the Large Intestine Microcrystalline cellulose is an energy source in humans21,22 as well as in herbivorous animals.23 Some species of bacteria such as Ruminococcus albus, Bacteroides succinogenes, and Clostridium lochhradii can metabolize crystalline cellulose in the gastrointestinal tract.23 Kelleher et al.24 reported that fecal recovery of insoluble 14C was 51% (34% to 72%) after administration of powdered 14C-cellulose. Cellulose is metabolized in the large intestine, and its end products are short-chain fatty acids,10 which are absorbed in the wall of the large intestine.25 The yield of short-chain fatty acids averages 1.05 mol for each 1 mol of hexose equivalent.26 Short-chain fatty acids correspond to 1200 kJ/mol (286 kcal/mol).27 If 51% of cellulose is fermented to short-chain fatty acids24 and 99% of short-chain fatty acids are absorbed in the gastrointestinal tract,27 cellulose should result in digestible energy of 3.4 kJ/g (0.81 kcal/g). Although fermentation of cellulose in the hindgut depends on the timing and chemical composition (particularly of ß-starch) of the diet, 4.0 g of finely powdered A4 copy paper (Biznet, Tokyo, Japan) might yield 14 kJ (3.3 kcal). Short-chain fatty acids modulate colonic motility,28 decrease lipolysis,29 stimulate the proliferation of gut epithelial cells,30 control appetite,31 and might affect colon tumorigenesis.32 Short-chain fatty acids from cellulose may have these effects.
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Dilution Effect Powdered and microcrystalline celluloses are widely used as bulking agents.4 Although crystalline cellulose can be fermented, cellulose provides less energy than proteins, carbohydrates, and fats. The use of microcrystalline cellulose in foods reduces its energy content.4 The addition of cellulose to foods compensatorily increased the intake amount, but still reduced the daily energy intake in cats,33 dogs,34 and rats.18 Hence, the dilution effect of cellulose might result in reduced energy intake by reducing total energy intake. Johnson et al.35 reported that the food conversion (weight gain/food intake) in rats whose diet was supplemented with 10% purified cellulose was lower than control rats due to the dilution effect of cellulose. Indeed, cellulose has recently become a popular form of weight control in humans.36 Effects on Carcinogenesis and Cell Proliferation Birkitt37 hypothesized that dietary fiber increases fecal bulk, dilutes intestinal contents, and shortens intestinal transit time (or mean retention time), which reduces the contact of carcinogens with the colorectal mucosa. This effect should occur in the intestinal lumen because the hypothesis refers to carcinogens in the lumen. However, carcinogens are usually injected subcutaneously in most studies.38 When carcinogens are administered orally, there is a protective effect of 4% powdered cellulose for 28 weeks.39 However, the protective effect of cellulose (4%) on carcinogenesis was smaller than that of wheat bran (10%) in rats.39 The consumption of microcrystalline cellulose with subcutaneous injection of carcinogens in rats also suppresses carcinogenesis.38 The protective effect of microcrystalline cellulose might have other explanations in addition to the hypothesis of Birkitt.37 Another protective mechanism of microcrystalline cellulose may occur. However, numerous epidemiological studies assessing the influence of dietary fiber on colon cancer are not all in agreement.40 Microcrystalline cellulose (10%)5 and kaolin (10%)41 in the diet and glass beads (2.5 mm diameter) injected into the ileal fistula (Takahashi unpublished data) enhanced the mass of the distal colon mucosa in rats, but did not stimulate the proximal colon. Digesta in the distal colon is usually a hardened residue rather than a fluid, whereas digesta in the cecum and proximal colon is more pliable and flows.42 Hence, the transport of intestinal contents in the distal colon should be different from that in the cecum and proximal colon. Hardened residue in the distal colon slips on the luminal mucin layer covering the mucosa,43 whereas such slipping of digesta in the cecum and proximal colon is poor because of its plasticity. Kaolin and glass beads should cause more friction on the mucosa of the distal colon, indicating that rubbing of the mucosa by indigestible solids such as cellulose might stimulate hyperplasia of the mucosa in the distal colon.
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Effects on Fats Epidemiologically, there is no relationship between cellulose intake and serum lipid levels in diabetic subjects.44 The administration of 10% microcrystalline cellulose over 12 weeks has no effect on type 2 diabetic patients.45 However, human fecal bile acid excretion increases with cellulose intake.46 Bile acids do not bind to cellulose in vitro.47 The binding effect of cellulose might not explain the high fecal bile acid excretion with cellulose. The reducing behavior of substances such as bile acids in the lumen with cellulose intake48 might explain the high fecal bile acid excretion with cellulose. Microcrystalline cellulose can interfere with lipase activity in the small intestine in rats.49 Microcrystalline cellulose delays triglyceride absorption and increases lipid absorption in the ileum of rats fed a 20% cellulose meal for 20 days.49 Microcrystalline cellulose (2%) decreases the absorption of linoleate after massive small-bowel resection in rats.50 If the effects of microcrystalline cellulose are exaggerated by increasing the intake of cellulose or shortening the small intestine in rats, powdered cellulose might decrease blood lipids. The effects of powdered cellulose on blood lipids do not seem to be completely negative. Modified cellulose derivatives such as hydroxypropylmethylcellulose and methylcellulose show high viscosity.51 Hamsters fed diets containing 4% hydroxypropylmethylcellulose for four weeks52 and rats fed 8% methylcellulose for 10 days51 showed lower plasma cholesterol concentrations through reduced cholesterol absorption efficiency and lowered plasma triacylglycerol levels compared to controls, respectively. The high viscosity of the supernatant of the intestinal contents slows the digestion and absorption of nutrients in the small intestine.51 Effects on Carbohydrates Few studies of the relationship between microcrystalline cellulose ingestion and blood glucose have been performed because cellulose is normally used in the control diet for animals.5 The effects of cellulose on blood glucose are summarized in Table 12.1. Long-term53–55 and acute48,56 (Takahashi et al. unpublished data) administration of microcrystalline cellulose decreased postprandial blood glucose and insulin levels changed in some cases (Table 12.1), whereas in other studies, postprandial blood glucose and insulin levels did not change significantly.14,52,55,57–59 The time to gastric emptying, which is an important factor influencing postprandial blood glucose levels, was delayed with the administration of microcrystalline cellulose in some studies and did not change in others (Table 12.1). However, there are no reports indicating that cellulose increases blood glucose and insulin or decreases gastric emptying time (Table 12.1). Following the intake of 45 g of different types of fiber in an oral glucose tolerance test, blood glucose levels were lowest in those that ate pectin, were
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Table 12.1 Effects of Cellulose on Gastric Emptying Blood Glucose, and Insulin. Cellulose Type Cellulose
Duration of Dose Single dose 5 weeks
Cellulose
8 months
Purified cellulose (15%)
1 week
Cellulose
4 weeks
Cellulose
4 weeks
Microcrystalline cellulose Microcrystalline cellulose Crystalline cellulose
One shot in the SI One shot in the SI Single dose
Wood cellulose
Single dose
Microcrystalline cellulose Cellulose phospate and crystalline cellulose
Single dose
Carboxymethylcellulose and crystalline cellulose Solubilized cellulose
10 days
Carboxymethylcellulose Methylcellulose
2 weeks
Single dose (OGTT)
Single dose
Single dose
Effects
Species
Reference
No effect on blood glucose Decreased blood glucose Decreased blood glucose No effect on insulin No effect on blood glucose, insulin, GIP and glucagons Decreased blood glucose No effect on blood glucose, insulin, and gastric empty Decreased blood glucose Decreased blood glucose Decreased blood glucose
Rat
Schwartz & Levine 1980
Dog with DM
Nelson et al. 1998
Pig
Nunes & Malmlof 1992
Cat with DM Healthy volunteers
Nelson et al. 2000 Schwartz et al. 1982
Pig
Low et al. 1987
Rat
Delayed gastric empty No effect on gastric empty Cellulose phosphate decreased blood glucose; No effect on blood insulin Both delayed gastric empty. Only CMC decreased blood glucose No effect on blood glucose; Decreasde blood CCK Decreased blood glucose Decreased blood glucose and insulin
Pig Healthy volunteers Patients with DM
Takahashi et al. 2005 Takahashi et al. unpublished data Johansen & Knudsen 1994 Bianchi & Capurso 2002 Monnier et al. 1978
Rat
Begin et al. 1989
Hypercholesterolemic volunteers Rat
Daniela Geleva et al. 2003
Healthy volunteers
Healthy volunteers
Vachon et al. 1988 Jenkins et al. 1978
Notes: SI: Small intestine; DM: Diabetes mellitus; GIP: Gastric inhibitory polypeptide; OGTT: Oral glucose tolerance test.
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intermediate in those that ate cellulose phosphate, and were highest in those that ate crystalline cellulose.61 Obviously, the effect of cellulose on blood glucose is smaller than for soluble fibers such as pectin,61 guar gum,59 and hydroxypropylmethylcellulose.65 However, 45 g of pectin are more difficult to consume in a normal diet than are 45 g of microcrystalline cellulose. The relationships among the effects of different fibers, dosage, and palatability must be considered when planning the administration of fiber for prevention or treatment of diabetes mellitus. Microcrystalline cellulose administration increases the viscosity of gastric, small intestinal, and cecal contents in rats.5 Glucose does not bind to microcrystalline cellulose in vitro.48 Microcrystalline cellulose in the small intestine injected via a catheter diminishes plasma glucose increases.48 Microcrystalline cellulose diminishes glucose absorption by retarding diffusion within the luminal contents because of the high digesta viscosity with cellulose intake.48 Several studies have estimated the effect of microcrystalline cellulose on digestibility in the small intestine. The ingestion of microcrystalline cellulose with a meal does not affect digestibility from the oral to the distal end of the small intestine in rats with operationally bypassed large intestines (Takahashi et al. unpublished data). Most carbohydrates are digested in the proximal part of the small intestine.62 The digestion ability in the small intestine might result in similar digestibility with cellulose and in a control. Ingested microcrystalline cellulose can produce short-chain fatty acids in the human colon. A short-chain fatty acid, butyrate, appears to increase the plasma concentration of glucagon-like peptide-2 in rats.63 The infusion of short-chain fatty acids other than acetate raises the blood insulin level in lambs.68 These studies suggest a relationship between short-chain fatty acids and blood glucose levels. However, acute ileal and rectal perfusion of shortchain fatty acids does not significantly alter the blood glucose or insulin concentrations in healthy humans.28,69 Effect on Water Absorption in the Intestine In general, water moves from areas of higher to lower water potential,70 and water transport in plant tissue and soil can be explained by the water potential.71,72 Water absorption in the intestine can also be estimated by examining the water potential in the intestinal lumen.48,70 The water potential is calculated by subtracting the solute potential from the pressure potential.70 Therefore, high pressure in the intestinal lumen should induce water absorption.48,70 Dietary microcrystalline cellulose increases the viscosity and elasticity of the intestinal contents,5 which require more pressure in the intestinal lumen to move. In fact, the pressure potential caused by segmental contractions and peristalsis in the small intestinal lumen with microcrystalline cellulose ingestion is estimated to increase based on a mathematical model48 developed from the Hagen-Poiseuille law.6 Consequently, the water potential in the small intestinal lumen with microcrystalline cellulose should increase,
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which would stimulate water absorption.48 Indeed, water absorption from the rat small intestine has been observed with microcrystalline cellulose ingestion.48 Therefore, microcrystalline cellulose stimulates water absorption from the rat small intestine by creating a higher water potential in the intestinal lumen.48 The ingestion of cellulose with a meal produces a high antral motility index and a high proportion of propulsive duodenal contractions, which is consistent with the higher pressure and water potential with microcrystalline cellulose ingestion. The addition of powdered cellulose to the diet increases water absorption in the jejunum of pigs with two re-entrant cannulas.56 The addition of powdered and microcrystalline cellulose, which increases digesta viscosity, is likely to reduce the incidence of diarrhea associated with enteral nutrition.48 Effects on Proteins The ingestion of cellulose increases or does not affect protein efficiency ratios,73,74 but increases fecal protein excretion in rats due to increased fecal bacterial nitrogen.73,75 Cellulose is fermented in the large intestine,24 which increases bacterial abundance in the large intestine. The true efficiency of bacterial protein synthesis was 5.2 g bacterial protein/100 g supplementary cellulose in rats.70 Extra bacteria will be excreted in the feces. Increased fecal protein excretion is also observed in humans fed dietary fiber.76 In contrast, urinary nitrogen decreases with cellulose consumption in rats, indicating a shift in nitrogen excretion from urine to feces with cellulose intake.70 Such a shift can be explained largely by the degree of microbial fermentation in the large intestine caused by the addition of dietary fiber.77 Microbial fermentation in the large intestine reduces blood urea.77 Hence, the ingestion of cellulose can affect nitrogen metabolism and can change the nitrogen excretion route. Physiological Benefits of Hydroxypropylmethylcellulose Hydroxypropylmethylcellulose (HPMC) is a high-viscosity food gum produced from cellulose. Health benefits of HPMC include cholesterol-lowering actions and attenuating postprandial glycemic reponses. High-molecularweight HPMC is not metabolized by the microbiota in the human colon and may therefore be tolerated better.78 In hamsters, adding 4% HPMC to the diet for four weeks decreased body weight, plasma and liver cholesterol,79 and cholesterol absorption52 and increased the viscosity of the supernatant of the small intestinal 79 compared to adding cellulose. In mid- to moderate hypercholesterolemia, 5 or 7.5 g HPMC per day significantly reduced total cholesterol and LDL (approximately 12% 20 mg/dL reduction at both levels of HPMC) without altering HDL levels.79 Accordingly, HPMC has a lipidlowering effect in animals and humans.
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Cellulose Table 12.2 Food Application of Cellulose and Its Derivatives Cellulose/Derivatives Powdered cellulose Microcrystalline cellulose Methylcellulose Sodium carboxymethylcellulose Hydroxypropylmethylcellulose
Application Breads, beef burgers, doughnuts, pasta, imitation cheese, cereal Dressings, beverages, whipped toppings, reduced-fat foods, ice cream, tablets Sauces, soups, breads, fried foods, reduced-fat foods, gluten-free bakery products Frozen desserts, dressings, sauces, syrups, beverages, reduced-fat foods Whipped toppings, mousses, frozen desserts, dressings, sauces, gluten-free bakery products, reduced-fat foods
HPMC also lowers blood glucose levels. In a 2007 study of Maki et al.,61 meals containing 75 g of carbohydrate plus 4 or 8 g of high-viscosity HPMC showed a reduced peak and incremental areas from 0 to 120 min of the glucose and insulin concentrations in overweight or obese men and women without diabetes.61 Peak glucose was significantly lower (P < 0.001) after HV-HPMCcontaining meals (7.4 mmol/l [4 g] and 7.4 mmol/l [8 g]) compared with the control meal (8.6 mmol/l). Peak insulin concentrations and the incremental areas for glucose and insulin from 0 to 120 min were also significantly reduced after both doses of high-viscosity HPMC versus control (all P < 0.01). The authors concluded that high-viscosity HPMC may favorably alter the risks for diabetes and cardiovascular disease.61 HPMC shows promise as a dietary intervention for reducing cardiovascular and diabetes risk. Food Applications Celluloses have many uses as emulsifiers, stabilizers, dispersing agents, and thickeners. Powdered and microcrystalline celluloses have been used to enhance textural attributes and as bulking agents due to their rheological properties. The addition of natural crystalline cellulose increases cake volume, reduces shrinkage, and improves the texture of beef burgers (Table 12.2).7 Powdered cellulose is also added to pasta, imitation cheese, and cereal (Table 12.2). The microcrystalline celluloses Ceolus and Avicel have diameters of 6 to 10 µm and 40 µm, respectively.80 Very fine microcrystalline cellulose with a smaller diameter has been developed. A water suspension of 10% very fine microcrystalline cellulose has a creamy texture.3 This suspension is used as an oil replacement agent, which can be added to dressings, sauces, beverages, and whipped toppings.81 Microcrystalline cellulose is also formed into tablets and used as a binding agent due to its excellent compression properties.80
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Fiber Ingredients: Food Applications and Health Benefits
Acetobacter xylinum produces bacterial cellulose with a width of approximately 25 nm from glucose,82 and this material is used to make “nata de coco.” In water, this fiber has a viscosity that is not lost at high temperatures. Dried bacterial cellulose films have very high elasticity, suggesting applications in techniques involving electronic speakers and filter paper.80 Food applications of cellulose derivatives such as HPMC, methylcellulose, and carboxymethylcellulose are shown in Table 12.2.
Physiological Benefits Significance of Mixing-In Behavior of Nutrients in the Lumen The physical properties of cellulose and cellulose derivatives are important for determining their physiological benefits. Insoluble particles such as powdered and microcrystalline cellulose, as well as soluble components, generally elevate the viscosity of fluids with suspended particles, such as blood,82 fiber suspensions,83 and coal-oil mixtures.84 Indeed, insoluble particles of both smaller and larger (> 1 mm) sizes and microcrystalline cellulose increase the viscosity of the digesta, including particulate matter, in the stomach, small intestine, and cecum of pigs,6,85 chickens,86 and rats.5 The viscosity of the intestinal contents is critical for understanding the effects of cellulose on the mode of digestion and absorption. Previous studies5,6,85,86 have led to the hypothesis that the viscosity of the digesta influences absorption by affecting the behavior of nutrients in the intestinal lumen.85,87 The behavior of nutrients in the lumen is directly involved in the “micromixing” of nutrients and enzymes in the lumen.85 Micromixing is the molecular-scale mixing of digesta that directly influences chemical reactions and absorption.88 The extent of nutrient micromixing can be estimated by the flow pattern of digesta in the lumen,85 which can be estimated from the Reynolds number.86 There are two possibilities involving the micromixing of digesta in the lumen: rapid mixing by turbulence and poor mixing by diffusion.88 Turbulence in the lumen can rapidly mix the intestinal contents at a molecular scale, while diffusion induces much slower micromixing, which occurs only when laminar flow exists in the lumen.85 In the rapid micromixing with turbulence, the influence of the translocation rate of a nutrient in the lumen on the overall absorption rate can be ignored, since the rapid micromixing of digesta can translocate the nutrient to the epithelial surface at a rate exceeding that of absorption. In other words, the overall absorption rate should depend on the transepithelial transport rate (Equation 12.1).
(Overall absorption rate) = (Transepithelial transport rate) × a
(12.1)
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273
where a is a constant. This should result in a homogenous concentration of nutriLumen ents across the intestine. However, in vivo Intestinal wall measurement of the short-chain fatty acid concentration across the contents of the cecum and colon does not support such homogenous concentration. The shortLumen (Laminar flow) chain fatty acids concentration is higher in the core than in the periphery of the Nutrient contents.90 Conversely, nutrients can reach the Diffusion epithelium by diffusion in laminar flow (Figure 12.1).85 If the diffusion rate of a nutrient in the lumen is lower than its transepithelial absorption rate, the overall absorption rate of the nutrient should Trans epithelial be proportional to either its diffusion transport rate in the lumen or its membrane transEpithelium port rate. The slower of these two factors is the rate-limiting factor for the over- Figure 12.1 all absorption process. Considering the Schematic drawing of the possible above-mentioned short-chain fatty acid translocation of nutrients to the epithelium in the intestinal lumen. gradient across the intestinal lumen,90 the diffusion rate in the lumen should be slower than the membrane transport rate. Therefore, the diffusion rate of nutrients in the lumen should correlate with the overall absorption rate in laminar flow (Equation 12).
(Overall absorption rate) = (Diffusion rate in lumen) × b
(12.2)
where b is a constant. In this regard, when defining the mode of digestion and absorption, it is important to know whether the flow behavior in the intestinal lumen is turbulent or laminar. The flow pattern of digesta in the lumen can be estimated using the Reynolds number, which expresses the ratio of inertial forces to viscous forces in a fluid.89 The inertial force is the tendency of the fluid to stay in motion or at rest unless acted upon by an outside force.91 Viscous force is an internal property of a fluid that offers resistance to flow.91 The ratio, the Reynolds number, is used to determine whether a flow will be dominated by inertial or viscous forces (i.e., whether it is turbulent or laminar). A Reynolds number below 2300 indicates that viscous force predominates over inertial force to keep the flow laminar (a in Figure 12.2), which results in poor micromixing along the transversal axis. A Reynolds number exceeding 2300 indicates that inertial force dominates and that flow becomes turbulent89 (b in Figure 12.2), which mixes digesta in a molecular level completely.88
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Fiber Ingredients: Food Applications and Health Benefits a. Laminar flow
Circular tube No radial mixing
Direction of flow
Poor micromixing with diffusion 0
Reynolds number <2300
Velocity
b. Turbulent flow
Quick micromixing 0
Reynolds number >2300
Velocity
c. Karman vortex
Moderate micromixing with folding
40< Reynolds number <9600
Obstruction d. Low Reynolds number situation
Lumen
Obstruction (constriction)
No vortex
Reynolds number <10
Poor micromixing with diffusion Intestinal wall
Figure 12.2 Schematic drawing of flow behavior in a tube. Arrows represent the flow line when (a) Reynolds number <2300, (b) Reynolds number >2300, (c) 40 < Reynolds number < 96000, and (d) Reynolds number <10.
A vortex can mix a flow moderately by folding the digesta.88 Obstructions in the flow can make a vortex (i.e., Karman vortex, which is a curl or rotation) in fluids with a Reynolds number between 40 and 10,000. A Reynolds number less than 40 indicates that a Karman vortex does not occur in the flow downstream from the obstruction92 (d in Figure 12.2). A Reynolds number between 40 and 2300 shows the existence of a vortex in the laminar flow, suggesting that diffusion is still important to homogenize the fluid completely.88 A vortex is particularly important in macroscopic mixing in laminar flow.85
275
Cellulose Table 12.3 Reynolds Numbers of Flows Produced Peristalsis in the Lumen of the Intestine in the Pig, Chicken, and Human Radius of GI Tract (mm)
Velocity of Peristalsis (mm · s–1)
Shear Rate (s–1)
Reynolds Number (no unit)
Pig Small intestine Cecum Chicken Small intestine Cecum Humana Small intestine Colon
5.0 15
50 11
49 3.8
4.4 0.15
2.5 4.0
50 1.0
97 1.9
1.7 0.00010
7.0 25
50 21
35 4.3
5.3 0.52
Estimated from viscosity of pig. Source: Takahashi T. and Sakata T., Foods & Food Ingredients J. Jpn. 210, 944, 2005 a
A mathematical simulation was used to calculate the Reynolds numbers of the flows in the small and large intestine of pigs, chickens, and humans with peristalsis (Table 12.3) and segmental contraction.84 Flow Behavior in the Lumen of the Intestine Produced by Peristalsis The Reynolds numbers of the flow produced by peristalsis were much lower than 2300 in the small and large intestines of pigs, chickens, rats, and humans (Table 12.3). Reynolds numbers below 10 suggest that the flow of digesta should be laminar without a vortex in the intestinal lumen. Therefore, micromixing of digesta by turbulence is unlikely in the small intestine or cecum. The theoretical absence of turbulence means poor micromixing,88 which supports the validity of Equation 12. At a very low Reynolds number of <10 (Table 12.1), a plica, constriction, or haustra should not shed a vortex in the intestine (d in Figure 12.2). This suggests that the macroscopic mixing of digesta by a vortex hardly occurs in the small intestine, cecum, or proximal colon. Furthermore, the roughness of the mucosal surface should not alter the frictional drag and should not disturb the flow of contents in the small and proximal large intestine in laminar flow.93 Laminar flow without a 94 is a fluid without macroscopic mixing along the transverse axis of the flow (Figure 12.2). Nutrients should reach the epithelium by diffusion, even in the existence of a plica, constriction, or haustra. The absorption rate should depend on the diffusion rate in such a situation (Equation 12).
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Flow Behavior of the Intestinal Contents with Segmentation There are two types of segmental contractions: segmental contraction with and without complete constriction. Segmental contraction in the cecum and proximal colon is incomplete, but leaves lumen space even when a segment constricts.95 Therefore, the calculated Reynolds number of the flow produced by segmental contraction in the cecum and proximal colon of pigs and humans was smaller than 0.5 when the duration exceeded 1 s, a physiological condition in pigs and humans.91,96 Accordingly, this type of segmental contraction should not mix the contents transversally. Therefore, segmental constriction cannot mix the contents completely in the intestinal lumen. Segmental contraction with complete constriction can bring the nutrients in the center of the lumen into close proximity with the intestinal walls.97 The laminar structure in the lumen should disappear in the area of constriction when a segmental contraction closes the lumen. The laminar structure is then reconstructed in the area of constriction along with the relaxation following contraction. The old laminar structure will be disturbed when reconstructing a new laminar structure in a low Reynolds number situation, suggesting that there is moderate mixing in the area of constriction. However, almost none of the old laminar structure in the lumen will remain, with the reconstruction of a new laminar structure. There should be no turbulence in segmental constriction with complete constriction. Since the Reynolds number produced by segmental constriction with complete constriction should be smaller than 0.5, it is essentially the same as that produced by incomplete constriction. Diffusion in laminar flow still is needed to homogenize the fluid completely.88 Interrelationship between the Behavior of Nutrients and Cellulose X-ray computed tomography after a single injection of model digesta containing barium sulfate into the ileum or cecum of rats confirmed the poor macroscopic mixing in the large intestine in vivo (Takahashi et al. unpublished data). Indeed, rapid mixing with turbulence is unlikely to occur in the intestinal lumen.48,98–101 Although some macroscopic mixing and folding of digesta is probably induced by segmental contractions of the small intestine85 and contributes to increased glucose absorption rates,90 the self-diffusion of nutrients is an important determinant of the absorption rate because of poor micromixing in the lumen. The diffusion of nutrients in the intestinal lumen should depend negatively on the viscosity of the digesta.102 Therefore, the overall absorption rate is likely to be limited by self-diffusion, rather than by transepithelial transport because the diffusion rate is slower than the transepithelial transport rate.85 Accordingly, the viscosity of the digesta containing microcrystalline cellulose and HPMC may diminish glucose absorption by depressing the diffusion rate in the lumen.5
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Safety and Technology The summary of evaluations performed by the joint FAO/WHO expert committee on food additives did not specify an acceptable daily intake of powdered and microcrystalline cellulose, methylcellulose, or HPMC because their toxicity is extremely low. However, cellulose might affect the absorption of minerals from the gut. The addition of 10 g of cellulose for 20 days increased the excretion of calcium and zinc in humans.103 Similarly, the addition of 16 g of cellulose for approximately one month increased fecal excretion of calcium and magnesium.12 These studies suggest that calcium, magnesium, and zinc should be added to the diet when long-term administration of cellulose is performed. Microcrystalline cellulose does not adversely affect iron,104 phosphorus, calcium, magnesium, iron, zinc, or copper balance in rats.105 Adamii et al.11 concluded that microcrystalline cellulose supplements could be protracted because they do not interfere with iron absorption in obese patients. Further study of the relationship between mineral balance and powdered or microcrystalline cellulose intake is necessary to determine the effects of long-term administration of cellulose.
References
1. Miles J. Carbohydrates, in Nutrition secrets, van Way CW, Ed., Hanley & Belfus, Inc. Philadelphia, PA 1998. 2. Chesson A. Dietary fiber, in Food polysccharides and their applications, Stephen AM. Ed., Marcel Dekker, Inc., New York 1995. 3. Takahashi R, Hirasawa Y, and Nishinari K. Cellulose and its derivatives, Foods & Food Ingredients J. Jpn. 208, 824, 2003. 4. Ang J.F. Water retention capacity and viscosity effect of powdered cellulose, J. Food Sci. 56, 1682, 1991. 5. Takahashi T et al. Influences of solid particles on the viscous properties of intestinal contents and intestinal tissue weight in rats, J. Jpn. Soc. Nutr. Food. Sci. 56, 199, 2003. 6. Takahashi T and Sakata T. Large particles increase viscosity and yield stress of pig cecal contents without changing basic viscoelastic properties, J. Nutr. 132, 1026, 2002. 7. Prakongpan T, Nitithamyaong A, Luangprtuksa P. Extraction and application of dietary fiber and cellulose from pineapple core. J. Food Sci. 67, 1308, 2002. 8. Roma E et al. Diet and chronic constipation in children: the role of fiber. J. Pediatr. Gastroenterol. Nutr. 28, 169, 1999. 9. Hillman L, Peters S, Fisher A and Pomare EW. Differing effects of pectin, cellulose and lignin on stool pH, transit time and weight, Br. J. Nutr. 50, 189, 1983. 10. Cummings JH. Cellulose and the human gut, Gut 25, 805, 1984.
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11. Adamii A, Dall’Aglio E and Strata A. Clinical research on a new microcrystalline cellulose dietetic supplement, Minerva Gastroenterol. Dietol. 44, 171, 1998. 12. Slavin JL and Marlett JA. Influence of refined cellulose on human bowel function and calcium and magnesium balance, Am. J. Clin. Nutr. 33, 1932, 1980. 13. Wichert B, Opitz B and Kienzle E. Dietary treatment for chronic colon problems, 2000 Purina Nutrition Forum St. Louis, MO, 2000. 14. Bianchi M and Capurso L. Effects of guar gum, ispaghula and microcrystalline cellulose on abdominal symptoms, gastric emptying, orocaecal transit time and gas production in healthy volunteers, Dig. Liver Dis. 34 Suppl 2, S129, 2002. 15. Fahey GC Jr et al. Dietary fiber for dogs: I. Effects of graded levels of dietary beet pulp on nutrient intake, digestibility, metabolizable energy and digesta mean retention time, J. Anim. Sci. 68, 4221, 1990. 16. Martínez del Rio C, Cork SJ and Karasov WH. Modelling gut function, in The digestive system in mammals, Chivers DJ and Langer P. Eds., Cambridge University Press, Cambridge, 1994, 287–309. 17. Wichert B et al. Influence of different cellulose types on feces quality of dogs, J. Nutr. 132, 1728S, 2002. 18. Delorme CB and Wojcik J. Interaction of dietary protein with cellulose in the adaptation of caloric dilution by weaning rats, J. Nutr. 112, 21, 1982. 19. Smith C, Hellebusch SJ and Mandel KG. Patient and physician evaluation of a new bulk fiber laxative tablet, Gastroenterol. Nurs. 26, 31, 2003. 20. Hamilton J, Wagner J, Burdick B and Bass P. Clinical evaluation of methylcellulose as a bulk laxative, Dig. Dis. Sci. 33, 993, 1988. 21. Milton-Thompson GJ and Lewis B. The breakdown of dietary cellulose in man, Gut 12, 853, 1971. 22. Livesey G and Elia M. Short-chain fatty acids as an energy source in the colon, in Physiological and clinical aspects of short-chain fatty acids, Cummings JH, Rombeau JL and Sakata T., Eds., Cambridge University Press, Cambridge, 1995, 427. 23. Stevens CE and Hume ID. Comparative physiology of the vertebrate digestive system, Cambridge University Press, Cambridge, 1995. 24. Kelleher J et al. Degradation of cellulose within the gastrointestinal tract in man. Gut 25, 811, 1984. 25. von Engelfardt W. Absorption of short-chain fatty acids in the large intestine, in Physiological and clinical aspects of short-chain fatty acids, Cummings JH, Rombeau JL and Sakata T., Eds., Cambridge University Press, Cambridge, 1995, 149. 26. Wrong OM. Definitions and history, in Physiological and clinical aspects of shortchain fatty acids, Cummings JH, Rombeau JL and Sakata T., Eds., Cambridge University Press, Cambridge, 1995, 1. 27. Jorgensen H, Larsen T, Zhao XQ, Eggum BO. The energy value of short-chain fatty acids infused into the caecum of pigs, Br. J. Nutr. 77, 745, 1997. 28. Cherbut C., Effects of short-chain fatty acids on gastrointestinal motility, Cummings JH, Rombeau JL and Sakata T. Eds., in Physiological and clinical aspects of short-chain fatty acids, Cambridge University Press, Cambridge, 1995, 191. 29. Anderson JW. Short-chain fatty acids and lipid metabolism, in Physiological and clinical aspects of short-chain fatty acids, Cummings JH, Rombeau JL and Sakata T. Eds., Cambridge University Press, Cambridge, 1995, 509. 30. Sakata T. Effects of short-chain fatty acids on the proliferation of gut epithelial cell in vivo, in Physiological and clinical aspects of short-chain fatty acids, Cummings JH, Rombeau JL and Sakata T. Eds., Cambridge University Press, Cambridge, 1995, 509.
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31. de Jong A. Short-chain fatty acids, pancreatic control and appetite control, in Physiological and clinical aspects of short-chain fatty acids, Cummings JH, Rombeau JL and Sakata T. Eds., Cambridge University Press, Cambridge, 1995, 257. 32. Lupton JR. Short-chain fatty acids and colon tumorigenesis: animal models, in Physiological and clinical aspects of short-chain fatty acids, Cummings JH, Rombeau JL and Sakata T. Eds., Cambridge 1995, 257. 33. Prola L, Dobenecker B and Kienzle E. Interaction between dietary cellulose content and food intake in cats, J. Nutr. 136, 1988S, 2006. 34. Dobenecker B and Kienzle E. Interactions of cellulose content and diet composition with food intake and digestibility in dogs, J. Nutr. 128, 2674S, 1998. 35. Johnson IT, Gee JM and Mahoney RR. Effect of dietary supplements of guar gum and cellulose on intestinal cell proliferation, enzyme levels and sugar transport in the rat, Br. J. Nutri. 52, 477, 1984. 36. Jones KR and Pillsbury HC III. Cellulose fiber diet pills. A new cause of esophageal obstruction, Arch. Otolaryngol. Head Neck Surg. 116, 1091, 1990. 37. Burkitt DP. Epidemiology of cancer of the colon and rectum, Cancer 28, 3, 1971. 38. Iwane S et al. Inhibitory effect of small amounts of cellulose on colonic carcinogenesis with low-dose carcinogen. Dig. Dis. Sci. 47, 1257, 2002. 39. Kritchevsky D and Klurfeld DM. Interaction of fiber and energy registration in experimental colon carcinogens. Cancer Lett. 114, 51, 1997. 40. Kritchevsky D. Diet and Cancer: What’s Next? J. Nutr. 133, 3827S, 2003. 41. Sakata T. Effects of indigestible dietary bulk and short chain fatty acids on the tissue weight and epithelial cell proliferation rate of the digestive tract in rats, J. Nutr. Sci. Vitaminol. 32, 355, 1986. 42. Björnhag G. Adaptations in the large intestine allowing small animals to eat fibrous foods, in The digestive system in mammals, Chivers D and Langer P. Eds., Cambridge University Press, New York, 1994, 287. 43. Sakata T and von Engelhardt W. Luminal mucin in the large intestine of mice, rats and guinea pigs, Cell Tissue Res. 219, 629, 1981. 44. Fatema K et al. Dietary fibre intake and prevalence of dyslipidemia in Type-2 diabetic subjects, Asia. Pac. J. Clin. Nutr. 12, S21, 2003. 45. Niemi MK, Keinanen-Kiukaanniemi SM and Salmela PI. Long-term effects of guar gum and microcrystalline cellulose on glycaemic control and serum lipids in type 2 diabetes, Eur J. Clin. Pharmacol. 34, 427, 1988. 46. Stanley MM et al. Effects of cholestyramine, metamucil, and cellulose on fecal bile salt excretion in man, Gastroenterol. 65, 889, 1973. 47. Story JA and Kritchevsky D. Comparison of the binding of various bile acids and bile salts in vitro by several types of fiber, J. Nutr. 106, 1292, 1976. 48. Takahashi T et al. Crystalline cellulose decreases blood glucose increment and stimulates water absorption associated with digesta viscosity in the rat, J. Nutr. 135, 2405, 2005. 49. Gallaher D and Schneeman BO. Effect of dietary cellulose on site of lipid absorption, Am. J. Physiol. 249, G184, 1985. 50. Toki A et al. Effects of pectin and cellulose on fat absorption after massive small-bowel resection in weanling rats, J. Parenter. Enteral Nutr. 16, 255, 1992. 51. Topping DL et al. A viscous fibre (methylcellulose) lowers blood glucose and plasma triacylglycerols and increases liver glycogen independently of volatile fatty acid production in the rat, Br. J. Nutr. 59, 21, 1988.
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52. Carr TP et al. Increased intestinal contents viscosity reduces cholesterol absorption efficiency in hamsters fed hydroxypropylmethylcellulose, J. Nutr. 126, 1463, 1996. 53. Schwartz SE and Levine GD. Effects of dietary fiber on intestinal glucose absorption and glucose tolerance in rats, Gastroenterol. 79, 833, 1980. 54. Nelson RW et al. Effect of dietary insoluble fiber on control of glycemia in dogs with naturally acquired diabetes mellitus, J. Am. Vet. Med. Assoc. 212, 380, 1998. 55. Nelson RW et al. Effect of dietary insoluble fiber on control of glycemia in cats with naturally acquired diabetes mellitus. J. Am. Vet. Med. Assoc. 216, 1082, 2000. 56. Low AG et al. Influence of wheat bran, cellulose, pectin and low or high viscosity guar gum on glucose and water absorption from pig jejnum, P. Nutri. Soc. 45, 55A, 1987. 57. Schwartz SE et al. Sustained pectin ingestion delays gastric emptying, Gastroenterology 83, 812, 1982. 58. Begin F et al. Effect of dietary fibers on glycemia and insulinemia and on gastrointestinal function in rats, Can. J. Physiol. Pharmacol. 67, 1265, 1989. 59. Nunes CS and Malmof K. Effects of guar gum and cellulose on glucose absorption, hormonal release and hepatic metabolism in the pig, Br. J. Nutr. 68, 693, 1992. 60. Monnier L et al. Influence of indigestible fibers on glucose tolerance, Diabetes Care 1, 83, 1978. 61. Maki KC et al. High-viscosity hydroxypropylmethylcellulose blunts postprandial glucose and insulin responses, Diabetes Care 2007. 62. Kiriyama S. Carbohydrates, in Shineiyoukagaku, Asakura Publishing, Tokyo, 1991, 53. 63. Tappenden KA et al. Glucagon-like peptide-2 and short-chain fatty acids: a new twist to an old story, J. Nutr. 1333717, 2003. 64. Husveth F, Szegleti C and Neogrady Z. Infusion of various short chain fatty acids causes different changes in the blood glucose and insulin concentrations in growing lambs deprived of food overnight. Zentralbl. Veterinarmed. A. 43, 437, 1996. 65. Wolever TM et al. Effect of rectal infusion of short chain fatty acids in human subjects, Am. J. Gastroenterol. 84, 1027, 1984. 66. Schmidt-Nielsen B. The renal concentrating mechanism in insects and mammals: a new hypothesis involving hydrostatic pressure, Am. J. Physiol. 268, R1087, 1995. 67. Hsieh JJ. The relationship of water potential and water content in a local soil. BNWL-714, BNWL Rep. 8, 19, 1968. 68. Millar AA, Duysen ME and Wilkinson GE. Internal water balance of barley under soil moisture stress, Plant Physiol. 43, 968, 1968. 69. Muller H and Harmuth-Hoene AE. The effect of cellulose on endogenous nitrogen excretion in rats, evaluated using N-15 technics, Z. Ernahrungswiss. 25, 38, 1986. 70. Kreuzer M et al. Cellulose fermentation capacity of the hindgut and nitrogen turnover in the hindgut of sows as evaluated by oral and intracecal supply of purified cellulose, Arch. Tierernahr. 41, 359, 1991.
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71. Pastuszewska B, Kowalczyk J and Ochtabinska A. Dietary carbohydrates affect caecal fermentation and modify nitrogen excretion patterns in rats. I. Studies with protein-free diets, Arch. Tierernahr. 53, 207, 2000. 72. Stephen AM and Cummings JH. The influence of dietary fibre on faecal nitrogen excretion in man, Proc. Nutr. Soc. 38, 141A, 1979. 73. Tetens I, Livesey G and Eggum BO. Effects of the type and level of dietary fibre supplements on nitrogen retention and excretion patterns, Br. J. Nutr. 75, 461, 1996. 74. Younes H et al. Fermentable fibers or oligosaccharides reduce urinary nitrogen excretion by increasing urea disposal in the rat cecum, J. Nutr. 125, 1010, 1995. 75. Maki KC et al. High-molecular-weight hydroxypropylmethylcellulose taken with or between meals is hypocholesterolemic in adult men, J. Nutr. 130, 1705, 2000. 76. Gallaher DD, Hassel CA and Lee KJ. Relationships between viscosity of hydroxypropylmethylcellulose and plasma cholesterol in hamsters. J. Nutr. 123, 1732, 1993. 77. Maki KC, Davidson MH, Malik KC, Albrecht HH, O’Mullane J and Daggy BP. Cholesterol-lowering with high viscosity hydroxypropylmethylcellulose, Am. J. Cardiol. 84, 1198–1203, 1999. 78. Okajima K and Yamane C. Cellulose, in Tennen seitai koubunshi zairyou no shintenkai Miyamoto T, Akaike T and Nishinari K. Eds., CMC Shuppan, Tokyo, 2003, 7. 79. Coffey DG, Bell DA and Henderson A. Cellulose and cellulose derivatives, in Food polysccharides and their applications Stephen AM. Ed., Marcel Dekker, Inc, New York. 80. Kaushal R, Walker TK, Drummond DG. Observations on the formation and structure of bacterial cellulose, Biochem. J. 50, 128, 1951. 81. Brooks DE, Goodwin JW and Seaman GVF. J. Appl. Physiol. 28, 172–177, 1970. 82. Stenuf TJ and Unbehend JE. Rheology and non-Newtonian flows, in Encyclopedia of fluid mechanics Volume 5, Cheremisinoff N.P. Eds., Gulf Publishing Company, Houston, 1986. 83. Borghesani AF. Rheology and non-Newtonian flows, in Encyclopedia of fluid mechanics volume 7, Cheremisinoff NP. Eds., Gulf Publishing Company, Houston, 1988, 89. 84. Takahashi T and Sakata T. Insoluble dietary fibers: the major modulator for the viscosity and flow behavior of digesta, Foods & Food Ingredients J. Jpn. 210, 944, 2005. 85. Takahashi T, Goto M and Sakata T. Viscoelastic properties of the small intestinal and caecal contents of the chicken, Br. J. Nutr. 91, 867, 2004. 86. Anderson BW et al. Influence of infusate viscosity on intestinal absorption in the rat. An explanation of previous discrepant results, Gastroenterology 97, 938, 1989. 87. Baldyage J and Bourne JR. Flow phenomena and measurement, in Encyclopedia of fluid mechanics Volume 1, Cheremisinoff NP. Ed., Gulf Publishing Company, Houston, 1986, 148–201. 88. Huttula T, Krogerus KZ and Virtanen M. Surface and groundwater flow phenomena, in Encyclopedia of fluid mechanics Volume 10, Cheremisinoff NP. Ed., Gulf Publishing Company, Houston, 1990, 212.
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89. Yajima T and Sakata T. Core and periphery concentrations of short-chain fatty acids in luminal contents of the rat colon, Comp. Biochem. Physiol. Comp. Physiol. 103, 353, 1992. 90. Sherman FS. Viscous flow, McGraw-Hill, Columbus, 1990, 3. 91. Potter MC and Wiggert DC. Mechanics of fluids, Prentice Hall, Englewood Cliffs, 1991, 317–389. 92. Cheremisinoff NP. Encyclopedia of fluid mechanics Volume 1, Flow Phenomena and Measurement, Gulf Publishing Company, Houston, 1986, 285–351. 93. Fox RW and McDonald AT. Introduction to fluid mechanics, 3rd edition, John Wiley & Sons, New York, 1985, 331–388. 94. Berne RM and Levy MN. Physiology, 3rd ed. Mosby-Year Book, St louis, MO, 1993, 615–652. 95. Cherbut C and Ruckebusch Y. The effect of indigestible particles on digestive transit time and colonic motility in dogs and pigs. Br. J. Nutr. 53, 549, 1984. 96. Ruckebusch Y and Fioramonti J. Motor profile of the ruminant colon: hard vs soft faeces production. Experientia 15, 1184, 1980. 97. Yates GT. Handbook of fluid dynamics and fluid machinery, Volume III, Schetz JA and Fuhs AE. Eds., John Wiley, New York, 1996, 1938–1951. 98. Takahashi T and Sakaguchi E. Behaviors and nutritional importance of coprophagy in captive adult and young nutrias (Myocastor coypus). J. Comp. Physiol. [B]. 168, 281, 1998. 99. Takahashi T and Sakaguchi E. Role of the furrow of the proximal colon in the production of soft and hard feces in nutrias, Myocastor coypus. J. Comp. Physiol. B. 170, 531, 2000. 100. Takahashi T, Karita S, Yahaya MS and Goto M. Radial and axial variations of bacteria within the cecum and proximal colon of guinea pigs revealed by PCRDGGE, Biosci. Biotechnol. Biochem. 69, 1790, 2005. 101. Takahashi T and Sakaguchi E. Transport of bacteria across and along the large intestinal lumen of guinea pigs. J. Comp. Physiol. B. 176, 173, 2006. 102. Antoon CB and Kirsch JF. Investigation of diffusion-limited rates of chymotrypsin reactions by viscosity variation, Biochemistry 21, 1302, 1982. 103. Ismail-Beigi F et al. Effects of cellulose added to diets of low and high fiber content upon the metabolism of calcium, magnesium, zinc and phosphorus by man, J. Nutr. 107, 510, 1970. 104. Catani M et al. Dietary cellulose has no effect on the regeneration of hemoglobin in growing rats with iron deficiency anemia, Braz. J. Med. Biol. Res. 36, 693, 2003. 105. Gordon DT, Besch-Williford C and Ellersieck MR. The action of cellulose on the intestinal mucosa and element absorption by the rat, J. Nutr. 113, 2545, 1983.
13 Oat β-Glucan Niina Tapola and Essi Sarkkinen
Contents Characteristics...................................................................................................... 283 β-Glucan................................................................................................................284 Functionality and Food Applications...............................................................284 Viscosity.......................................................................................................284 Molecular Weight........................................................................................ 285 Effects of Processing on β-Glucan............................................................ 285 Effects of Oat Bran on Food Characteristics........................................... 287 Food Applications....................................................................................... 287 Physiological Benefits.......................................................................................... 288 Lipid Metabolism........................................................................................ 288 General and Dose Response.......................................................... 288 Summary of Randomized Controlled Human Studies............. 289 Mechanism....................................................................................... 293 Glucose Metabolism................................................................................... 296 Postprandial Effects........................................................................ 296 Long-Term Effects........................................................................... 297 Mechanism....................................................................................... 297 Safety..................................................................................................................... 297 References............................................................................................................. 298
Characteristics Oats (Avena sativa) have been used as food for people from the seventeenth centuries, especially in Scotland. Porridge made from rolled oats is probably the most popular food use of oat. The five largest producers of oat are Russia, Canada, United States, Poland, and Finland, producing over 50% of the world’s total oat production.1 Consumers’ interest in oat products has been increased again mainly because of the beneficial health effects of oat. The beneficial cholesterol and glucose effects of oat are attributed primarily to water-soluble fiber, called β-glucan. 283
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Oat is a good source of different dietary fibers such as β-glucan, arabinoxylans, and cellulose. Oat groats (dehulled kernels) contain 10.2% to 12.1% fiber, 4.1% to 4.9% soluble fiber, and 6.0% to 7.1% insoluble fiber depending on genotype of oat.2 The soluble fiber of oat is composed of neutral sugars and uronic acid. Neutral sugars account for 98% of the total soluble fiber, and β-glucan accounts for at least 80% of the neutral sugars. The insoluble dietary fiber of oat is composed of neutral sugars (50%), Klason lignin (43%), which is a noncarbohydrate part of dietary fiber (such as lignin, unavailable protein, polymers originating from Maillard reaction and tannin-protein complexes), and uronic acid (7%). β-Glucan is located mainly in the endospermic cell walls and in the subaleurone layer of oats.3 Environmental factors and especially genetic variability of oats result in significant differences in β-glucan content of different genotypes.4, 5 In literature the β-glucan concentration of oat groats varies from 3.9% to 6.8% in North American cultivars.6 Typically the oat groats contain 4.5% to 5.5% of β-glucan.4
β -Glucan Oat β-glucan is a linear, unbranched polysaccharide that contains (1→4)and (1→3)-β-linked glucopyranosyl units.7 About 70% of β-d-glucopyranosyl units are four-O-linked and 30% three-O-linked. The main compositions of β-glucan molecules are β-(1→3)-linked cellotriosyl and cellotetraosyl units constituting about 90% of polysaccharides of β-glucan.8 The ratio of β-(1→3)linked cellotriosyl to cellotetraosyl units is lower for oats (2.1 to 2.4) than for barley (2.8 to 3.4), wheat (3.0 to 3.8), and rye (2.7 to 3.2), resulting in fewer cellotriosyl and more cellotetraosyl sequences in oat.8,9 There seems to be no differences in the structure of β-glucan between different oat cultivars and between the bran and groat of oat defined by the ratio of tri- to tetrasaccharides.8 The distribution of β-glucan in oat kernels has been studied by using scanning microspectroflurometry. In cultivars with high β-glucan content β-glucan is concentrated in the central endosperm. A high β-glucan concentration has been also seen in the subaleurone region of those cultivars that have low β-glucan content.3
Functionality and Food Applications Viscosity β-Glucan forms highly viscous solutions at low concentrations (>0.3%).10 The viscosity increases with concentration and molecular weight of β-glucan.11
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In addition, the viscosity can be increased by decreasing the particle size of the oat ingredient. There are great differences in viscosity between β-glucan solutions isolated from different oat varieties.12 The most significant differences in viscosity between the oat varieties are explained in terms of differences in mean molecular weight of β-glucan. The viscosity of β-glucan preparations decreases when the proteins are removed by trypsin. The viscosity curves are similar for β-glucan solutions at different pH (2.7 to 8.1), suggesting that pH has no effect on viscosity.12 However, viscosity has been shown to decrease significantly when the pH has changed to a highly alkaline region.13 Hydrolyzed β-glucan results significantly reduced molecular weight and viscosity due to depolymerization of β-glucan.10 Apparently the β-glucan of hydrolyzed samples tends to aggregate. Molecular Weight The molecular weight of β-glucan affects significantly viscosity properties of β-glucan solutions. Table 13.1 shows molecular weights of β-glucan in different oat ingredients measured by high-performance size exclusion chromatography and Calcofluor detection. When the β-glucan is isolated and purified from oat bran, the molecular weight of β-glucan decreases due to enzyme action or share forces.14,15 Effects of Processing on β-Glucan Food processes such as milling, malting, extrusion cooking, and baking produce microstructural changes in cell wall components. However, dry processing involving milling, sieving, and rolling as well as extraction with aqueous ethanol does not significantly degrade β-glucan.16 Table 13.2 shows average molecular weights of experimental foods prepared with oat bran or rolled oats and some commercial oat-based foods measured by Calcofluor Table 13.1 Average Molecular Weight (Mw) of β-Glucan in Different Oat Ingredients Sample Oats Instant oats Rolled oats Rolled oats Oat bran Oat bran Oat bran Oat bran Oat bran Oat bran
β -Glucan Content (% of Dry Matter) 3.4 4.5 4.2 5.0 8.3 8.7 8.8 13.6 16.4 20.0
Calcofluor Average MW (x 10-4 g/mol)
Reference
225 252 254 230 215 296 280 206 216 206
16 14 14 16 16 14 14 16 16 16
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Table 13.2 Average Molecular Weight (MW) of β-Glucan in Different Experimental and Commercial Oat-Based Foods Sample Oat ingredients Oats Rolled oats Oat bran Oat bran Oat bran Oat bran Experimental oat-based foods Apple juice Extruded flakes Fresh pasta Macaroni Muffin Teacake Commercial oat-based foods Bread loaf Crisp bread Porridge Pancake batter Pancake Extruded oats Yogurt-like product Fermented drink Breakfast cereal
β-Glucan (% of Dry Matter)
Calcofluor Average MW (x 10-4 g/mol)
3.4 5.0 8.3 13.6 16.4 20.0
225 230 215 206 216 206
2.8 3.1 1.4 1.6 1.9 1.5
58 189 57 188 192 45
1.1 2.5 4.9 0.99 0.97 3.2 2.8 0.24 16.6
63 95 201 19 20 193 83 39 194
Source: [16]
in the study of Åman et al.16 Apple juice, fresh pasta, and teacakes had low average molecular weight. The researchers suggested that acid in the juice hydrolyzes the glycosidic bonds of β-glucan and enzymatic hydrolysis has occurred during pasta preparation and baking of teacakes. Wood et al.14 found a large difference in the peak molecular weight of β-glucan in different commercial ready-to-eat cereals. Molecular weights ranged from 0.60 to 2.93 x 10-6. The difference can be explained by differences in ingredients and processing. Extrusion cooking, which is usually used for the production of fiber-rich breakfast cereals and snacks, damages the cell wall mechanically. Extrusion cooking involves heating at high temperature. Heating decreases the molecular weight of β-glucan.17 The higher the temperature and longer the duration time of heating, the more the molecular weight
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287
decreases. However, Jaskari and coworkers found no change in molecular weight of oat bran β-glucan during hydrothermal treatment.15 Baking yeast-leavened bread results in an enzymatic degradation of β-glucan in oat bran.16 The active enzymes capable to hydrolyze β-glucans may be present in the flour (e.g., β-glucanases in wheat flour) or in the added yeast. Particle size of oat bran and time of fermentation seem to have important roles in degradation. Using large oat bran particles and short fermentation time, the degradation of β-glucan can be reduced.16,18 Baking of oat bran bread, cookies, and muffins decrease molecular weight of β-glucan and consequently breadmaking process reduces the viscosity of the soluble fiber.11, 19-21 Cooking is more favorable, because it increases the extractability of β-glucan unlike baking.22 Beer et al.21 found that frozen storage of oat-bran-containing muffins decreased extractability of β-glucan. However, the freezing seems not to affect the molecular weight of β-glucan, unless it is repeated after thawing.17, 19,21,23
Effects of Oat Bran on Food Characteristics Baking absorption (i.e., the amount of water needed) increases and stability of dough decreases with increased oat bran concentration and with reduced particle size of oat bran. Loaf volume of bread decreases with increased bran substitution and reduced bran particle size. In sensory evaluations the appearance, texture, and taste of bread with 15% large size oat bran was preferred more than bread with smaller oat bran size.24 Beverages and soups containing high molecular weight (2,000,000) are thicker, slimier, and more extensible compared to beverages and soups containing low molecular weight (40,000 – 200,000) β-glucan at the same concentration.23 In soups and beverages high molecular weight β-glucan concentration above 0.5% results in too thick texture, while beverages and soups with 2% low-molecular-weight β-glucan still have feasible thickness.23 In the study of Björklund et al.25 total impression of beverage with 5 g oat β-glucan was more preferred than the beverage with 10 g β-glucan. Food Applications Three forms of oat fiber are commonly available for human consumption: oat groat, oat bran, and oat hulls. Oat hulls are very high in total fiber (79 to 95 g/100 g).26 Oat hulls contain mainly insoluble fiber and only very little soluble fiber and no β-glucan. Oat bran has a total β-glucan content of at least 5.5% (dry weight basis) and a total dietary fiber content of at least 16% (dry weight basis), and at least one-third of the total dietary fiber is soluble fiber according to the definition provided by The American Association of Cereal Chemists for oat bran.27 Commercial oat brans contain usually 8% to 10% of β-glucan,28 but as high as 22% of β-glucan–containing oat bran has been made.
288
Fiber Ingredients: Food Applications and Health Benefits
β-glucan concentration of oat ingredients has been increased by producing high β-glucan grain fractions through dry-milling or wet-milling processes. There are also patented processing methods for increasing the β-glucan contents of oat bran. The main commercially produced oat fiber products are produced by dry-milling (OatWell®, Nurture® 1500, and Natureal®), thermal and frozen extractions (Nutrim-OB, Glucagel®, and Cerogen®), enzymatic hydrolysis Table 13.3 (Oatrim, OatsCreme™), and alkaline extracDifferent Oat-Based Foods tion (OatVantage™, Vitacel®).29 Conventional Bread milling has produced oat brans with 1.28 Hot cereals to 1.60 times more β-glucan than in groats Breakfast cereals and the fractionating process increases the Cookies β-glucan content by three- or four-fold.6,12 In Cereal bars addition to the method, the cultivars with Pasta high levels of β-glucan are important for Power drink obtaining high β-glucan contents. Oat fiber Oat milk ingredients have been used in various food Oat ice cream applications (Table 13.3). Fermented oat bran porridge
Physiological Benefits Lipid Metabolism General and Dose Response The cholesterol-lowering effect of oat has been reported in several studies. In these studies oat bran, concentrated oat bran, oat meal, and oat gum have been used in various food matrices. Two meta-analyses of randomized and controlled oat studies have proven the cholesterol-lowering effect of oat.30,31 Ripsin and coworkers found that incorporating oat products into the diet caused a modest reduction (0.13 mmol/L) in blood cholesterol concentrations.30 The magnitude of reduction was of similar size in the meta-analysis of Brown et al.31 They found that 1 gram of soluble fiber reduced total cholesterol concentration by 0.040 mmol/L and LDL-cholesterol concentration by 0.037 mmol/L in studies in which 2 to 10 g of soluble fiber was used. In 1997, the U.S. Food and Drug Administration (FDA) allowed the use of generic health claims on reducing the risk of coronary heart disease for oat and oat products, when food contains at least 0.75 g of β-glucan per reference amount customarily consumed of the food product.32 Four portions of whole oat foods provide 3 g of β-glucan, which is associated with reduced risk of coronary heart disease. Davidson et al.33 conducted a controlled dose-response study with 148 hypercholesterolemic subjects. The study group found the dose-dependent reduction in LDL cholesterol levels. The daily consumption of 1.2, 2.0, and
Oat β-Glucan
289
2.4 g β-glucan resulted in 5.8%, 4.7%, and 3.5% decreases in LDL cholesterol concentrations, respectively. Statistically significant decreases in LDL cholesterol levels of 10.1%, 15.9%, and 11.5% in the treatment groups with daily β-glucan consumption of 3.6, 4.0, and 6.0 g were respectively found. According to other recent clinical studies the optimal β-glucan dose for cholesterol reduction seems to be between 3 and 9 g depending on the application used. β-glucan has not been demonstrated to affect serum cholesterol concentrations in subjects with low (< 5 mmol/l) serum cholesterol. The largest reductions are seen in studies in which subjects had the highest total cholesterol concentration initially. Noakes et al.34 in a crossover study with hypertriglyceridemic subjects showed significantly lower triglyceride concentrations during oat bran periods compared with high-amylose diet and low-amylose diet. This result suggested that oat bran can suppress the rise in plasma triglyceride concentration common with high-carbohydrate diets. Summary of Randomized Controlled Human Studies Oat as Hot and Cold Cereals Oat as hot and cold cereals has been shown to be an effective way to decrease serum cholesterol levels both as part of a low-fat diet and habitual diet (Table 13.4).35–38 In addition, oat-bran-containing ready-to-eat cereals have been shown to decrease serum cholesterol concentrations in several human studies (Table 13.4).37,39–43 The daily amount of cereals has varied from 25 g to 56 g. The decrease in total and LDL-cholesterol concentrations was quite similar in all studies with ready-to-eat cereals. In a study of Demark-Wahnefried and coworkers, cholesterol concentration was reduced in subjects who used oat bran ready-to-eat cereals for 12 weeks as effectively as in subjects who followed a low-fat diet.43 However, use of oat bran and oat bran concentrate as itself or mixed with other foods has not been shown to be more effective to reduce cholesterol concentrations than wheat or rice bran (Table 13.4).44–46 Oat in Bread and Bakery Application Significant reduction in cholesterol concentration was found in four of the 10 human controlled and randomized studies with oat-bran-enriched bread and other bakery products (muffins and cookies) illustrating the matrices challenge (Table 13.5).19,47–55 Oat bran bread and muffins reduced serum total cholesterol concentrations by 5.6% compared to the wheat bran period and 3.8% compared to the rice bran period in hypercholesterolemic subjects.47 In ileostomic subjects oat bran bread decreased serum total and LDL cholesterol levels by 9.0% and 12.1%, respectively.48 Pick et al.49 reported 14% and 23% lower serum total and LDL cholesterol concentration in eight subjects with type 2 diabetes after 12-week consumption of bread, buns, and muffins with oat bran concentrate compared to the white bakery consumption. Romero et al.50 found oat bran cookies decreased both serum total and LDL-
36 Hypercholesterolemic subjects 44 Hypercholesterolemic subjects 62 Hypercholesterolemic subjects
152 Hypercholesterolemic subjects 35 Hypercholesterolemic subjects 20 Hypercholesterolemic 110 Normo- and mildly hypercholesterolemic subjects
84 Healthy subjects 36 Overweight men 208 Healthy subjects
Parallel Studies
Subjects
N/A 3.0
Oat bran
Oat bran concentrate
N/A 7.3
Oat bran Oat bran+ oat meal
10.3
N/A
Oat bran
Oat bran
N/A 5.5 N/A N/A 3.0
Oat bran Oatmeal + oat bran Oat bran Oatmeal N/A
Oat Ingredient
Daily Amount of Beta-Glucan (g)
8
6
8
3 12
12
6
2 12 6
Study Duration (Weeks)
Human Studies of Effects of Oat in Hot and Cold Cereals on Blood Lipids
Table 13.4
With yogurt and milk
Sprinkle on, mixed into foods
In juice, yoghurt, and as porridge
Hot cereals and muffins Ready-to-eat cereals and muffins
Ready-to-eat cereals
Hot and cold cereals Hot and cold cereals Hot cereals, muffins, recipes for use Ready-to-eat cereals
Vehicle
46
45
↓TC, LDL-C NS
44
90 91
↓TC NS
NS
43
41
↓TC, LDL-C NS
35 36 38
References
↓TC, LDL-C ↓LDL-C NS
Changes in Blood Lipids
290 Fiber Ingredients: Food Applications and Health Benefits
6
N/A N/A N/A N/A
Oat bran Oat bran
Oat bran
1.4
4 4
2
N/A
Oat bran + oat bran concentrate Oat bran
Hot cereals and muffins
Ready-to-eat cereals Ready-to-eat cereals
Ready-to-eat cereals
Ready-to-eat cereals
Notes: NS = not significant, TC = Total Cholesterol, LDL-C = LDL-Cholesterol, N/A = not available.
12 Hypercholesterolemic subjects 145 Hypercholesterolemic subjects 23 Hypercholesterolemic men 64 Hypercholesterolemic subjects 8 Hypercholesterolemic subjects
Crossover Studies 40 39 37 42 60
↓TC, LDL-C ↓TC, LDL-C ↓TC, LDL-C ↓TC, LDL-C ↓TC, LDL-C
Oat β-Glucan 291
N/A N/A N/A
Oat bran Oat bran
N/A N/A
Oat bran Oat bran concentrate
Oat bran
N/A
2.31
Oat bran
Oat bran
5.9
11.2 N/A
Oat bran
Oat bran concentrate Oat bran
6 4
3
3 12
4
4
4
8 8
Study Duration (Weeks)
Entrees and muffins Bread
Bread Bread, bun and muffins Muffins
Bread and muffins
Muffins
Bread and cookies
Bread Cookies
Vehicle
NS NS
55 52
53
48 49
↓TC, LDL-C ↓TC, LDL-C NS
47
54
↑HDL-C
↓TC, LDL-C
19
51 50
References
NS
NS ↓TC, LDL-C
Changes in Blood Lipids
Notes: NS = not significant, TC = Total Cholesterol, LDL-C = LDL-Cholesterol, HDL-C = HDL-Cholesterol, N/A = not available
16 Hypercholesterolemic subjects 20 Healthy subjects 12 Hypercholesterolemic subjects
24 Hypercholesterolemic subjects 9 Ileostomic subjects 8 Type 2 diabetic subjects
Crossover Studies
30 Hypercholesterolemic men 66 Normal and hypercholesterolemic subjects 48 Hypercholesterolemic subjects 34 Overweight women
Parallel Studies
Subjects
Oat Ingredient
Daily Amount of Beta-Glucan (g)
Human Studies on Effects of Oat in Bread and Bakery Applications on Blood Lipids
Table 13.5
292 Fiber Ingredients: Food Applications and Health Benefits
Oat β-Glucan
293
cholesterol concentrations more than wheat bran cookies and similar to psyllium-enriched cookies. Oat in Drink Application The results of studies investigating the effects of oat in drinks on serum cholesterol concentration are inconsistent (Table 13.6). Subjects with hypercholesterolemia who were administered oat gum mixed in non-carbonated diet drinks or water providing 5.8 g β-glucan for four weeks showed 9% reduction in blood total and LDL-cholesterol concentrations in reference to baseline.56 Beer et al. found no significant changes in serum lipids in healthy young men given 9 g β-glucan as oat gum in the form of an instant whip containing milk during a 14-day period in a crossover study.57 Önning et al.58 reported no differences in blood lipids between oat milk and soy milk consumption or oat milk and cow’s milk consumption. In the other study of Önning et al.,59 they observed 6% lower serum total and LDLcholesterol concentrations in hypercholesterolemic men who consumed oat milk compared to those who consumed rice milk. Consumption of oat bran and oat bran concentration mixed in orange juice lowered serum total cholesterol concentrations by 3.8% and LDL-cholesterol concentrations by 6.7% compared to the placebo.19 More recently Björklund et al.25 showed 7.4% lower total cholesterol concentration after consumption of 5 g β-glucan in beverage compared to a rice starch beverage. However, the beverage with 10 g of β-glucan did not affect serum lipids significantly in comparison with control. The researchers supposed that solubility of β-glucan might have reduced more in the beverage with 10 g β-glucan than in the beverage with 5 g β-glucan. Added to this, Table 13.7 shows various cholesterol studies in which oat bran or meal has been used in several applications. Mechanism Braaten and coworkers showed that β-glucan is the principal agent for the cholesterol-lowering property of oat.56 Mechanisms behind the serum cholesterol-lowering effects of β-glucan are not fully understood, but increased bile acid excretion and altered cholesterol and fat metabolism are probably the two main mechanisms. Increased fecal and small bowel bile acid excretion has been reported after oat fiber intake.48,60–63 Increased bile acid excretion results in reduced serum cholesterol levels via increased removal of steroids from the body and enterohepatic cycle and consequently a decrease in lipoprotein cholesterol secretion. Whether this can fully explain the hypocholesterolemic effects of β-glucan have been postulated.64 Soluble viscous fiber may also alter different steps of fat digestion in the gut and consequently reduce absorption of dietary cholesterol.65 Inhibition of endogenous cholesterol synthesis is one possible, but not major, mechanism. The inhibitory effect is mediated by increased production of short-chain fatty acids, which are fermentation products of soluble fiber.64
9.0 5.8 3.4/4.5 3.8 5.0
Oat Oat flake and oat bran
Oat bran
5.0 10.0
Oat gum Oat gum
Oat bran
2
4 5
1.4 4
5
Study Duration (weeks) Vehicle
Mixed with orange juice
Instant whip Mixed in non-carbonated diet drink Oat milk Oat milk
Beverage
Notes: NS = not significant, TC = otal Cholesterol, LDL-C = LDL-Cholesterol, HDL= HDL-Cholesteroll.
14 Healthy men 19 Hypercholesterolemic subjects 24 Healthy subjects 52 Hypercholesterolemic subjects 25 Hypercholesterolemic subjects
Crossover Studies
54 Hypercholesterolemic subjects
Parallel Studies
Subjects
Oat Ingredient
Daily Amount of Beta-Glucan (g)
Human Studies on Effects of Oat in Drinks on Blood Lipids
Table 13.6
58 59 19
↓TC, LDL-C
57 56
25
References
NS ↓TC, LDL-C
↑HDL ↓TC, LDL-C
↓TC NS
Changes in Blood Lipids
294 Fiber Ingredients: Food Applications and Health Benefits
N/A N/A
Oat bran
4
6
12
8
6
Study Duration (weeks)
bread, hot cereals and recipes for use muffins, cereals, bread, pasta
As itself, muffins and recipes for use Recipes for use
Hot cereals, muffins, shakes
Vehicle
34
↓TG
94
93
43
92
33
References
NS
NS
NS NS NS ↓ TC, LDL-C ↓ TC, LDL-C ↓ TC, LDL-C NS
Changes in Blood Lipids
Oat bran 1.1–1.3 4 cereals, bread, muffins, chouder NS Oat bran 2.2–2.5 Oat bran 3.3–3.8 Notes: NS = not significant, TC = Total Cholesterol, LDL-C = LDL-Cholesterol, TG = Triglycerides, N/A = not available.
29 Hypercholesterolemic subjects 23 Hypertriglyceridemic subjects 40 Hypercholesterolemic subjects
Crossover studies
N/A
1.2 2.0 2.4 4.0 3.6 6.0 N/A
Oat bran
Oat bran
48 Hypercholesterolemic subjects
236 Healthy subjects
Oatmeal Oat bran Oatmeal Oat bran Oatmeal Oat bran Oatmeal
148 Hypercholesterolemic subjects
Parallel studies
Subjects
Oat Ingredient
Daily Amount of Beta-Glucan (g)
Human Studies of Effects of Oat in Various Vehicles on Blood Lipids
Table 13.7
Oat β-Glucan 295
296
Fiber Ingredients: Food Applications and Health Benefits
Glucose Metabolism Postprandial Effects There is a significant inverse linear relationship between amount of β-glucan/ log viscosity of the product and postprandial glucose and insulin responses in healthy and diabetic subjects.66,67 Wood et al.66 tested the dose-response of β-Glucan with 0, 1.8 g, 3.6 g, and 7.2 g of oat gum in liquids with 50 g glucose. They found that 79% to 96% of the changes in plasma glucose and insulin responses are attributable to viscosity of solution. Tappy et al.67 found that approximately 5 g of β-glucan decreases glycemic response by 50% after ingestion of 35 g carbohydrates. They tested extruded breakfast cereals with 4.0 g, 6.0 g, and 8.4 g of β-glucan compared with breakfast bread. Oat products or food products rich in β-glucan have lower glycemic index (GI) or have produced lower glycemic response compared to the wheat bread or oral glucose load.68–70 The GI and insulinemic index of raw and heat-treated oat flakes was 72 to 78 and 58 to 77, respectively, and GI of commercial oat bran breakfast cereal with 3.7 g β-glucan is 86 compared to white bread.68,69 β-glucan enrichment in cereals and bars has produced an even lower glycemic index (< 55).69 In the study of Jenkins et al.69 1 g of β-glucan decreased GI by 4.0 units. Tappy et al.67 found 33% lower area under glucose response curve and glucose maximum increase for breakfast cereals with 4.0 g β-glucan compared to bread-containing breakfast. Tapola et al.70 found a 34% reduction in glucose excursion and 22% reduction in area under glucose response curve during 2 hour follow-up, when 30 g oat bran flour with 4.6 g β-glucan was ingested with 25 g oral glucose load compared to a 25 g oral glucose load alone. On the other hand, a low-fiber test meal produced a similar glycemic response compared to the same meal with oat bran with 5.14 g soluble fiber, rice bran, or wheat fiber, when the amount of total carbohydrate was not adjusted among the meals.71 Ingestion of whole rye meal bread enriched with oat β-glucan concentrate lowered only the insulin response compared to wheat bread, when both meals contained 50 g available carbohydrates and rye bread contained 5.4 g β-glucan.72 Ordinary muesli with oat flakes or oat porridge cooked with oat flakes, oat flours, or oat bran seems not to have enough β-glucan to reduce postprandial glucose tolerance.73–75 However, in liquids as little as < 6.0 mg of β-glucan per kg of body weight has reduced glucose response significantly.76 In addition to the studies of Braaten et al.77 and Wood et al.66 who found that oat gum in glucose solution is efficient to lower postprandial plasma glucose and insulin response, Björklund et al.25 found that a beverage with 5 g of oat bran β-glucan improved glucose metabolism. Oat bran and oat gum with similar amounts of β-glucan incorporated into a meal lowers postprandial glucose and insulin levels to the same degree.78, 79 Since the amount of β-glucan, viscosity, and molecular weight of β-glucan account for the magnitude of the glycemic response, the breakdown of β-glucan should be minimized during processing of oat products. There are
Oat β-Glucan
297
conflicting results regarding the effect of particle size on glucose and insulin response in the literature.68,80 Mild heat treatment and agglomeration of β-glucan have not been found to lower the glycemic response of oat products, but reduction of viscosity by acid hydrolysis reduces the capacity of β-glucan to decrease postprandial glucose responses.66,68 Long-Term Effects Fasting plasma glucose has not been shown to decrease after a 10-day to 12-week use of different oat-fiber-enriched foods.25,34,36,44,46,58,61,81 After a 12-week use of oat bran concentrate products, the glucose profile was reduced during an 8-hour day, which included typical meals.49 In addition, the area under insulin response curve was reduced by oat products. In subjects with central obesity oat bran ready-to-eat cereals with 3.2 g β-glucan lowered postprandial insulin responses more while performed after a 12-week ingestion period of oat products with 7.7 g daily dose of β-glucan compared to the postprandial test at the beginning of the ingestion period.81 In non-diabetic subjects the long-term use (4 to 8 weeks) of oat bran was not shown to have an effect on glucose tolerance after a standard breakfast compared to the use of wheat or rice bran.46,47 Mechanism β-glucan increases the viscosity of the contents of the stomach and small intestine. The increased viscosity consequently reduces the absorption of the nutrients from the small intestine. Delayed carbohydrate digestion and absorption are suggested to be the major factors responsible for the reduced glycemic response for β-glucan.82 Rate of gastric emptying is probably not sufficient to affect glucose response.73
Safety Oat bran and oatmeal do have a history of safe use, and oat fiber is considered safe and non-toxic. As to the microbiological and chemical safety (contaminants like pesticide residues, fungal toxins among others), oat fiber does not raise any specific safety concerns compared to other cereal fibers. There is no data on obvious toxicity of β-glucan either.83 Oat fiber has been well-tolerated according to numerous clinical trials.84 Most common adverse events reported have been typical gastrointestinal (GI) symptoms (e.g., flatulence) related to a high-fiber diet in general. Related to efficient water-holding capacity, potential obstruction of GI-tract similar to that reported from guar gum cannot be ruled out.85 Incorporation of suf-
298
Fiber Ingredients: Food Applications and Health Benefits
ficient amount of water along with the oat fiber product should be emphasized, especially if ingested in tablet form. In general fiber and compounds associated with cereal fiber (e.g., phytates and phenolic compounds) have been found to reduce the apparent absorption of minerals such as calcium, magnesium, zinc, and manganese. However, the ultimate effect of oat fiber as a “soluble” fiber on mineral absorption is more difficult to estimate. Since soluble forms of fiber have been found to add viscosity to the gut contents, and promote fermentation and the production of volatile fatty acids in the cecum, it does have the potential to improve absorption of minerals as well.86 In some cases the addition of soluble oat fiber to the diet has been found to improve absorption of minerals like iron, zinc, and phosphorus.87 Although oat fiber is not considered a typical allergen source and β-glucan is of non-allergenic nature, some occasional allergic reactions have been reported, especially via inhalated non-food exposure.88,89 Only oat fiber products totally free from gluten could be considered safe for celiac patients.
References
1. Food and Agricultural Organization of the United Nations. Economic and Social Department. The Statistics Division. Major food and agricultural commodities and producers. http://www.fao.org/es/ess/top/comodity.html?lang=e n&item=75&year=2005 Accessed 31.1.2007. 2. Manthey, F.A., Hareland, G.A. and Huseby, D.J., Soluble and insoluble dietary fiber content and composition in oat, Cereal. Chem., 76, 417, 1999. 3. Miller, S.S. and Fulcher, R.G., Distribution of (1→3), (1→4)-β-D-glucan in kernels of oats and barley using microspectrofluorometry, Cereal. Chem., 71, 64, 1994. 4. Cho, K.C. and White, P.J., Enzymatic analysis of β-glucan content in different oat genotypes, Cereal. Chem., 70, 539, 1993. 5. Saastamoinen, M. et al., β-glucan contents of groats of different oat cultivars in official variety, in organic cultivation, and in nitrogen fertilization trials in Finland, Agr. Food. Sci., 13, 68, 2004. 6. Wood, P.J., Weisz, J. and Fedec, P., Potential for β-glucan enrichment in brans derived from oat (Avena sativa L.) cultivars of different (1→3), (1→4)-β-D-glucan concentrations, Cereal. Chem., 68, 48, 1991. 7. Wood, P.J., Physicochemical characteristics and physiological properties of oat (1→3), (1→4)-β-D-glucan, in Oat bran, Wood, P.J., Eds., the American Association of Cereal Chemists, St. Paul, 1993, chap. 4. 8. Wood, P.J., Weisz, J. and Blackwell, B.A., Molecular characterization of cereal β-D-glucans. Structural analysis of oat β-D-glucan and rapid structural evaluation of β-D-glucans from different sources by high-performance liquid chromatography of oligosaccharides released by lichenase, Cereal. Chem., 68, 31, 1991.
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9. Wood, P.J., Weisz, J. and Blackwell, B.A., Structural studies of (1→3), (1→4)-β-Dglucans by 13C-nuclear magnetic resonance spectroscopy and by rapid analysis of cellulose-like regions using high-performance anio-exchange chromatography of oligosaccharides released by lichenase, Cereal. Chem., 71, 301, 1994. 10. Doublier, J-L. and Wood, P.J., Rheological properties of aqueous solutions of (1→3) (1→4)-β-D-glucan from oats (Avena sativa L.), Cereal. Chem., 72, 335, 1995. 11. Anttila, H., Sontag-Strohm, T. and Salovaara, H., Viscosity of β-glucan on products, Agr. Food. Sci., 13, 80, 2004. 12. Autio, K. et al., Physical properties of (1→3), (1→4)-β-D-glucan preparates isolated from Finnish oat varieties, Food. Hydro., 5, 513, 1992. 13. Salmenkallio-Marttila, M. et al., Effect of pH on viscosity of oat β-glucan, Proceeding of the 7th International Oat Conference, Peltonen-Sainio, P., Topi-Hulmi, M. Eds., MTT Agrifood Research Finland, Jokioinen, Agrifood Research Reports, 51, 138, 2004. 14. Wood, P.J., Weisz, J. and Mahn, W., Molecular characterization of cereal β-glucans. II. Size-exclusion chromatography for comparison of molecular weight, Cereal. Chem., 68, 530, 1991. 15. Jaskari, J. et al., Effect of hydrothermal and enzymic treatments on the viscous behavior of dry- and wet-milled oat brans, Cereal. Chem., 72, 625, 1995. 16. Åman, P., Rimsten, L., and Andersson, R., Molecular weight distribution of β-glucan in oat-based foods, Cereal. Chem., 81, 356, 2004. 17. Suortti, T., Johansson, L. and Autio, K., Effect of heating and freezing on molecular weight of oat β-glucan, AACC Annual Meeting 2000, Abstract 332. 18. Frank, J. et al., Yeast-leavened oat breads with high or low molecular weight β-glucan do not differ in their effects on blood concentrations of lipids, insulin, or glucose in humans, J. Nutr., 134, 1384, 2004. 19. Kerckhoffs, D.A.J.M., Hornstra, G. and Mensink, R.P., Cholesterol-lowering effect of β-glucan from oat bran in mildly hypercholesterolemic subjects may decrease when β-glucan is incorporated into bread and cookies, Am. J. Clin. Nutr., 78, 221, 2003. 20. Degutyte-Fomins, L., Sontag-Strohm, T. and Salovaara, H., Oat bran fermentation by rye sourdough, Cereal. Chem., 79, 345, 2002. 21. Beer, M.U. et al., Effect of cooking and storage on the amount and molecular weight of (1→3) (1→4)-β-D-glucan extracted from oat products by an in vitro digestion system, Cereal. Chem., 74, 705, 1997. 22. Johansson, L., Structural analyses of (1→3), (1→4)-β-D-glucan of oats and barley, Ph.D. thesis, Department of Applied Chemistry and Microbiology, University of Helsinki, Helsinki, 2006. 23. Lyly, M. et al., The sensory characteristics and rheological properties of soups containing oat and barley β-glucan before and after freezing, Lebensm.-Wiss. u.-Technol., 37, 749, 2004. 24. Krishnan, P.G., Chang, K.C. and Brown, G., Effect of commercial oat bran on the characteristics and composition of bread, Cereal. Chem., 64, 55, 1987. 25. Björklund, M. et al., Changes in serum lipids and postprandial glucose and insulin concentrations after consumption of beverages with β-glucans from oats or barley: a randomized dose-controlled trial, Eur. J. Clin. Nutr., 59, 1272, 2005. 26. Vollendorf, N.W. and Marlett, J.A., Dietary fiber methodology and composition of oat groats, bran, and hulls, Cereal. Foods, 36, 565, 1991.
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27. AACC, American Association of Cereal Chemists committee adopts oat bran definition, Cereal. Foods. World., 34, 1033, 1989. 28. Wood, P.J. et al., Large-scale preparation and properties of oat fractions enriched in (1→3)(1→4)-β-D-glucan, Cereal. Chem., 66, 97, 1989. 29. Stevenson, D. and Inglett, G., Commercial oat fiber fractionation — development of functional food ingredients, http://www.ars.usda.gov7research/publications/publications.htm?SEQ_NO_115=177928 Accessed 28.2.2007. 30. Ripsin, C.M. et al., Oat products and lipid lowering. A meta-analysis, JAMA, 267, 3317, 1992. 31. Brown, L. et al., Cholesterol-lowering effects of dietary fiber: a meta-analysis, Am. J. Clin. Nutr., 69, 30, 1999. 32. US Food and Drug Administration, FDA final rule for federal labeling: health claims: oats and coronary heart disease. Fed. Regist. 62, 3584, 1997. 33. Davidson, M.H. et al., The hypocholesterolemic effects of β-glucan in oatmeal and oat bran. A dose-controlled study, JAMA, 265, 1833, 1991. 34. Noakes, M. et al., Effect of high-amylose starch and oat bran on metabolic variables and bowel function in subjects with hypertriglyceridemia, Am. J. Clin. Nutr., 64, 944, 1996. 35. Kasthan, H. et al., Wheat-bran and oat-bran supplements’ effects on blood lipids and lipoproteins, Am. J. Clin. Nutr., 55, 976, 1992. 36. Davy, B.M. et al., High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middleaged and older men, Am. J. Clin. Nutr., 76, 351, 2002. 37. Whyte, J.L. et al., Oat bran lowers plasma cholesterol levels in mildly hypercholesterolemic men, J. Am. Diet. Assoc., 92, 446, 1992. 38. Van Horn, L. et al., Serum lipid response to oat product intake with a fat-modified diet, J. Am. Diet. Assoc., 86, 759, 1986. 39. Anderson, J.W. et al., Oat-bran cereal lowers serum total and LDL cholesterol in hypercholesterolemic men, Am. J. Clin. Nutr., 52, 495, 1990. 40. Keenan, J.M. et al., Randomized, controlled, crossover trial of oat bran in hypercholesterolemic subjects, J. Fam. Pract., 33, 600, 1991. 41. Karmally, W. et al., Cholesterol-lowering benefits of oat-containing cereal in Hispanic Americans, J. Am. Diet. Assoc., 105, 967, 2005. 42. Poulter, N. et al., Lipid profiles after the daily consumption of an oat-based cereal: a controlled crossover trial, Am. J. Clin. Nutr., 59, 66, 1994. 43. Demark-Wahnefried, W., Bowering, J. and Cohen, P.S., Reduced serum cholesterol with dietary change using fat-modified and oat bran supplemented diets, J. Am. Diet. Assoc., 90, 223, 1990. 44. Uusitupa, M.I. et al., A controlled study on the effect of β-glucan-rich oat bran on serum lipids in hypercholesterolemic subjects: relation to apolipoprotein E phenotype, J. Am. Coll. Nutr., 11, 651, 1992. 45. Gerhardt, A.L. and Gallo, N.B., Full-fat rice bran and oat bran similarly reduce hypercholesterolemia in humans, J. Nutr., 128, 865, 1998. 46. Lovegrove, J.A. et al., Modest doses of β-glucan do not reduce concentrations of potentially atherogenic lipoproteins, Am. J. Clin. Nutr., 72, 49, 2000. 47. Kestin, M. et al., Comparative effects of three cereal brans on plasma lipids, blood pressure, and glucose metabolism in mildly hypercholesterolemic men, Am. J. Clin. Nutr., 52, 661, 1990. 48. Zhang, J.X. et al., Effect of oat bran on plasma cholesterol and bile acid excretion in nine subjects with ileostomies, Am. J. Clin. Nutr., 56, 99, 1992.
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49. Pick, M.E. et al., Oat bran concentrate bread products improve long-term control of diabetes: a pilot study, J. Am. Diet. Assoc., 96, 1254, 1996. 50. Romero, A.L., Cookies enriched with psyllium or oat bran lower plasma LDL cholesterol in normal and hypercholesterolemic men from Northern Mexico, J. Am. Coll. Nutr., 17, 601, 1998. 51. Törrönen, R. et al., Effects of an oat bran concentrate on serum lipids in freeliving men with mild to moderate hypercholesterolaemia, Eur. J. Clin. Nutr., 46, 621, 1992. 52. Bremer, J.M., Scott, R.S. and Lintott, C.J., Oat bran and cholesterol reduction: evidence against specific effect, Aust. N. J. Med., 21, 422, 1991. 53. Kahn, R. et al., Oat bran supplementation for elevated serum cholesterol, Fam. Pract. Res. J., 10, 37, 1990. 54. Robitaille, J. et al., Effect of an oat bran-rich supplement on the metabolic profile of overweight premenopausal women, Ann. Nutr. Metab., 49, 141, 2005. 55. Swain, J.F. et al., Comparison of the effects of oat bran and low-fiber wheat on serum lipoprotein levels and blood pressure, N. Engl. J. Med., 322, 147, 1990. 56. Braaten, J.T. et al., Oat β-glucan reduces blood cholesterol concentration in hypercholesterolemic subjects, Eur. J. Clin. Nutr., 48, 465,1994. 57. Beer, M.U., Arrigoni, E. and Amado, R., Effects of oat gum on blood cholesterol levels in healthy young men, Eur. J. Clin. Nutr., 49, 517, 1995. 58. Önning, G. et al., Effects of consumption of oat milk, soya milk, or cow’s milk on plasma lipids and antioxidative capacity in healthy subjects, Ann. Nutr. Metab., 42, 211, 1998. 59. Önning, G. et al., Consumption of oat milk for 5 weeks lowers serum cholesterol and LDL cholesterol in free-living men with moderate hypercholesterolemia, Ann. Nutr. Metab., 43, 301, 1999. 60. Kirby, R.W. et al., Oat-bran intake selectively lowers serum low-density lipoprotein cholesterol concentrations of hypercholesterolemic men, Am. J. Clin. Nutr., 34, 824, 1981. 61. Anderson, J.W. et al., Hypocholesterolemic effects of oat-bran or bean intake for hypercholesterolemic men, Am. J. Clin. Nutr., 40, 1146, 1984. 62. Marlett, J.A. et al., Mechanism of serum cholesterol reduction by oat bran, Hepatology, 20, 1450, 1994. 63. Lia, Å. et al., Oat β-glucan increases bile acid excretion and a fiber-rich barley fraction increases cholesterol excretion in ileostomy subjects, Am. J. Clin. Nutr., 62, 1245, 1995. 64. Anderson, J.W. and Bridges, S.R., Hypocholesterolemic effects of oat bran in humans, In Oat Bran, Wood, P.J., Eds., The American Association of Cereal Chemists, St. Paul, 1993, chap. 6. 65. Lairon, D., Dietary fibres: effects on lipid metabolism and mechanisms of action, Eur. J. Clin. Nutr., 50, 125, 1996. 66. Wood, P.J. et al., Effects of dose and modification of viscous properties of oat gum on plasma glucose and insulin following an oral glucose load, Br. J. Nutr., 72, 731, 1994. 67. Tappy, L., Gügolz, E., and Würsch, P., Effects of breakfast cereals containing various amounts of β-glucan fibers on plasma glucose and insulin responses in NIDDM subjects, Diabetes. Care., 19, 831, 1996. 68. Granfeldt, Y., Eliasson, A.C. and Björck, I., An examination of the possibility of lowering the glycemic index of oat and barley flakes by minimal processing, J. Nutr., 130, 2207, 2000.
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69. Jenkins, A.L. et al., Depression of the glycemic index by high levels of β-glucan fiber in two functional foods tested in type 2 diabetes, Eur. J. Clin. Nutr., 56, 622, 2002. 70. Tapola, N. et al., Glycemic responses of oat bran products in type 2 diabetic patients, Nutr. Metab. Cardiovasc. Dis.,15, 255, 2005. 71. Cara, L. et al., Effects of oat bran, rice bran, wheat fiber, and wheat germ on postprandial lipemia in healthy adults, Am. J. Clin. Nutr., 55, 81, 1992. 72. Juntunen, K.S. et al., Postprandial glucose, insulin, and incretin responses to grain products in healthy subjects, Am. J. Clin. Nutr., 75, 254, 2002. 73. Lia, Å. and Andersson, H., Glycemic response and gastric emptying rate of oat bran and semolina porridge meals in diabetic subjects, Scan. J. Nutr., 38, 154, 1994. 74. Granfeldt, Y., Hagander, B. and Bjorck, I., Metabolic responses to starch in oat and wheat products. On the importance of food structure, incomplete gelatinization or presence of viscous dietary fibre, Eur. J. Clin. Nutr., 49, 189, 1995. 75. Liljeberg, H.G.M. et al., Products based on a high fiber barley genotype, but not on common barley or oats, lower postprandial glucose and insulin responses in healthy humans, J. Nutr., 126, 458, 1996. 76. Hallfrisch, J., Scholfield, D.J. and Behall, K.M., Diets containing soluble oat extracts improve glucose and insulin responses of moderately hypercholesterolemic men and women, Am. J. Clin. Nutr., 61, 379, 1995. 77. Braaten, J.T. et al., Oat gum lowers glucose and insulin after an oral glucose load, Am. J. Clin. Nutr., 53, 1425, 1991. 78. Wood, P.J. et al., Comparisons of viscous properties of oat and guar gum and the effects of these and oat bran on glycemic index, J. Agric. Food. Chem., 38, 753, 1990. 79. Braaten, J.T. et al., High ß-glucan oat bran and oat gum reduce postprandial blood glucose and insulin in subjects with and without type 2 diabetes, Diabet. Med., 11, 312, 1994. 80. Heaton, K.W. et al., Particle size of wheat, maize, and oat test meals: effects on plasma glucose and insulin responses and on the rate of starch digestion in vitro, Am. J. Clin. Nutr., 47, 675, 1988. 81. Maki, K.C. et al., Effects of consuming foods containing oat β-glucan on blood pressure, carbohydrate metabolism and biomarkers of oxidative stress in men and women with elevated blood pressure, Eur. J. Clin. Nutr., 6, 1, 2006. 82. Würsch, P. and Pi-Sunyer, F. X., The role of viscous soluble fiber in the metabolic control of diabetes. A review with special emphasis on cereals rich in β-glucan, Diabetes. Care., 20, 1774, 1997. 83. Delaney, B. et al., Evaluation of the toxicity of concentrated barley β-glucan in a 28-day feeding study in Wistar rats, Food. Chem. Toxicol., 41, 477, 2003. 84. Kahn, R.F. et al., Oat bran supplementation for elevated serum cholesterol, Fam. Pract. Res. J., 10, 37, 1990. 85. Lewis, J.H., Esophageal and small bowel obstruction from guar gum-containing “diet pills”: analysis of 26 cases reported to the Food and Drug Administration, Am. J. Gastroenterol., 87, 1424, 1992. 86. Greger, J.L., Nondigestible carbohydrates and mineral bioavailability, J. Nutr., 129, 1434S, 1999. 87. De Schrijver, R. and Conrad, S., Availability of calcium, magnesium, phosphorus, iron, and zinc in rats fed oat bran containing diets, J. Agric. Food. Chem., 40, 1166, 1992.
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88. Rylander, R. and Lin, R.H., (1→3)-beta-D-glucan–relationship to indoor airrelated symptoms, allergy and asthma, Toxicol., 152, 47, 2000. 89. Douwes, J., (1→3)-beta-D-glucans and respiratory health: a review of the scientific evidence, Indoor. Air., 15, 160, 2005. 90. Anderson, J.W. et al., Lipid responses of hypercholesterolemic men to oat-bran and wheat-bran intake, Am. J. Clin. Nutr., 54, 678, 1991. 91. Chen, J. et al., A randomized controlled trial of dietary fiber intake on serum lipids, Eur. J. Clin. Nutr., 60, 62, 2006. 92. Van Horn, L. et al., Serum lipid response to a fat-modified, oatmeal-enhanced diet, Prev. Med., 17, 377, 1988. 93. Stewart, F.M., Neutze, J.M., and Newsome-White, R., The addition of oatbran to a low fat diet has no effect on lipid values in hypercholesterolaemic subjects, N. Z. Med. J., 105, 398, 1992. 94. Leadbetter, J., Ball, M.J. and Mann, J.I., Effects of increasing quantities of oat bran in hypercholesterolemic people, Am. J. Clin. Nutr., 54, 841, 1991.
14 Rice Bran: Production, Composition, Functionality and Food Applications, Physiological Benefits Talwinder S. Kahlon
Contents Production.............................................................................................................305 Composition.......................................................................................................... 307 Food Applications................................................................................................308 Safety.....................................................................................................................309 Physiological Benefits..........................................................................................309 Cholesterol Lowering with Rice Bran......................................................309 Hamster Studies..............................................................................309 Rat Studies....................................................................................... 312 Other Species................................................................................... 313 Human Studies................................................................................ 314 Bile Acid Binding by Rice Bran.......................................................................... 316 Whole Grain Recommendation......................................................................... 316 Market Potential................................................................................................... 316 Summary............................................................................................................... 316 References............................................................................................................. 318
Production The world production of rice paddy in 2006 was 631 million metric tons. It resulted in 421 million tons of milled rice, of which 372 million tons were consumed as food. At least 114 countries grow rice and more than 50 have an annual production of 100,000 metric tons or more. The 11 top rice-growing countries are China, India, Indonesia, Bangladesh, Vietnam, Thailand, Myanmar, Philippines, Brazil, Japan, and the United States, producing 28.2%, 22.4%, 8.8%, 6.5%, 5.9%, 4.6%, 4.2%, 2.4%, 1.7%, 1.7%, and 1.5% of the world 305
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rice crop, respectively. The United States contributes 9.5 million metric tons to the annual world rice production. Thailand, Vietnam, the United States, India, Pakistan, and China exported 8.9, 5.9, 4.5, 4.2, 4.2, and 1.2 million tons, respectively: a total of 28.9 million tons of milled rice. Rice, wheat, and corn contribute to 50% of the human caloric intake; rice comprises 23%, wheat 17%, and corn 10% of the calories consumed [1]. Rice is primarily used for human consumption, whereas a larger proportion of wheat and corn are used as animal feed. On average, per capita rice consumption is 56.9 kg per year. Consumption in the developing countries is around 68.5 kg per capita per year, and 12.8 kg per year for developed countries. More than 60% of the calories consumed by the populations of East Asian countries such as Bangladesh, Cambodia, Laos, Myanmar, and Vietnam come from rice. Most rice is consumed as white, milled, polished rice. Rice as harvested from the field is called paddy. In the rice milling process, first the outermost layer, the hull, is removed to produce brown rice. This process is least damaging to the nutritional value of the rice and avoids the unnecessary loss of nutrients that occurs with the further processing to produce white milled rice. Brown rice would be considered whole grain. One hundred kilograms of paddy on milling yields 56 to 58 kg white rice, 10 to 12 kg broken rice, 18 to 20 kg husk, and 10 to 12 kg rice bran. Rice bran, a byproduct of the milling process, contains the enzyme lipase, which rapidly degrades the oil making the bran rancid and inedible. Researchers at the Western Regional Research Center, USDA-ARS, Albany, California, successfully stabilized rice bran by heating it to 125°C–135°C for 1 to 3 seconds at 11% to 15% moisture, and holding the extruded bran at an elevated temperature 97°C–99°C for 3 minutes prior to cooling, thereby deactivating the lipase [2]. Stabilized rice bran (SRB) has an estimated shelf life of about six months and could potentially be used as a food ingredient. Oil can be extracted from the bran and used as a healthful food component. Each year, 63 to 76 million tons of rice bran (rice milling by-product) is produced in the world and more than 90% of rice bran is sold cheaply as animal feed. The remainder is stabilized and could be used as a value-added health food product. Currently there is some market for SRB as a horse-feed supplement. In the United States, rice oil is being extracted from 15% to 20% of the rice bran. Parboiling, a steam treatment of paddy, gelatinizes the starch beneath the bran layer of the rice kernel, and yields more white rice, less broken rice, and higher fiber bran. Parboiling stabilizes rice bran by deactivating lipase, but it could destroy the beneficial antioxidants responsible for its healthpromoting properties. Steam cooking conditions destroy antioxidants [3]. Antioxidants derived from the diet scavenge and neutralize free radicals, a by-product of metabolism. Free radicals have been implicated in heart disease and cancer.
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Rice Bran Table 14.1 Composition of Rice Bran Percent of Stabilized Rice Bran
Parboiled Rice Bran
20.9 1.9 2.4 22.4
27.0 1.9 3.0 29.6
Total Dietary Fiber Soluble Dietary Fiber Nitrogen Fat Source: [14]
Table 14.2 Composition of Rice Bran Oil Component Unsaponifiable Matter Saturated Fatty Acids: Palmitic Stearic Arachidic Monounsaturated Fatty Acids: Oleic Vaccenic Gadoleic Polyunsaturated Fatty Acids: Linoleic Linolenic
% 4.1 17.0 1.7 0.6 39.4 0.9 0.6 34.3 1.3
Source: [15]
Composition The composition of stabilized and parboiled rice bran is given in Table 14.1, and of rice bran oil in Table 14.2. Nutritional studies have identified dietary fiber, bran oil, unsaponifiable matter, sterols, and protein as rice bran’s healthful components. The total dietary fiber (TDF) content of rice bran ranges from 21% to 27%, with less than 2% as soluble dietary fiber (Table 14.1). The protein content of stabilized rice bran ranges from 12% to 16%, and in parboiled rice bran from 14% to 20%. Rice bran protein is efficiently digested and has high nutritional value; it has a protein efficiency ratio of 1.6. Concentrates from
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Fiber Ingredients: Food Applications and Health Benefits Table 14.3 Composition of Rice Bran Oil Unsaponifiable Matter Sterol Plant Sterols Campesterol Stigmasterol β-Sitosterol Triterpene Alcohols 24-Methylene Cycloartenol Cycloartenol Aliphatic alcohols, hydrocarbons 4-Methyl Sterols
% 43
28
19 10
Source: [7]
rice bran protein have an efficiency ratio of 2.0 to 2.2, comparable to casein (2.5), a milk protein [4]. Rice bran contains 22% to 30% crude fat including 1.8% gum and 0.4% wax [5]. The crude fat content of commercial stabilized rice bran is 18% to 22%. The fatty acid composition of rice bran oil consists of 41% monounsaturates, 36% polyunsaturates, and 19% saturates (Table 14.2). The composition of unsaponifiable matter (UM) in rice bran oil is listed in Table 14.3. Rice bran oil (RBO) contains over 4% of UM, but peanut oil contains only 0.3% to 1% UM [6]. UM is a mixture of 43% plant sterols (campesterol, stigmasterol, β-sitosterol, and others), 28% triterpene alcohols (24-methylene cycloartanol, and cycloartenol), 19% less polar compounds such as aliphatic alcohols and other hydrocarbons, and 10% 4-methyl sterols [7]. Oryzanol, a mixture of ferulic acid esters of triterpenoid alcohols, composes 20% to 30% of UM and 1.1% to 2.6% of bran oil.
Food Applications Rice bran has many food applications in prepared foods, nutraceuticals, and functional foods. Some of the common applications of rice bran are in snack foods, bakery products, cereals, crackers, pasta products, dough conditioners, beverages, gluten-free foods, and medical foods. The USDA in partnership with a nonprofit organization provides a nutritious rice bran drink to preschool children in the Latin American countries. Rice-bran-containing beverage base can be used for isotonic drinks, iced tea drinks, enhanced juices, mineral supplements, and sports beverages. “Rice Milk” non-dairy alternative to milk is made from organically grown rice. Healthy meal replacement drinks made from stabilized rice bran are being introduced in the market.
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Safety Stabilized rice bran has shown no negative influence on shelf life or organoleptic properties of the various foods when used as an ingredient. Stabilized rice bran has been shown to have no adverse effects on animal health or feed nutritional quality when fed at 60% of the diet in chicks [8, 9] or up to 40% of diet of pigs [10].
Physiological Benefits Cholesterol Lowering with Rice Bran Hamster Studies The hamster has become the preferred rodent model for cholesterol studies, since it has a gall bladder, which is absent in the rat, and the lipoprotein profile of hamster plasma by density gradient ultracentrifugation contains distinct very low-density (20%), low-density (25%), and high-density (55%) lipoprotein fractions. Furthermore, hamsters and humans are reported to be similar in having significant levels of circulating plasma cholesterol and an intrinsically low rate of hepatic cholesterol synthesis, and a similarity in their response to diet modification and drugs [11]. Cholesterol lowering in hamsters by stabilized or parboiled rice bran in the United States was first reported by USDA-ARS (Albany, California) scientists [12] and was acknowledged by a feature article in the Journal of the American Oil Chemists’ Society [13] in which the need was expressed for funding a human study to validate these findings in hamsters. Diets containing 10% TDF from intact full-fat rice bran (stabilized or parboiled) resulted in significantly lower plasma and liver cholesterol compared with the 10% cellulose control diet in hamsters fed 0.5% cholesterol [14]. Replacing one-third of the stabilized rice bran fiber with wheat bran fiber also resulted in significantly lower plasma and liver cholesterol (Table 14.4). In a subsequent study [15], diets containing 10% TDF from stabilized rice bran significantly reduced plasma cholesterol compared to those fed a cellulose control diet, both in the presence and absence of 0.3% cholesterol in the diet. In the cholesterolfed hamsters, diets containing 11%, 22%, 33%, and 44% rice bran resulted in plasma cholesterol reductions of 8%, 11%, 15%, and 21%, respectively, compared with control values. Plasma cholesterol reductions were significant only with the diet containing 44% rice bran. Although plasma cholesterol reductions were significantly correlated with the level of rice bran in the diet (r = 0.38), the low correlation coefficient suggested that the rice bran level alone was a poor predictor of plasma cholesterol lowering.
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Table 14.4 Hamster Studies: Plasma and Liver Cholesterol Lowering by Rice Bran Plasma cholesterol (mg/dL)
Liver cholesterol (mg/g)
Control
Rice Bran
402 327 322 302 281 376 57 37 36 54 46 56
274 255 237 276 266 338 31 28 23 43 32 49
Effect Significant Significant Significant Not significant Not significant Significant Significant Significant Significant Significant Significant Significant
Ref. 14 15 5 16 17 21 14 15 5 16 17 21
Several fractions of rice bran were evaluated for cholesterol-lowering properties. Defatted rice bran resulted in a loss of cholesterol-lowering ability [14, 15], suggesting that the lipid fraction was necessary for maximum cholesterol-lowering potential. A combination of defatted rice bran plus RBO or degummed, dewaxed RBO resulted in significant liver cholesterol reductions [5, 15]. However, RBO extracted at 4°C or 54°C and wax and gum fractions of RBO had no significant influence on cholesterol status compared with their respective oil controls [5]. When recombined, it appeared that defatted rice bran and RBO were less effective in lowering cholesterol compared with intact full-fat rice bran, suggesting that either intact RBO was less available or there was a loss/inactivation of cholesterol-lowering activity in the rice oil fractionation process. Since the liver is the principal organ responsible for the regulation of plasma cholesterol levels, liver cholesterol levels also provide a measure of the influence of diet on cholesterol metabolism. Liver cholesterol was significantly lowered in hamsters by diet containing 10% TDF from rice bran or a 5:5 TDF combination of rice bran and a β-glucan-enriched (19% total β-glucans) barley fraction in diets containing 0.25% cholesterol [16]. In the same study, a diet containing a combination of rice bran and oat bran (5:5, TDF) with 2.6% total β-glucans (0.3% from rice bran, 2.3% from oat bran) resulted in significant plasma and liver cholesterol reductions, suggesting that the contribution of rice bran in lowering cholesterol in hamsters is likely due to components other than β-glucans or soluble fiber (Table 14.4). Measurement of diet slurry viscosities revealed rice bran diet viscosity to be similar to that of the cellulose (insoluble fiber) control diet (<10 cP over a three-hour period), rather than to oat bran diet viscosity (104 cP), indicating that cholesterol lowering
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by rice bran is related to a mechanism other than gel forming and sequestering or entrapment of lipid, bile acids, or their metabolites. In the earlier studies [5, 14, 15] in which either 0.3% or 0.5% cholesterol was fed, rice bran resulted in significant plasma cholesterol reductions, but when dietary cholesterol was lowered to 0.25%, plasma cholesterol was not significantly reduced by the rice bran diet, suggesting that the plasma cholesterol response is dependent on the level of hypercholesterolemia induced in the animals [16]. The source of dietary protein is an additional influence on plasma cholesterol elevations. It is common knowledge that vegetarians have lower plasma cholesterol levels than persons consuming animal protein. In each of the aforementioned hamster studies, the control diets contained casein as the sole source of protein, while treatment diets contained some plant protein. Therefore, a study was designed in which the contribution of plant protein was made equal in all treatments [17]. Diets contained 0.3% cholesterol, 10% TDF, 10.1% fat, and 3% nitrogen with the same plant-to-animal N ratio (44:56), using soy protein and casein in the control diet. Plasma cholesterol was elevated in the control animals to 281 mg/dL, 13% lower than that (322 to 325 mg/dL) observed in previous studies [5, 15] in which hamsters were fed 0.3% cholesterol with casein as the sole source of protein in the control diet. In this study, the unsaponifiable matter (UM) was isolated from rice bran oil and added to cellulose or rice bran diets to provide a total of 0.4% or 0.8% UM in the diets. Probably as a result of the lower level of hypercholesterolemia in the control animals, plasma cholesterol was not significantly lower in animals fed rice bran without added UM but was significantly lower in animals fed stabilized or raw rice bran with 0.4% additional UM from RBO, compared to the control group. Liver cholesterol was significantly lowered by stabilized or raw rice bran with or without added U (0.8% or 0.4% U, respectively), and by cellulose diets with added U (0.8%). Plasma and liver cholesterol reductions were proportional to the amount of UM in the hamster diet. Rice bran diets lowered cholesterol up to twice as much as cellulose diets with equivalent levels of UM. Fecal fat excretion was significantly negatively correlated to liver (r = –0.97) and plasma (r = –0.83) cholesterol values. The results of these hamster studies suggest that UM and other components of rice bran have cholesterol-lowering activity, possibly through increased fecal excretion of lipids. Kahlon et al. [18] observed a reduction (49% to 65%) in foam cells in the inner bend of the aortic arch in hamsters consuming rice bran diets containing 20% fat and 0.5% cholesterol for six weeks. The size of the plaque area on the inner bend of the aortic arch is a marker for arteriosclerosis and heart disease. Adding a megadose of vitamin E (1000 IU/Kg) resulted in further reduction in the aortic plaque area, but the difference was not significant over animals fed an adequate level (50 IU/kg) of vitamin E. Animals on the rice bran diet excreted more neutral sterols compared to the control animals. Animals consuming megadoses (21 times the normal dosage) of vitamin E with their rice bran diets excreted more neutral sterols than animals receiv-
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ing an adequate level of vitamin E. Plant sterols as a major component of these rice bran diets inhibit cholesterol absorption in the intestinal tract and are a proposed mechanism for cholesterol lowering [19]. Rong et al. [20] reported significant reductions in plasma cholesterol (PC), very low density lipoprotein cholesterol (VLDL-C), and low density lipoprotein cholesterol (LDL-C) in hamsters fed 1% oryzanol in diets containing 5% coconut oil and 0.1% cholesterol for seven weeks. Areas of aortic foam cells were reduced (67%) in animals on the oryzanol diet. Kahlon et al. [21] reported significant reductions in PC, VLDL-C, and liver cholesterol in animals on rice bran diets compared with corn bran or wheat bran diets. Extrusion cooking (processing at two energy levels, 221 and 442 Wh/kg dm) did not change the hypocholesterolemic properties of the rice bran. Rat Studies Although the current preference among researchers is to use the hamster model for the evaluation of diet ingredient effects on cholesterol metabolism, earlier work was conducted primarily with the laboratory rat. In cholesterolfed rats, Ayano et al. [22] reported that the neutral detergent fiber fraction (high in hemicellulose) of rice bran had serum cholesterol-lowering effects, while the acid detergent fiber fraction was ineffective. The hemicellulose fraction was isolated from defatted rice bran and fed to rats at 2% of the diet, resulting in significantly reduced plasma cholesterol (PC) levels (23); however, liver cholesterol was not significantly influenced in either study. Data from the latter investigation suggested that the hypocholesterolemic effect of rice bran hemicellulose involved increased excretion of bile acid, but not liver accumulation of cholesterol or suppression of cholesterol absorption. Others reported no significant PC reductions with diet containing 10% stabilized rice bran from parboiled rice compared to 10% cellulose or fiber-free control diets fed to rats for four weeks [24]; however, none of the diets contained added cholesterol and the level of rice bran in the diet was low. When diets containing 1% cholesterol, 0.2% cholic acid, 10% TDF from raw or parboiled rice bran, and 17% to 19% fat were fed to rats for 21 days, both plasma and liver cholesterol levels were significantly reduced by the rice bran diets compared with the fiber-free control diet [25]. Topping et al. [26] found significantly lower plasma and liver cholesterol in rats fed cholesterol-free diets containing 7% TDF from heat-stabilized rice bran compared to 7% TDF from unprocessed wheat bran. The cholesterol reductions were related to increase in hepatic low-density lipoprotein (LDL) receptor activity. Supplementing 5% fish oil in the diet achieved further reductions in PC. Cholesterol-lowering effects of rice bran oil and rice bran oil UM were reported in rats fed 1% cholesterol and 0.5% cholic acid diets for eight weeks [27]. Results showed that either 10% RBO or 0.4% rice bran oil UM significantly lowered PC and liver cholesterol compared to peanut oil. In another study with cholesterol-fed rats, significantly lower PC, LDL-C, and VLDL-C were observed with 10% RBO compared with those fed peanut oil [28]. An
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addition of 0.5% oryzanol to RBO diet showed a further significant decrease in PC. Rice bran oil also lowered liver cholesterol and triglycerides significantly. Evidence of a possible mechanism for the hypocholesterolemic activ ity of oryzanol was reported in a subsequent study in which a significant increase in fecal cholesterol and bile acid excretion and a 20% reduction in cholesterol absorption in vitro were observed after rats were fed 0.5% oryzanol and 1% cholesterol diet [29]. An additional mechanism for reducing atherosclerotic risk with oryzanol was suggested by significantly lower ADPinduced platelet aggregation and total inhibition of aggregation by collagen when 0.5% oryzanol was added to 1% cholesterol rat diet [30]. Other components of rice bran reported to have cholesterol-lowering activity in rats include wax isolated from RBO, which significantly lowered plasma and liver cholesterol and increased fecal fat excretion when fed at 10% of the diet [31], and rice bran protein, which significantly lowered serum cholesterol compared to casein or fish protein in rats fed cholesterol-free diet [32]. The hypocholesterolemic effect of rice protein was attributed to the higher arginine/lysine ratio in rice protein relative to animal protein. Morita et al. [33] reported significant serum cholesterol reduction in rats fed a rice protein diet compared with those fed a casein diet. Sunitha et al. [34] observed significant reduction in PC, LDL-C, and liver cholesterol in rats fed rice bran oil plus safflower/sunflower oil in a 70:30 ratio for four weeks. The fecal neutral sterols and bile acid content increased in animals on a diet containing rice bran oil. Other Species Rabbits fed 20% rice protein diet had significantly lower PC, VLDL-C, and LDL-C compared to those fed casein [35]. In addition to the higher arginine/lysine ratio of rice protein compared to that of casein [1.13 vs. 0.44), the authors also suggested that the lower percentage of acetate-generating amino acids (valine, leucine, isoleucine, phenylalanine, tryptophan, and lysine) in rice protein versus casein (33.49% vs. 38.17%, respectively) may have been partly responsible for the cholesterol-lowering effects. In male cynomolgus monkeys, rice bran oil significantly lowered PC and LDL-C without affecting high density lipoprotein cholesterol (HDL-C) compared with a diet containing a mixture of butter oil, com oil, and olive oil in an eight-week feeding study [36]. In contrast, feeding a 50% rice bran diet to female cynomolgus monkeys fed increasing amounts of cholesterol for 9 months resulted in no PC reductions [37]. A stabilized rice bran diet with 7% TDF significantly lowered PC but not liver cholesterol in C57BL/6 mice compared to a fiber-free control diet when diets contained 0.06% cholesterol from ground beef [38]. In chicks fed a diet containing 0.5% cholesterol, 60% full-fat rice bran, and 24% fat, PC and LDL-C were significantly lowered while HDL-C was significantly increased, compared with the 7% fat control diet; however, when diets were made isocaloric (10.8% fat), LDL-C significantly increased and HDL-C
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Table 14.5 Human Studies: Plasma Cholesterol Lowering by Rice Bran (RB) and Rice Bran Oil (RBO) Plasma Cholesterol, mg/dL 21 days (100g RB) 21 days (100g RB) 15 days (RBO) 30 days (RBO) 4 weeks (60g RB) 21 days (15g RB) 21 days (30g RB) 42 days (84g RB)
Control
Treatment
235 217 247 247 245 176 176 267
211 208 204 183 242 172 169 245
Effect Significant Not significant Significant Significant Not significant Not significant Not significant Significant
Ref. 43 43 49 49 42 46 46 44
increased with no effect on PC [39]. Defatted rice bran increased PC, LDL-C, and HDL-C, suggesting that PC-lowering properties of rice bran in chicks may be associated with rice bran oil. Human Studies Unpolished rice showed a repressive effect on serum cholesterol and triglyceride elevations in adult males compared with those fed polished rice; the beneficial effect was attributed to the dietary fiber of the unpolished rice [40]. Five healthy young men consumed brown rice with 27.9 g of neutral detergent fiber (NDF) per day for 14 days, resulting in significant increases in fecal wet weight, dry weight, water, and fat excretion compared with those fed white rice with 13.7 g of NDF per day [41]. PC and HDL-C levels were not significantly different from those with a polished rice diet, possibly due to the fact that total cholesterol concentrations in the subjects were in the lower part of the normal range. In a four-week study, 24 mildly hypercholesterolemic men consuming 60 g/d of rice bran diet containing 11.8 g dietary fiber, had 4% (nonsignificant) reductions in LDL-C and apo-B, significant increases in their HDL-C/PC ratio, and no change in PC compared to those consuming wheat bran [42] (Table 14.5). It was concluded that a consumption of realistic amounts of a single food source of dietary fiber could provide a modest benefit to the antiatherogenic profile of plasma lipoproteins. In a three-week crossover design study, significant reductions in PC and LDL-C were observed in 11 subjects with moderately elevated blood cholesterol after consuming 100 g/d of rice bran or oat bran [43]. Reductions were 10% (significant) during the first three weeks and 5% (nonsignificant) during the second three-week period, with an overall reduction of 7% (Table 14.5). Cholesterol reductions with rice bran and oat bran were similar. In a six-week non-crossover design study [44], moderately hypercholesterolemic adults achieved significant reductions in serum total and LDL cholesterol by consuming 84 g/d
Rice Bran
315
of heat-stabilized, full-fat medium grain rice bran product or oat bran. The bran supplements were added to the subjects’ usual daily intake of a low-fat, low-cholesterol diet and did not replace any dietary components. There were no significant differences between the serum cholesterol reductions with the rice bran product (8.3%) versus those with the oat bran (13.0%). Addition of a mixture of 30 g each of rice bran and oat bran to the daily diets of 17 moderately hypercholesterolemic and hypertriglyceridemic individuals for six weeks resulted in no significant reductions in TC or HDL cholesterol [45]. The authors suggested that the level of dietary fiber tested may have been inadequate or that increasing soluble fiber intake may not be the sole answer to reduce hyperlipidemia. Consuming 15 or 30 g/d of rice bran by 18 normocholesterolemic subjects for three weeks resulted in no significant changes in TC, LDL cholesterol, or HDL cholesterol, although triglycerides (a risk factor) were significantly reduced with 15 g/d rice bran consumption compared with 15 g/d wheat bran [46]. Again, the normocholesterolemic state of the subjects may have been partly responsible for the lack of effect on TC and LDL-C and HDL-C. A 60 g mixture of rice bran oil and safflower oil (70:30) given for seven days to 10 females per group was more effective in lowering TC than either of the oils alone [47, 48]; most of the subjects had normocholesterolemic basal levels at the start of each treatment. Other investigators also reported a beneficial effect when customary cooking oil was replaced with rice bran oil for 15 and 30 days, resulting in significant reductions in TC and triglycerides in 12 hypercholesterolemic and hypertriglyceridemic subjects [49] (Table 14.5). Significant cholesterol-lowering effects of γ-oryzanol were reported in hyperlipidemic patients who were given 300 mg/d γ-oryzanol for three months [50]. Consuming a diet supplemented with 35.5 g/d of full-fat rice bran for 18 days significantly lowered serum cholesterol in 10 subjects, compared to a fiberfree control period, whereas 30 g/d of defatted rice bran was not effective [51], suggesting that cholesterol reductions were due to the lipid component of rice bran. Hypercholesterolemic human subjects showed the same cholesterollowering effect as the animal model when fed cereal fiber, rice bran, and oat bran diets. In experiments conducted over 15 and 30 days, Raghuram et al. [49] reported a reduction in TC among 12 hypercholesterolemic men, who replaced their normal diet of peanut cooking oil with rice bran oil (Table 14.5). However, there were no reductions in total cholesterol in normocholesterolemic men who ate 15 or 30 grams of dietary fiber per day [46]. Hypercholesterolemic subjects who consumed the NCEP step-1 diet and a tocotrienol-rich extract of rice bran oil significantly reduced TC and LDL-C [52]. Hypercholesterolemic individuals who consumed rice bran oil or the tocotrienol-rich fraction from rice bran oil reduced TC and LDL-C [53, 54]. Numerous and exhaustive human and animal studies have shown that stabilized rice bran, rice bran oil, and tocotrienol-rich fraction of rice oil lower TC, LDL-C, and improve the HDL/TC ratio.
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Fiber Ingredients: Food Applications and Health Benefits
Bile Acid Binding by Rice Bran Binding bile acids and increasing their fecal excretion has been linked with cholesterol lowering in plasma and liver [55–57]. In vitro bile acid binding by stabilized rice bran on dry matter basis has been observed to be 12% to 25% of that by cholestyramine (a bile acid binding drug) [58, 59].
Whole Grain Recommendation USDA’s new food guide (2005) recommends consuming 50% of grains as whole rather than refined. The healthful potential of rice bran has been documented by various in vitro, animal and human studies. It would be advisable to consume brown rice as whole grain rice rather than fortifying milled white rice with stabilized rice bran. Brown rice takes 45 minutes to cook as compared with 20 minutes for white rice. Process technologies need to be perfected to reduce cooking time for brown rice and consumers need to receive the information that brown rice is a preferred food. Instant brown rice, partially cooked brown rice, or rice flour blasted brown rice to facilitate water penetration are in the works at various research facilities to reduce the cooking time for brown rice and to facilitate its consumer acceptance.
Market Potential Currently only a small fraction of the rice bran produced worldwide is stabilized and sold as health food. Rice bran and its fractions are sold at different price levels depending upon the final use or application. The wholesale price for stabilized rice bran ranges from $2.92 to $4.25 per Kg. Retail prices vary from $6.14 to $58.64 per Kg (Table 14.6). If all the rice bran and rice oil produced were sold as health food, the price would lower to encourage consumer preference. The stabilized rice bran at $1 per Kg would have a potential market value of $63 to $76 billion per year (world production = 63 to 76 million tons). It would be utilized as a food ingredient and its full healthful potential could be realized.
Summary Animal and human studies show cholesterol lowering with rice bran in hypercholesterolemic individuals, with reductions occurring usually in the
317
Rice Bran Table 14.6 Stabilized Rice Bran Prices Source
$/Kg
Wholesale Rice Bran (spot price) Rice Bran Deoiled
2.92 4.25
Retail Health Foods Markets Rice Bran Organic Rice Bran Solubles Rice Bran Rice Bran Syrup Rice Bran (low fiber) Rice Bran (with fiber) Rice Bran (with fiber) Rice Bran Beverage Rice Bran Oil
9:50 87.89 6.14 27.48 55.01 58.64 49.50 102.65 4.45–15.38
Notes: 63–76 million tons/year, $63–76 billion potential value per year.
LDL (atherogenic) fraction. Specific rice bran fractions showing hypocholesterolemic activity include rice bran oil, unsaponifiable matter, dietary fiber, and protein. There is a dose response to the level of rice bran and rice bran oil unsaponifiable matter for cholesterol reductions, but intact full-fat rice bran appears to be the most effective. This suggests that incorporation of intact stabilized rice bran into food products would be more effective than the fortification of food with isolated individual concentrated fractions of rice bran. Consuming brown rice as whole grain would be highly desirable. Possible mechanisms for cholesterol lowering with rice bran include interference with absorption/reabsorption of dietary and/or endogenous lipid in the gastrointestinal tract and increased excretion of bile acids, which results in utilization of more cholesterol for bile acid synthesis. In addition, changes in hepatic LDL receptor activity have been reported with rice bran feeding [18], and the inhibition of cholesterol synthesis by tocols and tocotrienols present in rice bran oil may also contribute to cholesterol reduction [42]. The evidence to date suggests that several mechanisms may be simultaneously involved in the cholesterol-lowering effects of rice bran. Atherosclerosis is a disease that apparently takes from 40 to 50 years to develop. The concept of a 2% reduction in risk with each 1% reduction in cholesterol in high-risk individuals is well accepted. With reported plasma total and LDL cholesterol reductions of 4% to 10% in subjects with moderate hypercholesterolemia, the available information suggests that inclusion of rice bran in the diet, along with a reduction of fat calories to 30% and satu-
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Fiber Ingredients: Food Applications and Health Benefits
rated fat to less than one-third of total fat, could prove to be healthful for the general population. Commercial interest generated by the health effects of rice bran has contributed to the introduction of numerous value-added ricebran-containing foods and food products such as breads, breakfast cereals, cakes, cookies, extruded snacks, muffins, pies, and snack bars. The popularity of the new rice bran products is encouraging and expected to continue with health-conscious consumers. Incentives are needed for the rice industry to increase the production and availability of stabilized rice bran for its incorporation into more healthful, value-added foods for human consumption.
References
1. Khush, G. 2003. Productivity improvements in rice. Nutr. Rev. 61:114–116. 2. Randall, J. M., R. N. Sayre, W. G. Schultz, R. Y. Fong, A. P. Mossman, R. E. Tribelhorn, and R. M. Saunders. 1985. Rice bran stabilization by extrusion cooking for extraction of edible oil. J. Food Sci. 50:361–364. 3. Steinhart, H., T. Rathjen. 2003. Dependence of tocopherol stability on different cooking procedures of food. Int. J. Vitam. Nutr. Res. 73:141–151. 4. Connor, M. A., R. M. Saunders, G. O. Kohler. 1976. Rice bran protein concentrates obtained by wet alkaline extraction. Cereal Chem. 53:488–496. 5. Kahlon, T. S., R. M. Saunders, R. N. Sayre, F. I. Chow, M. M. Chiu, and A. A. Betschart. 1992. Cholesterol-lowering effects of rice bran and rice bran oil fractions in hypercholesterolemic hamsters. Cereal Chem. 69:485–489. 6. Sharma, R. D., C. Rukmini. 1986. Rice bran oil and hypocholesterolemia in rats. Lipids 21:715–717. 7. Itoh, T., T. Tamura, and T. Matsumoto. 1973. Sterol composition of 19 vegetable oils. J. Am. Oil Chemists Soc. 50:122–125. 8. Sayre, R. N., L. Earl, F. H. Kratzer, and R. M. Saunders. 1987. Nutritional qualities of stabilized and raw rice bran for chicks. Poultry Sci. 66:493–499. 9. Sayre, R. N., L. Earl, F. H. Kratzer, and R. M. Saunders. 1988. Effects of diets containing raw and extrusion-cooked rice bran on growth and efficiency of food utilization of broilers. Brit. Poultry Sci. 29:815–823. 10. Calvert, C., K. Parker, Z. J. Parker, R. N. Sayre, and R. M. Saunders. 1985. Rice bran in swine rations. Calif. Agric. May–June, 19. 11. Spady, D. K., J. M. Dietschy. 1985. Rates of cholesterol synthesis and low-densilipoprotein uptake in the adrenal glands of the rat, hamster and rabbit in vivo. Biochim. Biophys. Acta 836:167–175. 12. Kahlon T. S., R. M. Saunders, R. N. Sayre, F. I. Chow, M. M. Chiu, and A. A. Betschart. 1989. Effect of rice bran and oat bran on plasma cholesterol in hamsters. Cereal Foods World 34:768 (Abstract). 13. Haumann, B. F. 1989. Rice bran linked to lower cholesterol. J. Am. Oil Chemists Soc. 66:615–618. 14. Kahlon T. S., R. M. Saunders, R. N. Sayre, F. I. Chow, M. M. Chiu, and A. A. Betschart. 1990. Influence of rice bran, oat bran, and wheat bran on cholesterol and triglycerides in hamsters. Cereal Chem. 67:439–443.
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15. Kahlon T. S., F. I. Chow, R. N. Sayre, and A. A. Betschart. 1992. Cholesterollowering in hamsters fed rice bran at various levels, defatted rice bran and rice bran oil. J. Nutr. 122:513–519. 16. Kahlon T. S., F. I. Chow, B. E. Knuckles, and M. M. Chiu. 1993. Cholesterollowering effects in hamsters of β-glucan-enriched barley fraction, dehulled whole barley, rice bran, and oat bran and their combinations. Cereal Chem. 70:435–440. 17. Kahlon T. S., F. I. Chow, M. M. Chiu, C. A. Hudson, and R. N. Sayre. 1996. Cholesterol-lowering by rice bran and rice bran oil unsaponifiable matter in hamsters. Cereal Chem. 73:69–74. 18. Kahlon, T. S., F. I. Chow, and D. F. Wood. 1999. Cholesterol response and foam cell formation in hamsters fed rice bran, oat bran, and cellulose + soy protein diets with or without added vitamin E. Cereal Chem. 76:772–776. 19. Mattson, F.H., S. M. Grundy, and J. R. Crouse. 1982. Optimizing the effect of plant sterols on cholesterol absorption in man. Am. J. Clin. Nutr. 35:697–700. 20. Rong, N. L., L. M. Ausman, and R. J. Nicolosi. 1997. Oryzanol decreases cholesterol absorption and aortic fatty streaks in hamsters. Lipids. 32:303–309. 21. Kahlon, T. S., R.H. Edwards, and F. I. Chow. 1998. Effect of extrusion on hypocholesterolemic properties of rice, oat, corn, and wheat bran diets in hamsters. Cereal Chem. 75:897–903. 22. Ayano Y., F. Ohta, Y. Watanabe, and K. Mita. 1980. Dietary fiber fractions in defatted rice bran and their hypocholesterolemic effect in cholesterol-fed rats. J. Nutr. Food (Japan). 33:283–291. 23. Aoe S., F. Ohta, and Y. Ayano. 1989. Effect of rice bran hemicellulose on the cholesterol metabolism in rats. Nippon Eiyoshokuryo Gakkaishi. 42:55–61. 24. Johnson I. T., J. M. Gee, and J. C. Brown. 1989. A comparison of rice bran, wheat bran and cellulose as sources of dietary fibre in the rat. Food Sci. Nutr. 42:153–163. 25. Rouanet, J-M, C. Laurent, and P. Besancon. 1993. Rice bran and wheat bran: selective effect on plasma and liver cholesterol in high-cholesterol fed rats. Food Chem. 47:67–71. 26. Topping D. L., R. J. Illman, P. D. Roach, R. P. Trimble, A. Kambouris, and P. J. Nestel. 1990. Modulation of the hypolipidemic effect of fish oils by dietary fiber in rats: studies with rice and wheat bran. J. Nutr. 120:325–330. 27. Sharma R. D., and C. Rukmini. 1987. Hypocholesterolemic activity of unsaponifiable matter of rice bran oil. Indian J. Med. Res. 85:278–281. 28. Seetharamaiah, G. S., and N. Chandrasekhara. 1989. Studies on hypocholesterolemic activity of rice bran oil. Atherosclerosis 78:219–223. 29. Seetharamaiah, G. S., and N. Chandrasekhara. 1990. Effect of oryzanol on cholesterol absorption & biliary & fecal bile acids in rats. Indian J. Med. Res. [B] 92:471–475. 30. Seetharamaiah, G. S., T. P. Krishnakantha, and N. Chandrasekhara. 1990. Influence of oryzanol on platelet aggregation in rats. J. Nutr. Sci. Vitaminol. 36:291–295. 31. Ishibashi, G., and M. Yamamoto. 1980. Effect of rice wax, garlic, and gingko seed component on plasma and liver cholesterol levels in rats. Kyushi Women’s Univ. 16:115–127. 32. Sugano, M., N. Ishiwaki, and K. Nakashima. 1984. Dietary protein-dependent modification of serum cholesterol level in rats. Ann. Nutr. Metab. 28:192–199.
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33. Morita, T., A. Oh-hashi, K. Takei, M. Ikai, S. Kasaoka, and S. Kiriyama. 1997. Cholesterol-lowering effects of soybean, potato and rice proteins depend on their low methionine contents in rats fed a cholesterol-free purified diet. J. Nutr. 127:470–477. 34. Sunitha, T., R. Manorama, and C. Rukmini. 1997. Lipid profile of rats fed blends of rice bran oil in combination with sunflower and safflower oil. Plant Foods for Human Nutr. 51:219–230. 35. Alladi S., R. Gilbert, and K. R. Shanmugasundaram. 1989. Lipids, lipoproteins and lipolytic activity in plasma with dietary protein changes. Nutr. Rep. Int. 40:653–661. 36. Nicolosi R. J., L. M. Ausman, and D. M. Hegsted. 1991. Rice bran oil lowers serum total and low density lipoprotein cholesterol and apo B levels in nonhuman primates. Atherosclerosis 88:133–142. 37. Malinow, M. R., P. McLaugwin, L. Papworth, H. K. Naito, and L. A. Lewis. 1976. Effect of bran and cholestyramine on plasma lipids in monkeys. Am. J. Clin. Nutr. 29:905–911. 38. Hundemer, J. K., S. P. Nabar, B. J. Shriver, and L. P. Forman. 1991. Dietary fiber sources lower blood cholesterol in C57BL/6 mice. J. Nutr. 121:1360–1365. 39. Newman, R. K., A. A. Betschart, C. W. Newman, and P. J. Hofer. 1992. Effect of full-fat or defatted rice bran on serum cholesterol. Plant Foods Hum. Nutr. 42:37–43. 40. Suzuki, M. 1982. Repressive effect of dietary fiber fractions in unpolished rice on the increase in cholesterol and triglyceride. J. Nutr. Food (Japan) 35:155–160. 41. Miyoshi, H., T. Okuda, Y. Oi, and H. Koishi. 1986. Effects of rice fiber on fecal weight, apparent digestibility of energy, nitrogen and fat, and degradation of neutral detergent fiber in young men. J. Nutr. Sci. Vitaminol. 32:581–589. 42. Kestin M., R. Moss, C. M. Clifton, and P. J. Nestel. 1990. Comparative effects of three cereal brans on plasma lipids, blood pressure, and glucose metabolism in mildly hypercholesterolemic men. Am. J. Clin. Nutr. 52:661–666. 43. Hegsted M., M.M. Windhauser, S. K. Morris, and S. B. Lester. 1993. Stabilized rice bran and oat bran lower cholesterol in humans. Nutr. Res. 13:387–398. 44. Gerhardt, A. L., and N. B. Gallo. 1998. Full-fat rice bran and oat bran similarly reduce hypercholesterolemia in humans. J. Nutr. 128:865–869. 45. Ranhotra, G. S., J. A. Gelroth, R. D. Reeves, M. K. Rudd, W. R. Durkee, J. D. Gardner. 1989. Short-term lipidemic responses in otherwise healthy hypercholesterolemic men consuming foods high in soluble fiber. Cereal Chem. 66:94–97. 46. Sanders, T. A. B., and S. Reddy. 1992. The influence of rice bran on plasma lipids and lipoproteins in human volunteers. Eur. J. Clin. Nutr. 46:167–172. 47. Suzuki, S., and S. Oshima. 1970. Influence of blending of edible fats and oils on human serum cholesterol level (Part 1). Blending of rice bran oil and safflower oil. J. Nutr. (Japan). 28:3–6. 48. Suzuki, S., and S. Oshima. 1970. Influence of blending oils on human serum cholesterol (Part 2). Rice bran oil, safflower oil, sunflower oil. J. Nutr. (Japan) 28:194–198. 49. Raghuram, T. C., D. B. Rao, and C. Rukrnini. 1989. Studies on hypolipidemic effects of dietary rice bran oil in human subjects. Nutr. Rep. Int. 39:889–895. 50. Yoshino, G., T. Kazumi, M. Amano, M. Tateiwa, T. Yamasakim, S. Takashima, M. Iwai, H. Hatanaka, and S. Baba. 1989. Effects of gamma-oryzanol and probucol on hyperlipidemia. Current Therap. Res. 45:975–982.
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51. Tsai, C. E., H. Ting, L. J. Wang, and T. Lin. 1992. The effect of rice bran on blood lipids in man. J. Chinese Agric. Chem. Soc. 30:484–495. 52. Qureshi, A. A., B. A. Bradlow, W. A. Salser, and L. D. Brace. 1997. Novel tocotrienols of rice bran modulate cardiovascular disease risk parameters of hypercholesterolemic humans. J. Nutr. Biochem. 8:290–298. 53. Rajnarayana, K., M. C. Prabhakar, and D. R. Krishna. 2001. Influence of rice bran oil on serum lipid peroxides and lipids in human subjects. Indian J. Physiol Pharmacol. 45:442–444. 54. Qureshi, A. A., S. A. Sami, W. A. Salser, and F. A. Khan. 2002. Dose-dependent suppression of serum cholesterol by tocotrienol-rich fraction (TRF25) of rice bran in hypercholesterolemic humans. Atherosclerosis 161:199–207. 55. Trowell, H. C. 1975. Refined Foods and Disease, Burkitt and Trowell, Eds., Academic Press, London, 195–226. 56. Lund, E. K., J. M. Gee, J. C. Brown, Wood, P. J., and Johnson, I. T. 1989. Effect of oat gum on the physical properties of the gastrointestinal contents and on the uptake of D-galactose and cholesterol by rat small intestine in vitro. Br. J. Nutr. 62:91–101. 57. Anderson, J. W., and A. E. Siesel. 1990. Hypocholesterolemic effects of oat products, in New Developments in Dietary Fiber: Physiological, Physiochemical, and Analytical Aspects, Furda, I., Brine, C.J., Eds., Plenum Press, New York, 17–36. 58. Kahlon, T. S., and F. I. Chow. 2000. In vitro binding of bile acids by rice bran, oat bran, wheat bran and corn bran. Cereal Chem. 77: 518–521. 59. Kahlon, T. S., and Woodruff, C. L. 2003. In vitro binding of bile acids by rice bran, oat bran, barley and β-glucan enriched barley. Cereal Chem. 80:260–263.
15 Barley Fiber Christine E. Fastnaught
Contents Characteristics...................................................................................................... 323 Functionality and Food Applications............................................................... 329 Extrusion...................................................................................................... 329 Bakery Products.......................................................................................... 332 Meats.............................................................................................................334 β-glucan Extracts........................................................................................334 Miscellaneous.............................................................................................. 336 Physiological Benefits.......................................................................................... 337 Digestion...................................................................................................... 337 Cardiovascular Disease............................................................................. 338 Glucose and Insulin Response..................................................................342 Blood Pressure.............................................................................................344 Cancer and Immune Response.................................................................344 Safety/Toxicity......................................................................................................346 References............................................................................................................. 347
Characteristics Barley is a unique cereal grain because soluble and insoluble fibers are distributed throughout the mature seed. The content and balance of these fibers in the whole grain is effected by genetics and growing environments. Genetics controls the type of hull, cemented or loose, and the subsequent processing required prior to consumption. Malt and feed barley have a cemented hull (referred to as covered or hulled), which must be removed by abrasion, while hulless barley has a loose hull, which can be removed by air. Barley food ingredients produced with either type contain significant levels of fiber and include whole grain barley, pearled barley, barley flour, and barley fiber concentrates produced through dry milling, malting, and wet extraction. The importance of barley fiber in the human diet was recently validated by the FDA authorizing the use of a health claim on food packages for the role 323
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Fiber Ingredients: Food Applications and Health Benefits
Table 15.1 Average Fiber Composition of 14 Covered and 14 Hulless Barley Cultivars2, 5 Component Total Fiber Arabinoxylan A-X ratioa Cellulose β-glucan Klason lignin Uronic acid Galactose Mannose a
Covered
Hulless
20.03 7.50 0.44 4.60 4.91 1.50 0.80 0.30 0.40
15.00 5.01 0.72 2.39 5.64 0.81 0.70 0.30 0.40
= Ratio of arabinose to xylose.
of β-glucan soluble fiber from barley in reducing the risk of coronary heart disease.1 The fiber in barley is found in the hull, pericarp, and cell walls of the aleurone and starchy endosperm. The hull fiber is equal parts cellulose and arabinoxylan and about 20% lignin.2 The hull is removed for most barley products, but is the main component of brewers’ spent grains which have been utilized in foods.3 The pericarp and aleurone cell walls are 70% arabinoxylan and 25% β-glucan.4 In contrast, the cell walls of the starchy endosperm are 75% β-glucan and 20% arabinoxylan. All of the cell walls have small amounts of cellulose and glucomannan. The fiber characteristics of whole grain hulled and hulless barley reflect these different sources2,5 (Table 15.1). Since the hull of hulless barley is lost in harvesting and cleaning, the resulting fiber in the grain has less cellulose and arabinoxylans but more β-glucans. Endosperm characteristics can have a significant effect on the fiber content of barley. Fastnaught6 and Newman and Newman7 recently reviewed the effects of endosperm starch and protein on the levels and type of fiber and β-glucan in barley. Both hulled and hulless barley cultivars that have waxy starch (95% to 100% amylopectin) can have 25% to 100% higher levels of soluble fiber in the form of β-glucan (Table 15.2). Cultivars that combine the waxy endosperm, hulless and high protein genes can have up to 400% more β-glucan fiber than the normal cultivars but typically have an associated shrunken endosperm, which has a negative affect upon yield. Cultivars that have high amylose starch also tend to have higher levels of β-glucan.8 While β-glucan is one of the primary components of the cell walls of both barley and oats, there are definite differences in regard to the anatomical distribution of β-glucan, especially in the traditionally grown varieties of the two cereals. The (1→3),(1→4)-linked β-D-glucans can be identified visually in both barley and oats using Calcofluor White M2R New stain.9 Stained crosssections of barley and oats show that the oat aleurone cell walls (outer tissue
325
Barley Fiber Table 15.2
Range of Total and Soluble Dietary Fiber and β-Glucan Content in Diverse Barley Genotypes6-8 Dietary Fiber (% dry wt) Total Soluble
Genotype
Na
Hulled (covered) Hulless Waxy starch, hulled Waxy starch, hulless Waxy starch, high protein, hulless High amylose starch, hulless
126 19 3 20 2
15.0–24.1 11.0–15.7 20.0–21.0 13.1–20.1 33.4–34.0
3.3–6.7 3.0–7.0 6.4–7.2 5.2–10.2 18.1–19.6
2
17.2–17.9
6.8–7.5
a b
Nb 243 55 10 35 4 6
Total β-Glucan (% Dry Wt) 2.0–5.9 4.1–6.4 4.7–7.3 5.1–11.3 14.7–17.5 6.0–9.7
= number of cultivars/samples reported for range of dietary fiber. = number of cultivars/samples reported for range of total β-glucan.
layer of the grain) are thicker than the same cell walls in barley.10 Miller and Fulcher11 compared five oat and five barley cultivars ranging in β-glucan content from 2.8% to 11% using microspectrofluorometric scans of cross-sections of the central region of individual grains. The oat cultivars, which ranged in β-glucan from 3.7% to 5.1%, typically had a higher concentration of β-glucan located in the aleurone. The barley cultivars ranging in β-glucan from 2.8% to 11% had β-glucan distributed evenly throughout the grain with much higher concentrations in the endosperm than found in oats. Pearling hulled barley grain removes the outer layers, which contain much of the cellulose and arabinoxylan found in barley. Pearling hulless barley grain removes the pericarp, testa, and aleurone, producing a “true bran.”12 Pearl barley has from 35% to 78% less total and insoluble fiber depending on the degree of pearling.12–14 Soluble fiber and β-glucan content can decrease slightly or show increases from 5% to 32%.12–16 Barley fiber can be a by-product of other processing (malting, brewing, ethanol production) or one of the primary products from dry or wet milling. The by-products of malting and fermentation processes have been called brewers’ spent grains (BSG) or spent barley grain (SBG) or dried distillers’ grains (DDG). They consist of the hull and other water-insoluble components remaining after the grain is malted, macerated, and washed to remove soluble components. These products are a rich source of insoluble (98%) dietary fiber containing 48% to 59% TDF3,17 and can be further processed by milling and sieving to concentrate the high glutamine protein.18,19 Conventional roller-milling or impact and abrasive milling (pin mill, hammer mill, etc.) followed by air classification or sieving can be used to produce concentrated β-glucan fractions. Regardless of the type of milling, hulled cultivars are generally dehulled to eliminate the husk. Products derived
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from conventional milling are classified as flour, shorts, or bran, depending on particle size. Often the bran and shorts are combined because the brittleness of barley bran precludes a clean separation from the shorts.12 Thus, this type of barley bran will contain pericarp, testa, aleurone, and subaleurone, and the fiber content will increase as flour yield increases. Flour yields of 26.3% to 83.1% have been reported for barley.6,20–24 Bhatty20 milled a hulless and a waxy hulless barley at six different moisture levels and concluded that the highest flour yield for both cultivars (83.1% and 66.4%, respectively) was obtained by milling grain at 5% moisture. Compared to raw grain, β-glucan concentrations were 15% and 29% higher in the bran and 4% and 16% lower in the flour, respectively. Impact and abrasive milling followed by sieving or air classification produce coarse fractions high in fiber and β-glucan. The effectiveness of these procedures varies with type of mill and cultivar but fractions containing 12% to 23% β-glucan have been reported6 and are available commercially.25 Studies of barley β-glucan structure have focused on characterization of molecular weight and the products of enzyme digestion. Barley β-glucan is composed of glucose molecules linked by approximately 30% β-(1→3) and 70% β-(1→4) linkages. Lichenase digestion produces oligosaccharides of glucose with a degree of polymerization (DP) ranging from 3 to 15. Approximately 92% of the oligosaccharides are DP3 (cellotriosyl) or DP4 (cellotetraosyl). The molar ratio of DP3/DP4 is reported to range from 2.4 to 3.4 in barley and 2.0 to 2.7 in oat.26-29 Jiang and Vasanthan30 reported that watersoluble β-glucan from 10 barley cultivars (two pearled) had a lower molar ratio ranging from 2.1 to 2.8. In contrast, the DP3/DP4 ratio of wheat β-glucan is 4.531 and lichenin is 24.5.28 It has been suggested that a higher proportion of β-(1-3)-linked cellotriosyl units (higher molar ratio) could lead to a greater structural regularity resulting in decreased solubility.32 The peak molecular weight of barley β-glucan has been reported to vary from 0.2 x 106 to 2.66 x 106 (Table 15.3). However, when reviewing the data, several factors must be taken into consideration. First, solvent type and extraction temperature have a significant effect on the molecular weight of extracted β-glucan.27 Strong acid or base is often used to “completely” extract total β-glucan from barley and oats, and some studies suggest that β-glucans extracted with water tend to have lower molecular weight. Second, the cultivar genetics and growing environments also affect β-glucan molecular weight.33 And finally, enzyme activity is a critical factor that must be considered when reviewing β-glucan molecular weight data. Both oats and barley may have significant quantities of active β-glucanase. Hot ethanol or NaOH treatments prior to extraction have been recommended.34,35 If researchers do not take proper precautions, the reported β-glucan molecular weights may be significantly lower than actual values. This factor may also have an impact on solubility and viscosity. Total β-glucan content is being used as a marker for β-glucan soluble fiber in barley and oat products. Under most of the methods in which β-glucan solubility has been measured, barley and oats are comparable. However a
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Barley Fiber Table 15.3 Weight Average and Peak Molecular Weight of β-glucan from Barley and Oats. Solvent
Barley
Oat
Number of Cultivars
— 0.45 — — — — — — 2.25 185 181
24 barley58 1 barley, 1 oat59 6 barley, Greek60 1 normal, 3 waxy hulless barley33 2 waxy hulless barley33 1 normal, 2 waxy hulless barley34 1 normal, 2 waxy hulless barley34 1 normal, 2 waxy hulless barley34 1 barley, 1 oat35 1 barley, 1 oat35 1 barley, 1 oat35
Molecular Weight (weight average g/mol × 106) Water, 10˚C Water Water, 90˚C /enzymes Water, 23˚C NaOH-NaBH4 Water, 23˚C NaOH NaOH pre- + NaOH Water, 100˚C NaOH Na2CO3
1.2–1.6 0.67 0.45–1.32 0.72–2.34 2.92–3.30 0.27–0.66 0.8–1.2 1.32–1.87 1.64 173 162
Peak Molecular Weight (g/mol × 106) Water, 90˚C /enzyme NaOH Water, 40˚C & 65˚C Water / NaOH Water, 65˚C NaOH Na2CO3, pH 10 Na2CO3, pH 10
1.32–1.69 1.26 0.2–0.3 0.4–1.6 0.58–1.31 1.02–1.6 3.2 1.70–2.66
2.09–2.51 1.27 — — — — — 2.89–3.03
8 barley, 6 oat39 1 normal barley, 1 oat39 Sequential extracts, 1 barley61 Sequential extracts, 1 barley62 Sequential extracts, 24 barley47 Sequential extracts, 24 barley47 1 waxy hulless barley63 4 normal barley, 4 oat26
review of the data has not established a clear relationship between an in vitro level of solubility and the cholesterol-lowering abilities of barley or oat β-glucan fiber. Still, some general points and conclusions can be made about methodology and the relationship between total and soluble β-glucan in barley and oats. There are four general procedures that have been used to measure β-glucan solubility. • Aqueous extract at 38ºC for two hours – temperature, time can be modified.36 • Aqueous extract with a hot ethanol pretreatment – temperature, time vary.37,38 • Aqueous extract with hot ethanol pretreatment followed by thermostable α-amylase – temperature 80-100ºC, times vary.39 • Soluble dietary fiber analysis with buffered extractions and enzymes, β-glucan or glucose measured in the soluble portion of fiber.40–42
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Aqueous extraction at 38ºC is confounded by β-glucanase activity that can be present. Limited digestion of the β-glucan molecule increases its solubility. Oat varieties have higher soluble β-glucan than barley varieties under these conditions, but processed oatmeal and oat bran do not since β-glucanase is destroyed by processing.36,43–45 β-glucanase can be inactivated by pretreatment with hot ethanol, by heat processing of materials, by low or high pH during extraction, or by high temperature during extraction.37–39,46 β-glucan solubility of enzyme-inactivated barley and oats increases with increasing temperature and the addition of amylase and/or protease enzymes.26,47,48 Soluble β-glucan of barley and oats measured as the β-glucan content of extracted soluble fiber (using any of the enzymatic dietary fiber methods) represents from 68% to 96% of total β-glucan. Oatmeal has the highest β-glucan solubility reported (80% to 96%) with oat bran (71% to 77%), oat groats (68% to 75%) and barley products (69% to 83%) being similar.40-42,49–53 Limited research has examined the relationship between in vitro and in vivo β-glucan solubility.49,54–57 In general, the amount of β-glucan soluble in ileal effluent following consumption of either a barley or oat product is similar or slightly lower than the amount of soluble β-glucan as measured in extracted soluble fiber from the product. β-glucan solubility measured in extracted soluble fiber was related to lipid response in rats by Shinnick et al.42 All of the oat products, having from 51% to 88% soluble β-glucan, were identical in lowering cholesterol in rats compared to a cellulose control. Processes to purify β-glucan have developed from the research on molecular weight and solubility. Various combinations of solvents, pH, temperature, and enzymes have been utilized in the production of barley β-glucan isolates.64 Hot water (up to 100oC) with or without enzyme digestion is reported to solubilize up to 86% of the β-glucan in barley-producing concentrates having 33.1% to 89.1% β-glucan.48,65,66 Temelli48 reported soluble β-glucan yield and viscosity increased as temperature increased up to 55oC. Extractions at four temperature (40oC to 55oC) and pH (7 to 10, using sodium carbonate) combinations gave the highest yields at pH 7 and 8 but the highest viscosity at pH 9 indicating the need to balance extraction yield with functionality. Bhatty65 also observed the highest viscosity when β-glucan was extracted with sodium carbonate but the highest solubility and recovery using 4% NaOH (54% vs. 81%, respectively). Solubility increased to 98% using 1N NaOH (80) but recovery decreased to 77% lowering overall yield. Knuckles et al.44 reported 100% β-glucan solubility in 1N NaOH + NaBH4 (1%) at 65oC. The extracted β-glucan, which represented the total β-glucan, had a higher molecular weight than β-glucans extracted in water. Burkus and Temelli68 reported that viscosity stability is improved by refluxing with 70% ethanol prior to purification of β-glucan. Extracted β-glucans are typically precipitated with alcohol. However, Morgan and Ofman69 developed a new method of β-glucan isolation using hot
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water extraction followed by freeze-thawing of the extract to precipitate the β-glucans. The presence of endogenous enzyme resulted in lower molecular weight β-glucan unless extraction time was kept to a minimum. Inglett70 developed a process of extracting β-glucan soluble fiber from oat and barley along with gelatinized, soluble starch resulting in a dietary fiber-maltodextrin product containing 7% to 8% dietary fiber. Patents for barley β-glucan extraction methods have been reviewed,6 but new processes have been disclosed for utilizing water alone or combined with an enzyme digestion,71,72 or NaOH alone or combined with enzyme digestion.73 Resistant starch (RS) can be enhanced in some types of barley through heat and chemical processing. Formation of resistant starch increases with increasing amylose content in barley starch.74,75 Sundberg and Falk76 found that bread and porridge made from barley having normal starch had higher RS (0.8% and 1.1%) than the same products made from barley with waxy starch (0.2%). Szczodrak and Pomeranz77 increased RS in isolated starch of High Amylose Glacier (45% amylose) from 0 to 26% by repeated cycles of autoclaving and found that lipids and emulsifiers interfered with the formation of RS in barley.78 Vasanthan and Bhatty79 found that starch gels made with high-amylose barley starch had 7% RS. After three heating and cooling cycles, the RS was increased to 13%. Further processing of the dried retrograded starch gels with pullanase or acid increased RS to 20% and 21.5%, respectively. Topping et al.8 recently described a new barley, Himalaya 292 that has 70% amylose starch, thus the potential for increased levels of RS.
Functionality and Food Applications The wide range of fiber products available from barley suggests that food applications would be diverse. Similar to other cereal grains, barley can be minimally processed into flakes and grits to be utilized as a hot breakfast cereal or a baking ingredient.6,80,81 Minimal processing also produces the pearled barley most often found in soups. In Japan, barley is pearled and split to look similar to rice and can be used to supplement fiber content without changing traditional recipes.12,82 The amount of β-glucan reported in these types of raw materials vary considerably (Table 15.4) and the amount of β-glucan found in a serving of a particular food is a function of the formulation and the β-glucan in the raw barley (Table 15.5). Brewers’ spent grains are a high-fiber, high-protein ingredient that is plentiful and inexpensive but has little soluble fiber.3 Extrusion Extrusion processing of barley for foods has significant benefits over other processing. High temperature and high pressure increases the solubility of
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Fiber Ingredients: Food Applications and Health Benefits
Table 15.4 Typical β-glucan Soluble Fiber Levels in Barley Food Raw Materials Reported in Published Articles. Barley Raw Material Whole berries14,15,20,83,84 Covered-dehulled Hulless Pearl 14,15, 20,83,85 Covered Hulless Flakes22 Cracked/Grits86 Meal83,87,88 Flour concentrate –ground and sieved 24,25,83,89 Flour – impact milled/air-classified fractions 90 β-glucan enriched Other Flour – roller-milled 45% to 70% flour extraction20,21,84,91,92 Covered Hulless Bran – roller-milled 45% to 70% flour extraction20,21,84,92-94 Covered Hulless Bran – pearled 20% to 32% 14,20,83,85 Covered Hulless a
No.
β-glucan % (dwb)a Range Mean
6
3.3–4.6
8
4.1–7.3
4.2 5.8
4 6 3 1 6 3
3.4–4.7 4.1–6.8 2.8–5.7 7.1 4.1–6.9 9.0–23.0
4.2 5.7 4.5 7.1 5.6 16.8
15 27
8.0–23.0 3.0–9.5
12.4 5.4
3 10
2.7–4.2 3.0–6.0
3.3 3.9
4 10
5.9–8.7 5.4–13.4
7.2 8.1
2 5
3.6–4.5 2.8–6.6
4.1 4.7
Dwb = dry weight basis.
β-glucan and can increase resistant starch producing an increase in both soluble and insoluble fiber of the products.88,95–98 Ostergard et al.97 reported significantly higher soluble dietary fiber in all of the whole grain barley extruded products and higher insoluble dietary fiber in products extruded at a temperature greater than 120°C and feed moisture greater than 18%. Marlett98 made a ready-to-eat cereal using an oven-puffing process that increased the solubility of the fiber and β-glucan by 23%. Lee and Schwarz95 extruded barley and barley/corn blends and found that increasing feed moisture and temperature increased bulk density and breaking strength. The bulk density of 100% barley was 2.5 times greater than corn extrudates. Extrudates containing 50% barley had a similar bulk density to 100% corn but slightly less expansion, higher breaking strength, higher water holding capacity (8%) and higher oil absorption capacity (25%). These products had 2.3% soluble and 5.8% total dietary fiber compared to only 0.4% and 2.6%, respectively, in
331
Barley Fiber Table 15.5 Grams of β-glucan Found in a Single Serving of Typical Barley Foods When Raw Barley Grain Contains 4%, 5.5%, or 7% β-glucan on a Dry Basis
Food Product Pearl barley, uncooked Hot barley cereal (flakes) - uncooked Granola Tortilla, soft – 50% barley meal or flour Tortilla chips – 50% barley meal or flour Muffin – 50% barley meal or flour No-bake cookie – 100% barley flakes Lemon cookie – 100% barley flour Extruded barley/rice crisp – 50% barley Extruded barley/corn puff snack – 50% barley Turkish flat bread – 40% barley Barley waffles a Spaghetti – 40% barley Angel Barley Pilaf a Stew with pearl barley a Barley almond vegetable salad a Tuna barley garden salad a Barley Caponata a a,
Serving Size (g) 48.0 40.0 49.0 51.0 28.4 57 90.0 30.0 33.0 28.4 64.0 1 waffle 56.0 ¼ recipe 1/6 recipe ¼ recipe 1/6 recipe 1/8 recipe
β-Glucan/Serving (g) If Raw Barley Has 4%
5.5%
7%
1.7 1.4 1.3 0.7 0.6 0.5 1.2 0.3 0.6 0.6 0.7 0.75 0.8 1.0 0.9 1.3 1.2 0.7
2.4 2.0 1.8 0.9 0.8 0.6 1.6 0.6 0.8 0.8 0.9 1.0 1.1 1.3 1.2 2.0 1.6 0.9
3.0 2.5 2.3 1.2 1.0 0.8 2.0 0.9 1.1 1.0 1.2 1.3 1.4 1.7 1.5 2.3 2.0 1.2
Recipes found at www.barleyfoods.org.
the corn products. Berglund et al.88 extruded four barley cultivars, rice and barley/rice blends in the production of a crisp rice cereal. Cereals made with 100% barley had 165% to 238% higher bulk density as the rice cereal. But 50% barley cereals were only 30% higher. Cereals containing 2.7% soluble and 8% total dietary fiber were scored similar in hedonic sensory testing to the rice cereal with 1.3% total dietary fiber. Extrusion of barley flours containing variable levels of lipid (1.3% to 3.8%) and fiber (10% to 17.3%) into snack products indicated that expansion ratio was negatively correlated to fiber content.83 However, the product having the best expansion and rated highest by a trained sensory panel still had 5% soluble and 10% total dietary fiber. Koksel et al.99 extruded barley flour (milled to 54% yield) using low and high shear, three die temp and three moisture levels. The low shear extrusion, the highest temperatures, and lowest moisture produced extrudates with the lowest bulk density and the highest cross-sectional expansion index. Foehse et al.100 described extruded cereals made with specially milled barley flour that contained from 20% to 50% β-glucan. Noodles containing small amounts of barley are reported to have acceptable cooking and sensory qualities and increased β-glucan contents. Baik
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Fiber Ingredients: Food Applications and Health Benefits
and Czuchajowska101 found that the texture profile analysis of udon noodles containing 15% ground pearled non-waxy barley was similar to 100% wheat flour noodles but required a shorter cooking time. Waxy barley reduced hardness and chewiness of this type of noodle. Spaghetti102 made with 15% barley had similar cooking quality to 100% durum spaghetti and 0.5% to 1.4% β-glucan (depending on the cultivar). Knuckles et al.103 used milledfiber-enriched barley fractions and an extracted water-soluble barley fiber to make pasta containing 4.1% to 8.6% β-glucan. A pasta made with 20% of the extracted fiber (7.1% β-glucan) had an overall acceptability rating and color equal to the durum pasta. Pastas containing 5% β-glucan that were made with 50% to 70% barley flour or brans have been rated as having acceptable cooking qualities and being similar to a whole wheat control.14,87,104 Bakery Products Barley β-glucan incorporated at low levels in yeast bread is similar to other gums used as gluten substitutes. Lee et al.105 reported that 1% of an extracted 85% pure barley β-glucan increased water absorption and dough development time but improved bread grain and texture while maintaining loaf volume. Higher levels (5% to 26%) of barley β-glucan isolates,103,106 flours ,87,107-109 flakes80 have been incorporated into breads to provide consumers with adequate levels of fiber and β-glucan in their diet. All of these studies have reported a decrease in loaf volume as barley β-glucan or fiber is increased in bread. However, sensory tests showed that breads with significant levels of barley β-glucan (1% to 3%) or fiber are rated similar in overall acceptability to the control breads. Bhatty111 reported that hulless barley flour has twice the water holding capacity and alkaline water retention capacity as wheat flour but similar oil absorption. Heavier type breads,86,104,107,112 flatbreads,113 and biscuits87,104 can been made using 30% to 100% barley flour or bran. Izydorczk et al.114 attempted to separate the effect of barley flour components (i.e., starch, β-glucan, and arabinoxylan) on rheological properties of wheat dough. They prepared dough with 20% whole meal barley, or 15% isolated barley starch, or 4% isolated barley β-glucan or arabinoxylan made from four barley cultivars with varying amylose starch contents (waxy, 6% amylase; normal, 26% amylase; high amylase, 42% amylase; and zero amylose). β-glucan contents ranged from 3.9% to 8% (dwb). β-glucan and arabinoxylan reduced mixing time while increasing peak dough resistance, mixing stability, and work input. Conversely, addition of the barley starch increased mixing time, and decreased peak dough resistance, mixing stability, and work input. There did not appear to be any effects due to the amylose content of the starch. The effects on dough properties observed with the whole meal flours were small because the effects of the starch and non-starch polysaccharides canceled themselves out. The authors concluded that the combination of high amounts of non-starch polysaccharides and unusual starch characteristics in barley seem to balance the negative effects associated with gluten dilution brought about by addition of barley into wheat flour.
Barley Fiber
333
Recent studies have focused on overcoming the loaf volume reduction resulting from the substitution of barley for wheat in bread. Gill et al.115,116 reported that high-temperature, high-moisture extrusion of waxy barley flour improved loaf volume significantly at the 15% substitution level. Basman et al.117 reported no significant effects when transglutaminase, an enzyme involved in protein cross-linking, was utilized in breads that contained 10% to 50% barley flour. Trogh et al.118 produced a composite flour which was 60% strong wheat flour and 40% of barley flour (2.5% β-glucan) and made breads with increasing levels of a xylanase that was resistant to xylanase inhibitors found in wheat. Compared to the control wheat bread the loaf volume of the barley bread was reduced by 32%. By using the xylanase this reduction was improved to 19%, still lower than the wheat bread. They reported that these breads had good crumb structure, were palatable, and remained softer over a longer period than the wheat bread. Upon optimizing the recipe for industrial-scale production, loaf volumes were the same as the wheat breads. They also examined the molecular weight of the β-glucan and found, like others, that molecular weight decreased with mixing and fermentation but was not affected by baking.119 Substitution of barley flour for wheat flour produces very acceptable baked goods such as muffins, pancakes, biscuits, and cookies and tortillas. The β-glucan in whole-grain barley flour mimics fat and allows for some reduction in added fat in muffins and quick breads. Berglund et al.87 incorporated 50% to 100% waxy hulless barley flour (6.6% β-glucan) into cookies, a nofat muffin, and quick breads, which were rated by consumer panels as having overall acceptability similar to the control products. Muffins made with 100% barley flour91 having β-glucan content ranging from 3.8% to 4.9% have been described as moister and gummier, but were preferred over the wheat control. High β-glucan mill fractions used at lower levels (25%) in muffins and cookies108 produce products comparable to whole wheat products but containing twice as much soluble dietary fiber. Hudson et al.89 used a similar fraction to develop a muffin that had three times the total dietary fiber (7 g in a 100 g muffin), four times (3.8 g in a 100 g muffin) the β-glucan content, and one-third of the fat of a commercial oat bran muffin mix. It was necessary to increase leavening by 10% and liquid by 20% to 25% because of the moistureabsorbing characteristic of the barley fraction. Fastnaught et al.120 found that muffins containing between 1% to 3% β-glucan had higher volume and were more tender when fat was decreased as much as 66%. An extracted barley fiber concentrate containing 55.6% β-glucan was used to develop tortillas with 12.5% total dietary fiber, which were slightly more tender and had similar storage stability as control tortillas.121 Ames et al.82 reports that tortillas formulated with barley flour containing less starch and amylose and more β-glucan are easier to roll, less breakable, softer, and less dry and chewy. Robertson et al.57 reported β-glucan extractability in biscuits was increased as a result of cooking. A milled barley bran that contained 45% total dietary fiber and 10.8% soluble dietary fiber was recently compared to wheat, rice, and oat bran in
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Fiber Ingredients: Food Applications and Health Benefits
dough and biscuits at substitution levels from 10% to 40%.122 The barley bran had the highest water absorption of all the brans, from 64% to 77% and the lowest dough development times. Dough stability also increased but mixing tolerance decreased significantly for both the oat and barley bran. Increasing bran caused a decrease in diameter of the biscuits. The barley bran biscuits were more similar to the control in color than the other bran biscuits. Sensory testing found that the rice bran was least liked of all the products, the 10% bran biscuits of barley, wheat, and oat were liked as well as the control. The authors concluded that biscuits containing 20% barley or wheat bran and 30% oat bran were highly acceptable resulting in products that contained significantly higher levels of dietary fiber, the highest being the barley at 9.3% total dietary fiber and 2.4% soluble dietary fiber. Meats Barley may have a role in meat products for fat replacement, and improvements in purge control, texture, and storage stability. Shand123 reported that 4% waxy barley flour provided better purge control in pork bolognas than wheat or regular barley. Bond et al.124 described adding 10% cracked, hydrated barley to 90% lean hamburger. Texture profile analysis revealed that the beefbarley burger was less chewy, springy, and hard than the 80% and 90% lean beef controls. Sensory panels preferred the beef-barley patties as they were more juicy and soft, and less chewy and crumbly than the controls.125 Pork, chicken, and beef patties containing 4% to 10% barley have improved moisture retention and improved storage characteristics.124,126–129 Low-fat sausages containing 0.3% of a barley β-glucan extract were liked as well as the high-fat sausage and rated more acceptable than those containing 0.8% β-glucan or 0.3% carboxymethyl cellulose.130,131 Whole grain barley may contain levels of antioxidants that improve storage stability of some end products.67 β-Glucan Extracts Barley β-glucan isolates offer food manufacturers the ability to incorporate β-glucan into products where the other components (starch, protein, insoluble fiber, and lipids) may present problems in formulation. As mentioned previously there are numerous wet milling methods for extracting β-glucan from barley, thus each β-glucan product has specific characteristics and functionality. Symons and Brennan138 examined the effect of 1% and 5% β-glucan on wheat starch gelatinization and pasting characteristics using β-glucan extracted by five different methods. Final β-glucan levels ranged from 63.5% to 73% and water retention capacity of 1 g of extracted barley β-glucan ranged from 6.5 g to 8.5 g. The 1% barley β-glucan added to wheat starch had no effect on pasting properties but 5% lowered peak and final viscosity and breakdown. These authors went on to substitute a 70% β-glucan extract at the 2.5% and 5% substitution level in bread.139 The 5% substitution increased dough exten-
Barley Fiber
335
sibility but loaf volume was reduced 10% and 27% with the 2.5% and 5% substitutions, respectively. The addition of the β-glucan did result in reducing sugars being released more slowly in an in vitro digestion process. Similar results were reported when the β-glucan extract Glucagel® was used.140 Loaf volume was reduced 11% and 46% with the 2.5% and 5% substitutions, respectively. Gill et al.115 proposed that water binding of β-glucan reduces steam production leading to an underdeveloped gluten network and lower loaf volume and increased firmness. While molecular weight was never reported in this research, their next study examined two purified β-glucans (95%, Megazyme™ International Ireland Ltd.), a high molecular weight (HMW, 510,000 Da), and a low molecular weight (LMW, 160,000 Da ) in breads at the 5% level of substitution.141 Dough containing β-glucan exhibited increased resistance to extension and the resulting breads had reduced loaf height and volume. Water was increased by 7% to account for the increased water absorption of the β-glucan, and the authors suggested that additional water may overcome the stiffness of the dough but may not rectify reduced elasticity. Except for bread firmness, the HMW β-glucan had greater negative effects than the LMW β-glucan. The molecular weight of the HMW β-glucan was reduced by one-half during the bread-making process; the LMW did not change. The release of reducing sugars from breads containing β-glucan during in vitro digestion was significantly slower than the control bread. Temelli et al.142 has compared beverages made with 0.3%, 0.5%, or 0.7% pectin or purified β-glucan (85%). Beverages made with 0.5% and 0.7% β-glucan were more viscous than comparable pectin beverages but consumer acceptability was similar. Color, viscosity, and pH were shelf stable over a 12-week period. Zheng et al.71 has described using a 70% barley extract, Barliv™ Barley Betafiber, in beverages at the 0.45% level which supplies 0.75 g of β-glucan in an 8 oz serving. This product is described as a white to tan powder that is soluble in water. Also described was a yogurt containing 0.65% of the extracted β-glucan and soup containing 1.2%. Dry products such as extruded corn flakes were made to provide 3 g of β-glucan per 30 g serving and bread which supplied 0.75 g β-glucan per 50 g serving. Lyly et al.143 also described the use of extracted β-glucan (35%) in soups at levels from 0.25% to 2.0%. They noted increasing viscosity but stable flavor attributes as concentration increased. They also noted that two weeks of being frozen resulted in a decrease in viscosity. Inglett70 has described soluble hydrocolloid compositions made from cereals including barley that can be used to replace fat in bakery and dairy products. Some of these compositions retain only the soluble portion of the fiber,70,144 while in others insoluble fiber is processed to make it soluble.145 Similar compositions have been used in the production of meat products.146 More recently Inglett147 describes a process involving shear, steam jet-cooking, and drum drying to produce compositions that are low in starch, rich in protein, have from 20% to 47% β-glucan and unique pasting curves. Lee and Inglett148 report that steam jet-cooking increased water absorption of
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processed barley flour and significantly lowered oil uptake in batters made with this product. Miscellaneous A few barley products have been described that are processed to improve convenience during preparation. Fox132,133 describes a process of precooking hulless grains, drying and cutting to produce an easily rehydrated product. Forsberg134 also describes a process for precooking, grinding, and drying barley into a powder that can be consumed in beverages. This product is called Aktivated Barley® and was used in the clinical trial described by Aman.135 Ames has described tortillas136 and whole grain products137 that are tempered, heated by infrared or microwave energy, and dried for consumption as a rice-like product or formulated in snack foods. Hulless barley cultivars can be used to produce malt and malt extract containing higher levels of soluble fiber. Vis and Lorenz149 malted waxy hulless barley to produce a beer containing 1.5% β-glucan compared to 0.35% in the control. Malted hulless barley or “food” malt contains no hulls thus can be used to make malt extracts with 1.5% β-glucan compared to 0.1% in commercial extracts.150 Brewers’ spent grains have been used as a fiber source in bakery products.3,110 This material has high water-absorption capacity, low fat absorption, and provides valuable minerals as well as fiber and protein. Addition of 10% to breads can double the fiber content and increase protein by 50%.151 Whole grain products are typically associated with finished products that are darker in color. Barley products can develop a dark gray color, which may be affected by a number of factors. Barley contains compounds (polyphenols, phenolic acids, proanthocyanidins) and enzymes (polyphenoloxidase (PPO), peroxidase) that cause discoloration upon oxidation. Ames et al.82 reported that infrared heat treatment of barley flour reduced peroxidase activity and improved tortilla brightness. But there is considerable genetic variation in barley for total phenolics and enzyme levels including a gene that significantly reduces the content of proanthocyanidins.152 Quinde et al.153 examined total polyphenolic content and PPO activity in 22 barley genotypes and found that the hulless cultivars had the highest levels of polyphenols, which was negatively correlated (r = 0.91) to brightness. Protein and ash also had negative effects on brightness, while PPO level had little effect among these genotypes. Abrasion and treatment with ascorbic acid at 1500 ppm were most effective at increasing the brightness of barley products.154 Barley fiber can be utilized in its many forms in a variety of food products. The genotypic, environmental, and processing effects on barley fiber necessitate strict definition and characterization of the individual fiber products by processors. The health benefits associated with barley fiber and whole
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grain barley will generate demand by the medical community and consumers. Development of foods containing barley fiber can increase to meet this demand when manufacturers understand the benefits, unique attributes, and impact on specific products.
Physiological Benefits Digestion The effect of barley insoluble fiber in the digestive system has been clearly documented in both animal and human studies. Ingestion of BSG (brewers’ spent grains, 97% insoluble fiber) or derived products is associated with increased fecal weight, accelerated transit time, increased cholesterol and fat excretion, and a decrease in gallstones.6 Germinated barley foodstuff (GBF) derived from the aleurone and scutellum fractions of brewers’ spent grains mainly consists of low-lignified hemicellulose and glutamine-rich protein. Animal studies18 suggested GBF improves the proliferation of intestinal epithelial cells and defecation, through the bacterial production of short-chain fatty acids (SCFA), especially butyrate. Mitsuyama et al.155 reported that GBF feeding resulted in an increase in stool butyrate concentrations in improved clinical activity index scores in patients with ulcerative colitis (UC). A separate study reported a similar response in healthy volunteers consuming GBF as well as a significant increase in fecal Bifidobacterium and Eubacterium and suggesting a prebiotic effect of GBF.156 A four-week trial that involved patients with mild to moderate active ulcerative colitis consuming 30 g of GBF daily reported significant clinical and endoscopic improvement.157 This research was extended to a 24-week trial, which reported similar results.158 Animal studies suggested that GBF has the potential to reduce the epithelial inflammatory response by depressing mucosal STAT-3 (signal transducer and activator of transcription) expression and inhibiting NFkB (nuclear factor kappa B) binding activity.159 Hanai et al.160 reported that GBF appeared to be effective and safe as a maintenance therapy to taper steroid dose and prolong remission in patients with UC. Barley soluble fiber is also associated with increased fat and cholesterol excretion from the digestive system and prebiotic effects.161 Lia et al.162 reported 55% higher cholesterol excretion in ileostomists consuming 13 g/d β-glucan from barley flour. Increased fecal fat excretion ranging from 70% to 200% has been reported in hamsters, chicks, and rats consuming significant quantities of β-glucan-containing barley products.6 Robertson et al.56 reported increased solubility and decreased molecular weight of β-glucan collected from ileal effluents, indicating substantial degradation prior to reaching the colon.
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Cardiovascular Disease The FDA authorized the use of a health claim on food labels for the role of β-glucan soluble fiber from barley in reducing the risk of coronary heart disease (CHD) in May 2006.1 This ruling modified 21CFR101.81, which authorizes a health claim on the relationship between soluble fiber of certain foods and CHD risk to include β-glucan soluble fiber from barley. The FDA concluded that consuming whole grain barley and/or dry milled barley products that provide at least 3 g of β-glucan soluble fiber per day is effective in lowering blood total and LDL cholesterol; and that the cholesterol-lowering effects of β-glucan soluble fiber is comparable to that of the oat sources of β-glucan soluble fiber which was already listed in 21CFR101.81(c)(2)(ii)(A).163 Barley foods containing β-glucan soluble fiber have been included as a dietary intervention in 13 human clinical trials and 40 animal trials measuring changes in lipid profiles and risk reduction for CHD.6,164,165 These studies include barley processed by dry-milling (including meal or flour, flakes, bran, and pearl) and wet-milling (high β-glucan extracts). Products made from barley that do not contain β-glucan soluble fiber, including the oil and brewers’ spent grains (BSG), have also been studied. Human clinical trial data (Table 15.6) clearly demonstrate that consumption of barley β-glucan soluble fiber is an effective dietary approach for lowering LDL cholesterol and total serum cholesterol. The observed decreases in total serum cholesterol and LDL cholesterol associated with consumption of barley β-glucan soluble fiber are equal to the changes brought about by dietary oat β-glucan soluble fiber. Similarly, as seen with consumption of oat products, the desirable HDL cholesterol is unchanged in individuals consuming barley products. Finally, the decreases in serum cholesterol reported in appropriately designed barley clinical trials are consistent with the dose response mechanism observed in the oat clinical trials. Higher levels of β-glucan in the diet may provide benefits beyond cholesterol reduction. An increase in HDL cholesterol and decrease in triglycerides was reported by Behall et al.170 The greatest differences were for the diet that contained 6 g of β-glucan from the barley foods. Keenan et al.166 also reported a significant decrease in triglycerides in participants consuming 5 g of the high molecular weight extracted β-glucan. A few of the studies reported no change in cholesterol when participants consumed a barley product. Keogh et al.171 concluded that the method of isolating the extracted β-glucan may have reduced the size of the molecules, causing a reduction in viscosity. Biorkland et al.168 reported that the molecular weight of the processed barley β-glucan used in the study was 40,000 but did not suggest the low molecular weight as the reason for lack of cholesterol reduction. These studies reinforce the possible importance of viscosity and/ or molecular weight as one mechanism for cholesterol reduction and the need to identify a functional molecular weight for the relationship between β-glucan and risk of CHD.
Extracted Barley β-glucanBarliv™ 1. Low molecular weight (LMW) 2. High molecular weight (HMW)
Pearl barley
Aktivated® Barley — 5% BG
β-glucan extracts: barley — 36% BG oat — 18% BG
Barley Pearl, Flakes, Sieved Flour — 5.0% BG
Hinata et al.167 52 men
Aman135 39 subjects
Biorkland et al.168 89 subjects
Behall et al.169 7 men and 18 women
Diet Intervention
Keenan et al.166 155 men and women
Reference/Subjects
Randomized, double blind, controlled crossover with Latin Square design of three 5-week diet periods; 3 treatments: 0, 3 g, 6 g barley soluble fiber; all with NCEP Step 1 diet
Rice: barley mix at a ratio of 7:3; SDF intake increased from 3.4 g to 18.7 g; Avg. period of 14 months Randomized, single blind, controlled, crossover with 4-week diet period; 2 treatments: 0 and 3 g BG Randomized, single blind, controlled, parallel with 5-week diet period; 4 treatments: 5 and 10 g of barley or oat β-glucan
Randomized, double-blind, controlled, five-arm parallel for 6-week diet period 5 treatments: 0, 3 g LMW BG, 3 g HMW BG, 5 g HMW BG, 5 g HMW BG β-glucans prepared in ready-to-eat corn flakes and juice beverage
Methods
Oat- 5 vs. Baseline TC: – 12.4 (– 4.8%) LDL: – 9.3 (– 5.5%) Oat- 10, Barley- 5 and Barley- 10 showed no difference to baseline Barley 3 g vs. Control - All TC: – 10.3 (– 4.9%) LDL: – 9.7 (- 6.5%) Barley 6 g vs. Control - All TC: – 12.3 (– 5.8%) LDL: – 12.4 (– 8.4%) (continued)
Barley 3 g vs. Control LDL: no data (– 5.0%)
Treatment vs. Control 3 g LMW: TC: – 17.1 (- 7.2%) LDL: – 13.4 (- 8.7%) 3 g HMW: TC: – 19.1 (- 8.2%) LDL: – 14.0 (- 9.2%) 5 g LMW: TC: – 26.4 (- 11.1%) LDL: – 20.3 (- 13.1%) 5 g HMW: TC: – 29.2 (- 12.4%) LDL: – 22.5 (- 14.6%) Barley vs. baseline TC: – 16.0 (- 9.7%)
Changes (mg/dl)a
Summary of Human Clinical Trials Utilizing Barley Foods Containing β-Glucan Soluble Fiber as a Dietary Intervention to Reduce Risk of Coronary Heart Disease
Table 15.6
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Barley extract – Glucagel — 75% β-glucan
Barley — whole grain
Pearled barley 13.6% TDF calculated
Keogh et al.171 18 men
Li et al.172 10 women
Ikegami et al.173 Trial 1: 5 men
Barley flour — whole grain
Barley — bran 50% extraction — 4.9% BG flakes — 4.4% BG
Narain et al.174 5 men and 1 woman
McIntosh et al.104 21 men
Trial 3: 7 women
Trial 2: 20 men
Barley Pearl, Flakes, Sieved Flour — 5.0% BG
Behall et al. 18 men
Diet Intervention
170
Reference/Subjects
Table 15.6 (Continued)
Randomized crossover, 2–4 week periods with no rest; BG g/day: TDF g/day: barley = 8.0 barley = 38.4 wheat = 1.5 wheat = 38.4
4 wk crossover, 1 wk rest; Barley = 100 g/day
Trial 3: 2 weeks
12-week crossover; 4-week washout between two 4-week diet periods; 2 treatments: 0 and 9.9 g barley β-glucan as part of a controlled Westernized diet 12-week crossover; 4-week washout between two 4-week diet periods; 2 treatments: 0 or 89 g barley/day as part of a controlled Japanese standard diet All studies: 280 g/day barley/rice 50:50 mix = 6.1 g TDF/day from barley Trial 1: 4 weeks Trial 2: 2 weeks
Randomized, double blind, controlled crossover with Latin Square design of three 5-week diet periods; 3 treatments: 0, 3 g, 6 g barley soluble fiber; all with NCEP Step 1 diet
Methods
Barley vs. baseline TC: – 11.3 (– 5.4% ns) LDL: – 11.6 (– 8.2% ns) TC: – 27.5 (– 9.9%) LDL: – 23.9 (– 12.8%) TC: – 24.8 (– 9.8%) LDL: – 23.2 (– 13.4%) Barley vs. baseline TC: +2.0 (+ 0.9%) ns HDL: +14.8 (+ 29.2%) Barley vs. wheat TC: – 15.1 (– 6.0%) LDL: – 12.8 (– 6.8%)
Barley vs. Control TC: – 20.0 (– 14.5%) LDL: – 11.1 (– 21.0%)
Barley 3 g vs. Control TC: – 1.0 (– 1.0% ns) LDL: – 0.4 (– 0.3% ns) Barley 6 g vs. Control TC: – 17.9 (– 8.8%) LDL: – 14.3 (– 11.0%) Barley vs. Control TC: – 1.3%, ns LDL: –- 3.8%, ns
Changes (mg/dl)a
340 Fiber Ingredients: Food Applications and Health Benefits
b
a
Barley flour — whole grain waxy hulless barley — 9.6% BG 32.6% EDF Barley flour — whole grain waxy hulless barley
Randomized parallel, 4 weeks EDF g/day: barley = 42 wheat = 42 Randomized parallel, 6 weeks TDF intake g/day: barley diet = 40 oat diet = 27
Barley vs. wheat TC: – 24.3 (– 12.3%) LDL: – 18.9 (– 14.3%) HDL: – 4.3 (– 10.5% ns) Barley vs. baseline TC: – 12.0 (– 4.7%) LDL: – 24.0 (– 13.9%) HDL: + 5.0 (+ 10.2%) Oat vs. baseline TC: – 12.0 (– 4.8%) LDL: – 11.0 (– 7.0%) HDL: – 6.0 (– 9.5%)
All changes reported are significant (p < 0.05) unless followed by ns (nonsignificant). Abbreviations: LMW = low molecular weight; HMW = high molecular weight; BG = β-glucan; TC = total cholesterol; LDL = low density lipoprotein cholesterol; HDL = high density lipoprotein; TDF = total dietary fiber; IDF = insoluble dietary fiber; SDF = soluble dietary fiber; EDF = estimated dietary fiber; NCEP = National Cholesterol Education Program.
Newman et al.176 22 subjects
Newman et al.175 14 men
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Overall, the scientific evidence has clearly demonstrated the health benefits of barley and barley (1→3),(1→4)-β-d-glucan soluble fiber. In summary, barley foods (hulless, dehulled, or pearled and derived products) contain as much or more β-glucan soluble fiber as oats. Controlled human clinical trials show that barley products that provide 3 g to 6 g of β-glucan soluble fiber daily significantly lower total and LDL cholesterol more than 5%. Barley β-glucan extracts vary in their functionality with respect to cholesterol reduction. At least one barley β-glucan concentrate, Barliv™ barley Betafiber, has demonstrated the ability to lower cholesterol in a human clinical trial.166 Thirty-six out of 40 animal nutritional studies reported that barley β-glucan soluble fiber significantly lowered total and/or LDL cholesterol from 8% to 80%. Barley products tested include meal, flour, bran, sieved flour (β-glucan enriched flour) and extracts.164,165,177 Barley and oats were directly compared in 14 animal studies. Twelve of these studies reported that barley lowered total and LDL cholesterol greater than or the same as oats.164 Two barley products, barley oil and brewers’ spent grain (BSG), neither of which contains soluble fiber, have been investigated for their potential positive impact on lipid metabolism. Brewers’ spent grain (BSG) is a by-product of the brewing industry and typically contains 98% insoluble dietary fiber and is high in protein (20% to 30%) and lipid (6% to 10%) and contains three times more tocotrienols than the whole grain. The combined animal and human studies on barley oil and brewers’ spent grains suggest that some components, possibly the tocotrienols, which are an antioxidant, have the ability to affect lipid-controlling enzymes and lower cholesterol.6,178 This material certainly warrants further research. Glucose and Insulin Response The physiological impact of individual foods on plasma glucose and insulin response varies depending upon the type and concentration of carbohydrate present in the product. Typically, foods with a low degree of starch gelatinization (more compact granules) such as spaghetti, and whole grains that contain high levels of viscous soluble fiber, such as barley, oats, and rye have a slower rate of digestion and lower glycemic index (GI) values.179 Pearl barley has one of the lowest GI values, and rolled barley is equivalent to quick oatmeal.180 GI is a function of structure, starch type, fiber content, and the interaction of these characteristics.75 Livesey et al.181 found that ileostomists eating finely ground barley had 2% undigested starch compared to 17% when they consumed barley flakes. Light microscopy of the ileal effluent showed starch granules surrounded by intact cell walls. Liljeberg and Bjorck112 reported breads made with ground whole meal barley were similar to white bread (GI=100), while breads containing 80% intact barley kernels were significantly lower (GI=33). Granfeldt et al.75 reported GI was lowered to 66 when ground whole meal barley flour was boiled and eaten as a porridge and suggested
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that boiling released the soluble fiber more effectively than baking. More recently, Liljeberg et al.113 reported a lower GI (71 to 77) for both porridge and bread made from a barley flour containing 18% β-glucan. Cavallero et al.182 reported a GI of 69 for bread containing 6.7% β-glucan extracted from barley with water. Yokoyama et al.183 reported that pasta containing 7.7% β-glucan, made from a β-glucan enriched barley flour, produced a 63% lower peak glucose and 53% lower insulin response in subjects compared to the control durum pasta. In a longer study involving 11 non-insulin-dependent diabetics eating barley bread products that provided 5.2 g/d β-glucan, Pick et al.86 reported a lower glycemic response, but in contrast to studies with healthy test subjects, a higher insulin response. This resulted in four subjects reducing their dosage of hypoglycemics. Wursch and Pi-Sunyer184 reported that foods containing 10% viscous β-glucan soluble fiber from oats and barley can reduce glucose and insulin response in the bloodstream by 50% compared to white bread. Behall et al.185 compared three levels of resistant starch and three levels of barley β-glucan in a factorial design. They reported significant decreases in glucose and insulin areas under the curve following consumption of 5 g of barley β-glucan in muffins and concluded that the β-glucan was more effective than the resistant starch at lowering glucose and insulin response. Ostman et al.186 reported further decreases of glycemic and insulin indexes as β-glucan levels increased to 12.2 g in breads. A direct comparison has been made of barley, oats, and β-glucan extracts from barley and oats (Nu-trim X) on glucose and insulin responses in nondiabetic men and women.187 Glucose responses to the barley and oats and β-glucan extracts from both grains, as measured by the areas under the curve, were significantly lower than the glucose control (P < 0.0001). Insulin responses for the barley extract were the lowest and were significantly lower than the glucose control. Wood et al.188 related glucose and insulin response to concentration and molecular weight of β-glucans in a drink consumed by subjects. They reported that viscosity was positively correlated (R2 = 0.97) to molecular weight times concentration, which was inversely related to glucose and insulin response. Biorklund et al.168 reported no change in areas under the curve for serum glucose or insulin when subjects consumed a beverage containing 5 g or 10 g of extracted β-glucan from barley that had a molecular weight of 40,000. In the same study, a beverage that contained extracted oat β-glucan with a molecular weight of 70,000 lowered postprandial glucose and insulin at the 5 g level but not the 10 g level. Only a few studies have examined the long-term effects of barley soluble fiber on risk factors for diabetes and the results are somewhat conflicting. Decreases in HbA1c were reported in the longest trials (Hinata et al.167 – 14 months; Hawrysh et al.189 – six months) but not in trials lasting from four to 12 weeks (Li et al.172; Pick et al.86; Narain et al.174). Fasting plasma glucose was decreased in the study by Hinata et al.167 that utilized pearl barley but not in the other long-term study by Hawrysh et al.189 where participants consumed barley in bread products.
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In summary, there is considerable evidence showing that consumption of foods with a low glycemic index may provide considerable health benefits, especially for diabetic subjects.190 The accumulating data indicate that low-GI foods containing soluble fiber (β-glucans) not only prevent certain metabolic ramifications of insulin resistance, but also reduce insulin resistance.191 Yokoyama and Shao192 conclude that some soluble fibers, including barley, can overcome the adverse metabolic effects of diets high in saturated fats. Since over 16 million Americans are diabetics, with 90% having type 2 DM, this has extremely important ramifications in regards to the health and welfare of the U.S. population. Increased consumption of barley products containing β-glucan soluble fiber in conjunction with diet moderation as outlined in the USDA/USDHHS guidelines will help address this health problem and in the process may reduce the risk of CHD. Blood Pressure Epidemiological studies have shown that increased consumption of dietary fiber is associated with lower levels of systolic and diastolic blood pressure.193 Clinical studies have shown blood pressure reductions associated with consumption of soluble fiber from barley. Hallfrisch et al.194 and Behall et al.195 reported that barley foods (providing 3 g or 6 g β-glucan/day) lowered diastolic and mean arterial blood pressure 5% after five weeks of consumption by moderately hypercholesterolemic men and women. These barley foods were made from a dehulled (lightly pearled) barley, which does not retain all of the pericarp and germ, though it can be considered whole grain and did contain significant levels of both soluble and insoluble fiber. The barley diets were compared to a whole wheat and brown rice diet that also lowered blood pressure but which contains little soluble fiber. The Dietary Approaches to Stop Hypertension (DASH) Study Group concluded that intake of whole grains, along with fruits and vegetables, has a significant effect in decreasing systolic and diastolic blood pressure.196 These studies agree with those findings but do not clarify the metabolic mechanism for blood pressure reduction. Cancer and Immune Response A growing body of scientific evidence has linked whole grain and fiber consumption with a reduced risk of several types of cancer. As a result a whole grain/cancer and heart disease health claim was allowed by the FDA in 1999.197 Several potential biological mechanisms have been identified that might be involved in reducing cancer risk. Whole grains are rich sources of fermentable carbohydrates (dietary fiber, resistant starch, and oligosaccharides) that are fermented by intestinal microflora in the colon. The primary fermentation end products are short-chain fatty acids such as acetic, butyric, and propionic acids. These short-chain fatty acids have been correlated to lower serum cholesterol and reduced risk of cancer.198 Whole grains also
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contain a wide range of antioxidants such as phenolic acids, tocotrienols, phytoestrogens, and phytic acid, all of which have been associated with reduced risk of cancer. Phytic acid, which is sometimes referred to as an antinutrient, has a useful antioxidant function. It forms chelates with various metals, which suppresses iron-catalyzed redox reactions.199 This mechanism is proposed to suppress the oxygen radicals produced by colonic bacteria fermentations. A few animal studies have addressed the role of barley fiber in reducing risk of cancer. McIntosh et al.200 compared barley bran diets that varied in insoluble and soluble fiber content to a wheat bran diet in tumor-induced rats. Some of the barley brans were comparable to wheat bran in decreasing tumor incidence and tumor mass index. One of the most effective barley brans was prepared in a manner similar to oat bran and contained 13% total fiber that was 40% soluble. Zhang et al.201 reported that ingestion of brewers’ spent grains reduced the secondary to primary bile acid ratio in hamsters and in vitro preferential adsorption of lithocholic acid by barley fiber has been demonstrated.202 Snart et al.161 reported a prebiotic effect of high-molecular-weight β-glucan isolate fed to rats. They reported differing denaturing gradient gel electrophoresis profiles from rats fed cellulose versus HMW BG and found that a rRNA fragment that was more conspicuous had sequence identity with Lactobacillus acidophilus. The cell walls of many bacteria and fungi contain hemicelluloses similar to the β-glucans found in barley and oats but comprised of β(1→3)-linked glucosyl residues with small numbers of β(1→6)-linkages rather than the β(1→4)-linkages. These glucans have the ability to enhance the immune system resulting in antitumor, antibacterial, antiviral, anticoagulatory, and wound healing activities.203 A leukocyte membrane receptor, CR3, has been identified as the binding site that recognizes β-glucans, including barley β-glucan.204–206 Jaramillo and Gatlin207 reported that 0.1% of a purified barley β-glucan had no effect on disease resistance of hybrid striped bass to Streptococcus iniae. However, Misra et al.208 reported that barley-derived β-glucan injected into Labio rohita juvenile fish enhanced immune parameters and lowered mortality when the fish were challenged with two pathogens. Modak et al.209 (2005) reported that Rituximab therapy of lymphoma in mice is enhanced by orally administered purified barley β-glucan. Using the same purified barley β-glucan, Hong et al.210 demonstrated that barley β-glucan molecules are transported from the intestinal system of mice by macrophages to the spleen, lymph nodes, and bone marrow. Dr. N.-K.V. Cheung of the Sloan-Kettering Cancer Center has submitted a U.S. patent application “Therapy-Enhancing Glucan,” which describes a barley β-1,3-1,4-glucan between 250,000 and 450,00 Da that enhances the efficacy of antibodies.211 The application describes a series of animal experiments and successful preliminary data from a Phase I human study among patients with metastatic neuroblastoma.
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Fiber Ingredients: Food Applications and Health Benefits
Safety/Toxicity Barley has mainly been consumed in the form of pearled barley or ground meal and as such has a long history of safe use. In the United States, it has a defined reference amount per eating occasion of 45 g dry and 140 g prepared and an annual per capita consumption of 0.6 kg (barley alone) is reported.212 But as recently as 1961, barley was consumed at levels as high as 226 g/day in Morocco. This would be equivalent to approximately 9 g of soluble fiber and 24 g of insoluble fiber. Presently, Morocco is the largest food user of barley with an annual per capita intake of 63 kg (reported between 1980 and 1995).213 In that region, barley is used in a variety of traditional foods (bread, soup, porridge), resulting in an average intake of up to 172 g/person/day. With this intake of barley, about 6 g/person/day of pure β-glucan is consumed. The published human clinical trials generally take note of potential gastrointestinal disturbances that could be associated with barley consumption. Subjects in these studies have consumed from 44 to 175 g of barley or up to 10 g of extracted barley β-glucan on a daily basis. Some bloating and flatulence have been reported but nothing more than what would be expected in adjusting to a high-fiber diet. Overall, no serious adverse effects have been reported for barley foods86,169,170,174,175 or barley β-glucan extracts.166,168,187 Potential toxicity of barley β-glucan soluble fiber extracts has been studied in animals. Delaney et al.214 fed Wistar rats three levels of extracted barley β-glucan for 28 days and concluded there were no adverse effects on general condition and behavior, growth, feed and water consumption, feed conversion efficiency, red blood cell and clotting potential parameters, clinical chemistry values, and organ weights. Overall, no signs of toxicity were detected even when large amounts were consumed. In a further study, Delaney et al.215 used the same protocols in CD-1 mice, used frequently to evaluate inflammatory responses. Following 28 days of consumption and 14 days of recovery, no treatment-related adverse effects were observed in hematology or clinical chemistry measurements or in organ weights and immunopathology. The researchers concluded that concentrated barley β-glucan did not cause treatment-related inflammatory or other adverse effects. Vitamin and mineral malabsorption associated with barley fiber has been examined in a few human and animal studies. Wisker et al.216 examined the calcium, magnesium, and zinc balances and iron absorption in young women eating a diet that contained 15 g/day of barley fiber that was 97% insoluble and low in phytic acid (0.06%). This fiber was derived from the outer layers of the grain and contained no husk. The fiber had no effect on the mineral balances or absorption of iron except when protein intake was decreased. Sandstrom et al.217 reported that individuals absorbed significantly higher levels of zinc when consuming barley porridge and bread than when consuming oatmeal, whole wheat or triticale porridges or breads. Harrington et al.218 reported that calcium absorption in rats was unaffected by a barley
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fiber but was decreased by a wheat fiber. The barley fiber was 88% insoluble and 12% soluble. In vitro binding studies parallel the in vivo studies. Kennefick and Cashman219 reported barley bound significantly less calcium than wheat. Weber et al.220 analyzed the calcium-binding capacity of 18 fibers including barley that had 3.5% soluble and 57.1% insoluble fiber. The barley fiber ranked four out of 18 for level of phytic acid, but only nine out of 18 for amount of calcium bound. The scientists reported that in this study there was no correlation between total calcium bound and phytic acid (r = –0.12). In a similar study, barley fiber bound more copper than 16 other brans, but less magnesium than 11 and less zinc than four other brans.221 Persson et al.222 analyzed in vitro binding of copper, cadmium, and zinc to the soluble fiber from barley, oats, and rye. All of the fibers bound more copper than zinc or cadmium, and barley appeared to bind more of the minerals than the oats and rye but no statistics were reported. However, none of these soluble fibers bound as much zinc as wheat bran. And, purified barley β-glucan did not bind to any of the minerals. Barley contains a type of protein called hordeins, which are in the class of proteins called glutens. The gluten proteins of wheat can trigger an autoimmune disease called celiac disease in genetically susceptible individuals. While barley glutens are very different from wheat glutens, the effect of barley glutens on individuals with celiac disease is not well understood. Thus, products that contain barley cannot carry the “gluten-free” label. Individuals that have the disease will recognize barley in the ingredient label and can choose accordingly.
References
1. FDA, Food labeling: health claims; soluble dietary fiber from certain foods and coronary heart disease, final rule, Fed. Reg., 71, 29248, 2006. 2. Xue, Q. et al., Influence of the hulless, waxy starch and short-awn genes on the composition of barleys, J. Cereal Sci., 26, 25, 1997. 3. Musatto, S.I., Dragone, G., and Roberto, I.C., Brewers’ spent grain: generation, characteristics and potential applications, J. Cereal Sci., 43, 1, 2006. 4. Fincher, G.B., Cell wall metabolism in barley, in Barley: Genetics, Bioochemistry. Molecular Biology and Biotechnology, Shewry, P.R., Ed., CAB International, Oxford, 1992, 413. 5. Oscarsson, M. et al., Chemical composition of barley samples focusing on dietary fibre components, J. Cereal Sci., 24, 161, 1996. 6. Fastnaught, C.E., Barley fiber, in Handbook of Dietary Fiber, Cho, S. and Dreher, M., Eds., Marcel Dekker, New York, 2001, chap. 27. 7. Newman, C.W. and Newman, R.K., Hulless barley for food and feed, in Specialty Grains for Food and Feed, Abdel-Aal, E. and Wood, P., Eds., AACC Press, Minneapolis, 2004, chap. 7.
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168. Biorklund, M. et al., Changes in serum lipids and postprandial glucose and insulin concentrations after consumption of beverages with β-glucans from oats or barley: a randomized dose-controlled trial. Eur. J. Clin. Nutr., 59, 1272, 2005. 169. Behall, K.M., Scholfield, D. and Hallfrisch, J., Diets containing barley reduce lipids significantly in moderately hypercholesterolemic men and women. Am. J. Clin. Nut., 80, 1185, 2004. 170. Behall, K.M., Scholfield, D.J. and Hallfrisch, J.G., Lipids significantly reduced by diets containing barley in moderately hypercholesterolemic men. J. Am. Coll. Nutr., 23, 55, 2004. 171. Keogh, G. F. et al., Randomized controlled crossover study of the effect of a highly β-glucan-enriched barley on cardiovascular disease risk factors in mildly hypercholesterolemic men. Am. J. Clin. Nutr., 78, 711, 2003. 172. Li, J. et al., Effects of barley intake on glucose tolerance, lipid metabolism, and bowel function in women. Nutrition, 19, 926, 2003. 173. Ikegami, S. et al., Effect of boiled barley-rice-feeding in hypercholesterolemic and normolipemic subjects. Plant Foods Hum. Nutr., 49, 317, 1996. 174. Narain, J.P. et al., Metabolic responses to a four week barley supplement. Int. J. Food Sci. Nutr., 43, 41, 1992. 175. Newman, R.K. et al., Hypocholesterolemic effect of barley foods on healthy men. Nutr. Rep. Int., 39, 749, 1989. 176. Newman, RK., Newman, C.W. and Graham, H., The hypocholesterolemic function of barley beta-glucans. Cereal Foods World, 34, 883, 1989. 177. Yang, J.-L. et al., Barley β-glucan lowers serum cholesterol based on the upregulation of cholesterol 7α-hydroxylase activity and mRNA abundance in cholesterol-fed rats. J. Nutr. Sci. Vitaminol., 49, 381-387, 2003. 178. Lupton, J., Robinson, M.C. and Morin, J.L., Cholesterol-lowering effect of barley bran flour and oil. J. Am. Diet. Assoc., 94, 65, 1994. 179. Liu, S., Dietary carbohydrates, whole grains, and the risk of type 2 diabetes mellitus, in Whole-Grain Foods in Health and Disease, Marquart, L. et al., Eds., American Association of Cereal Chemists, St. Paul, 2002, 155. 180. Behall, K.M. and Hallfrisch, J., Effects of grains on glucose and insulin responses, in Whole-Grain Foods in Health and Disease, Marquart, L. et al., Eds., American Association of Cereal Chemists, St. Paul, 2002, 269. 181. Livesey, G. et al., Influence of the physical form of barley grain on the digestion of its starch in the human small intestine and implications for health. Am. J. Clin. Nutr., 61, 75, 1995. 182. Cavallero, A. et al., High (1→3), (1→ 4)-β-glucan barley fractions in bread making and their effects on human glycemic response. J. Cereal Sci., 36, 59, 2002. 183. Yokoyama, W.H. et al., Effect of barley beta-glucan in durum wheat pasta on human glycemic response. Cereal Chem., 74, 293, 1997. 184. Wursch, P. and Pi-Sunyer, F.X., The role of viscous soluble fiber in the metabolic control of diabetes. Diabetes Care, 20, 1774, 1997. 185. Behall, K.M., Scholfield, D.J., and Hallfrisch, J.G., Barley β-glucan reduces plasma glucose and insulin responses compared with resistant starch in men. Nutr. Res., 26, 644, 2006. 186. Ostman, E. et al., Glucose and insulin responses in healthy men to barley bread with different levels of (1→3), (1→ 4)-β-glucans; predictions using fluidity measurements of in vitro enzyme digests. J. Cereal Sci., 43, 230, 2006.
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187. Hallfrisch, J., Scholfield, D.J. and Behall, K.M., Physiological responses of men and women to barley and oat extracts (Nu-trimX). II. Comparison of glucose and insulin responses. Cereal Chem., 80, 80, 2003. 188. Wood, P.J., Beer, M.U. and Butler, G., Evaluation of role of concentration and molecular weight of oat beta-glucan in determining effect of viscosity on plasma glucose and insulin following an oral glucose load. Br. J. Nutr., 84, 19, 2000. 189. Hawrysh, Z.J. et al., Barley bread products in the diet: community study with diabetic subjects. Cereal Foods World, 42, 620, 1997. 190. McLaren, D.S., Not fade away — the glycemic index. Nutrition, 16, 151, 2000. 191. Reaven, G.M., Role of insulin resistance in the pathophysiology of non-insulin dependent diabetes mellitus. Diabetes Metab. Rev., 9 Suppl 1, 5S, 1993. 192. Yokoyama, W.H. and Shao, Q., Soluble fibers prevent insulin resistance in hamsters fed high saturated fat diets. Cereal Foods World, 51, 16, 2006. 193. Ascherio, A. et al., Prospective study of nutritional factors, blood pressure, and hypertension among US women. Hypertension, 27, 1065, 1996. 194. Hallfrisch, J., Scholfield, D.J. and Behall, K.M., Blood pressure reduced by whole grain diet containing barley or whole wheat and brown rice in moderately hypercholesterolemic men. Nutr. Res., 23, 1631, 2003. 195. Behall, K.M., Scholfield, D.J. and Hallfrisch, J., Whole-grain diets reduce blood pressure in mildly hypercholesterolemic men and women. JADA, 106, 1445, 2006. 196. Sacks, F. M. et al., Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. N. Engl. J. Med., 344, 3, 2001. 197. FDA, Health claims notification for whole grain foods, Govt. Printing Office, Washington, D.C., 1999. 198. Cummings, J. H. et al., Fecal weight, colon cancer risk, and dietary intake of nonstarch polysaccharides (dietary fiber). Gastroenterology, 103, 1783, 1992. 199. Graf, E. and Eaton, J.W., Suppression of colonic cancer by dietary phytic acid. Nutr. Cancer, 19, 11, 1993. 200. McIntosh, G. et al., A comparative study of the influence of differing barley brans on DMH-induced intestinal tumours in male Sprague-Dawley rats. J. Gastroenterol. Hepatol., 11, 113, 1996. 201. Zhang, J. X. et al., Dietary effects of barley fibre, wheat bran and rye bran on bile composition and gallstone formation in hamsters. APMIS, 100, 553, 1992. 202. Huang, C. and Dural, N., Absorption of bile acids on cereal type food fibers. J. Food Pro. Eng., 18, 243, 1995. 203. Bohn, J.A. and BeMiller, J.N., (1-3)-β-d-glucans as biological response modifiers: a review of structure-functional activity relationships. Carb. Poly., 28, 3, 1995. 204. Vetvicka, V., Thornton, B.P., and Ross, G.D., Soluble β-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-Opsonized target cells. J. Clin. Invest, 98, 50, 1996. 205. Czop, J.K. and Austen, F.K., Properties of glycans that activate the human alternative complement pathway and interact with the human monocyte β-glucan receptor. J. Immun., 135, 3388, 1985.
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206. Thornton, B.P. et al., Analysis of the sugar specificity and molecular location of the β-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). J. Immun., 156, 1235, 1996. 207. Jaramillo, F. and Gatlin, D.M., Comparison of purified and practical diets supplemented with or without β-glucan and selenium on resistance of hybrid striped bass Morone chrysops x M.saxatilis to Streptococcus iniae infection. J. World Aquac. Soc., 35, 245, 2004. 208. Misra, C.K. et al., Effect of multiple injections of β-glucan on non-specific immune response and disease resistance in Labeo rohita fingerlings. Fish Shellfish Immun., 20, 305, 2006. 209. Modak, S. et al., Rituximab therapy of lymphoma is enhanced by orally administered (1→3),(1→ 4)-D-β-glucan. Leukemia Res., 29, 679, 2005. 210. Hong, F. et al., Mechanism by which orally administered β-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. J. Immun., 173, 797, 2004. 211. Cheung, N.-K.V., Therapy-enhancing glucan, U.S. Patent Appl. Publ., US 2006/0020128 A1, 2006. 212. ERS (USDA/Economic Research Service), Food consumption data system: barley and oats, www.ers.usda.gov/Data/FoodConsumption, ERS/USDA, 2002. 213. FAO (Food and Agriculture Organization), Food balance sheets. Barley, 1961 and 2001, faostat.fao.org/site/345/default.aspx, FAO, 2007. 214. Delaney, B. et al., Evaluation of the toxicity of concentrated barley β-glucan in a 28-day feeding study in Wistar rats. Food Chem. Tox., 41, 477, 2003. 215. Delaney, B. et al., Repeated dose oral toxicological evaluation of concentrated barley β-glucan in CD-1 mice including a recovery phase. Food Chem. Tox., 41, 1089, 2003. 216. Wisker, E. et al., Calcium, magnesium, zinc, and iron balances in young women: effects of a low-phytate barley-fiber concentrate. Am. J. Clin. Nutr., 54, 553, 1991. 217. Sandstrom, B. et al., Zinc absorption in humans from meals based on rye, barley, oatmeal, triticale and whole wheat. J. Nutr., 117, 1898, 1987. 218. Harrington, M.E., Flynn, A., and Cashman, K.D., Effects of dietary fibre extracts on calcium absorption in the rat. Food Chem., 73, 263, 2001. 219. Kennefick, S. and Cashman, K., Investigation of an in vitro model for predicting the effect of food components on calcium availability from meals. Int. J. Food Sci. Nutr., 51, 45, 2000. 220. Weber, C. et al., Binding capacity of 18 fiber sources for calcium. J. Agric. Food Chem., 41, 1931, 1993. 221. Idouraine, A. et al., In vitro binding capacity of various fiber sources for magnesium, zinc, and copper. J. Agric. Food Chem., 43, 1580, 1995. 222. Persson, H. et al., Binding of mineral elements by dietary fibre components in cereals — in vitro (III). Food Chem., 40, 169, 1991.
16 Sugar Beet Fiber: Production, Characteristics, Food Applications, and Physiological Benefits Marie-Christine Ralet, Fabienne Guillon, Catherine Renard, and Jean-Francois Thibault
Contents Introduction.......................................................................................................... 360 Fiber Production................................................................................................... 361 Characteristics...................................................................................................... 361 Sugar Beet Fiber Composition.................................................................. 362 Structure of Sugar Beet Fiber Polysaccharides....................................... 365 Pectins ........................................................................................... 365 Hemicelluloses................................................................................ 369 Cellulose........................................................................................... 369 Sugar Beet Fiber Physicochemical Properties......................................... 370 Hydration Properties...................................................................... 370 Adsorption/Binding of Ions and Organic Molecules............... 372 Functionality and Food Applications............................................................... 372 Extracted Polysaccharides......................................................................... 372 Whole Sugar Beet Fiber.............................................................................. 373 Ready-to-Eat Breakfast Cereals..................................................... 373 Bakery Products.............................................................................. 374 Meat Products.................................................................................. 374 Physiological Benefits.......................................................................................... 374 Apparent Fermentability or Apparent Digestibility.............................. 374 Transit Time and Stool Output................................................................. 375 Minerals Adsorption.................................................................................. 376 Glucose Metabolism................................................................................... 376 Lipid Metabolism........................................................................................ 378 Colorectal cancer......................................................................................... 381 Tolerance to Sugar Beet Fiber.................................................................... 382 Safety/Toxicity...................................................................................................... 383 Conclusion............................................................................................................. 383 References.............................................................................................................384 359
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Introduction Beets originate from the Middle East and have been grown as vegetables or for fodder since antiquity. However, their use as a sugar crop began only in the 18th century. At that time, consumption and production of sugar from sugar cane were very widespread and France had an important place in this trade. The French Revolution drastically modified the sugar world order and conflicts seriously disrupted shipping transport with the colonies. The Napoleonic Wars at the beginning of the 19th century made worse an already critical situation. In 1807, the British began a blockade of France, preventing the import of cane sugar from the Caribbean. Prices exploded and France had to find an alternative to the production of sugar from sugar cane in the overseas territories. In 1747, a Prussian chemist, Andreas Sigismund Marggraf, had been successful in recovering crystallized sugar from sugar beet. In France, Benjamin Delessert improved the Marggraf process and opened the first beet sugar factory in 1811. By the end of the wars, over 300 beet sugar mills operated in France and central Europe. The first U.S. beet sugar mill opened in 1838. Today, sugar beet provides approximately 25% to 30% of the world’s sugar production, which was around 150 million tons in 2005. The European Union (130 million tons for the 2005–2006 campaign), the United States (25 million tons), and Russia (22 million tons) are the world’s three largest sugar beet producers. The new sugar reform (2006) will probably have only a moderate impact on sugar beet production. Indeed, agricultural surfaces devoted to alternative fuel production will certainly compensate the decrease in those devoted to sugar production. Sugar beet roots contain ~18% sucrose and ~5% cell wall polysaccharides on a wet weight basis. Beet-sugar producers slice the washed beets and then extract the sugar with hot water in a diffuser. These treatments typically consist of heating at 85°C for approximately 15 min followed by diffusion by water, typically 2 h at ~65°C and pH ~6.5. An alkaline solution (“milk of lime” and carbon dioxide from the lime kiln) then serves to precipitate impurities. After filtration, evaporation concentrates the juice to a content of about 70% solids, and controlled crystallization extracts the sugar. A centrifuge removes the sugar crystals from the liquid, which gets recycled in the crystallizer stages. When economic constraints prevent the removal of more sugar, the manufacturer discards the remaining liquid known as molasses. Sugar beet pulp is a very abundant by-product (500 kg wet weight per ton of beets). On a wet weight basis (~90% humidity), 120 million tons of beet pulp are produced in the world each year. The wet pulp can be used directly (dry matter ~10%), pressed (dry matter ~27%), or dried (dry matter ~90%). The pulp is a popular feed for ruminants. However, alternative uses are currently proposed in order to increase the value of the pulp. The extraction of polysaccharides (pectins, arabinans, cellulose) or monomeric components (arabinose, galacturonic acid, rhamnose, ferulic acid) may be one way of upgrading [1–3]. For example, arabinan may be extracted from the pulp
Sugar Beet Fiber
361
and its potential as fat replacer has been investigated [4]. Another possibility is to find direct uses for the pulp. As this residue consists mainly of cell wall polysaccharides, several if not all sugar companies have studied the use of sugar beet pulp as a high-fiber food ingredient or a dietary fiber.
Fiber Production Larrauri [5] indicated that the ideal fiber preparation should meet several requirements among which are bland in taste, color, texture, and odor. In that context, beet pulp must be processed before it can be used in food systems because it has a typical unpleasant flavor, may be too colored, and also may contain too high amounts of soil or sand [6]. Essentially physical treatments including cleaning, extraction, sieving, and heating have been described, although some chemical treatments have also been proposed. With special processing, it is possible to produce a dietary fiber, with an off-white color and unobtrusive flavor, suitable for human food. The fibers may be milled to a given particle size from coarse to fine depending on the intended use, or treated with steam in a flaking process. Several processes have been patented and trade names have been given for such fibers. today, the sole commercial sugar beet fiber is Fibrex® developed by Danisco Sugar A/S (Denmark) and marketed as an ingredient all over the world. Annual Fibrex® production is less than 5000 tons. It includes two steam-drying steps with optimized temperature, pressure, and time, as well as a milling and screening step to remove sand from the end product. Fibrex® is proposed with a variety of particle sizes (from < 32 µm to flake) for easy blending with other ingredients (Figure 16.1).
Characteristics Dietary fiber in sugar beet comes exclusively from its cell walls, and is devoid of resistant starch or other reserve polysaccharides. Plant cell walls vary enormously in their compositions and physical properties depending on the cell type and plant species (7). Three plant groups are generally defined: dicotyledons (most fruit and vegetables), non-commelinid monocotyledons (mostly alliums), and commelinid monocotyledons (grasses and cereals). Among those groups, two major wall types are typically recognized: primary and secondary, the latter being often lignified (8). The polysaccharide compositions of the wall types in the different plant groups differ widely (Table 16.1). Fiber preparations from fruits or fruit residues and sugar beet pulp (dicotyledons) contain predominantly primary cell walls while cereal
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Fiber Ingredients: Food Applications and Health Benefits
Figure 16.1 Fibrex® of different particle sizes. This picture was kindly provided by Danisco Sugar A/S (Denmark).
Table 16.1 The Polysaccharide Compositions of Cell Wall Types in the Different Plant Groups Wall Type Plant Group Dicotyledons and Monocotyledons noncommelinid Monocotyledons commelinid
Non-Lignified Primary
Lignified Secondary
Cellulose ~ Pectins > Xyloglucan
Cellulose > Heteroxylans > Glucomannans
Heteroxylans (+ mixed β-glucans in Poaceae and other families) > Cellulose >> Pectins and Xyloglucans
Cellulose ~ Heteroxylans >> Glucomannans
Source: Adapted from Harris and Smith, 2006 [8]
brans (commelinid monocotyledons) contain both primary and secondary cell walls. This leads to very different cell wall architectures, polysaccharide compositions, and physicochemical properties. Sugar Beet Fiber Composition Sugar-beet pulp has a high dietary fiber content, typically >75%, and is known for its high soluble fiber content (Table 16.2) (9–11). The AOAC method, because of its lengthy enzyme incubations at pH close to neutral and at high temperature, may however overestimate the amount of fiber actually solubilized in the upper parts of the digestive tract. Lignin content of beet fiber is low (< 5%) (12–14). The remainder of the fiber preparations consists of pro-
363
Sugar Beet Fiber Table 16.2
Dietary Fiber (Total, Insoluble and Soluble, % Dry Weight) of Native and Modified Sugar Beet Fiber Preparations Native sugar beet fiber Autoclaved at 122°C Autoclaved at 136°C Native sugar beet pulp Fibrex® Native sugar beet fiber H2O2-treated
TDF
IDF
SDF
87.1 78.4 78.6 76.9 73.0 70.0 94.3
71.7 52.5 48.9 52.1 49.0 57.8 61.1
15.4 25.9 29.7 24.8 24.0 12.2 33.2
Ref. (9)
(10) Data provided by the supplier (Danisco) (11)
teins (< 10%) (13–15); ash (3% to 8%) (13–15); and lipids (< 2%) (15). Some sugar beet pulp fractions may be high in ash (16) arising from contamination by soil particles. In detailed studies of their composition, beet cell walls, and therefore sugar beet fiber, are characterized by very high pectin content, with about 20% each of galacturonic acid (GalA) and arabinose (Ara) (Table 16.3) (17–20). This amount of pectin and more specifically of Ara is exceptionally high, even in comparison to cell walls from other dicotyledons. Arabinans, which are part of pectins, are still often mistaken for hemicelluloses. Sugar beet fiber also contains approximately 20% of glucose (Glc), mainly of cellulosic origin. In total, sugars account for about 80% of the dry weight, with remarkably low amounts of xylose (Xyl) and mannose (Man). Several non-sugar constituents are also present: methanol, acetic acid, phenolic acids, proteins, lignin, and ash (Table 16.3). There are little differences in global sugar composition between cell wall material directly isolated from raw beets and sugar beet pulp (Table 16.3). Le Quéré et al. (21) found 4.5% of water-soluble pectin from beet slices alcoholinsoluble solids (AIS) and, surprisingly, still 3.3% from AIS arising from beet pulp after diffusion. Fares et al. (22) also showed that few polysaccharides, mainly of pectic origin, are extractable from sugar beet by water in the sugar factory. This low extraction of pectins could be due to physical limitations to diffusion of the pectic polymers from the cell wall network or to the structure of beet cell walls. Little material is extracted from beet cell walls in mild, non-degradative conditions. Dea and Madden (23) extracted only a total of 5% dry matter from whole beets by successive cold and hot water treatments at pH 3.7. Renard and Thibault (24) and Levigne et al. (19) extracted only 5% to 5.6% of whole beet AIS by buffer or water at pH 4.5 and room temperature. This extracted material is of pectic nature, rich in GalA and Ara. As pointed out above, the AOAC method leads to higher extraction yields with SDF values around 20%. Compositional analysis reveals that sugar beet SDF is also of pectic nature. Sugar beet IDF still contains large quantities of pectic material and is rich in Glc of cellulosic origin (Table 16.3).
Native pulp Acid- and alkali-treated pulp Native pulp Acid- and alkali-treated pulp Native fiber Acid- and alkali-treated fiber AIS from fresh roots Water-extraction at 20°C Residue Soluble (polymeric) IDF SDF
1.4 1.0 2.4 2.3 1.5 1.2 2.0 1.2 1.2 1.6 0.9
82 2 60 13
Rha
100 35 100 53 100 46 4
Yield (%)
19.2 16.1 24.6 7.9
19.1 11.0 19.6 10.0 23.6 5.3 17.2
Ara
1.4 tr 1.6 tr
1.6 3.6 1.4 2.1 1.4 2.5 1.1
Xyl
1.0 tr 1.4 4.2
1.3 2.7 1.3 2.1 1.4 2.6 1.0
Man
Sugar Composition of Different Sugar Beet Fiber Preparations (% dry weight)
Table 16.3
4.9 6.1 6.1 3.1
4.6 2.3 5.5 5.7 5.4 4.5 4.5
Gal
22.2 1.2 29.6 0.6
20.6 54.2 21.5 38.9 24.3 51.0 18.8
Glc
21.7 31.6 19.6 43.4
20.2 4.9 20.6 16.0 23.2 12.0 20.0
GalA
71.6 56.2 84.5 60.1
68.8 69.8 72.3 77.1 80.8 79.1 64.6
Total sugars
20
20
19
17
18
17
Ref.
364 Fiber Ingredients: Food Applications and Health Benefits
Sugar Beet Fiber
365
Structure of Sugar Beet Fiber Polysaccharides Sugar beets are mainly composed of parenchymal tissue with thin, supple, and hydrophilic cell walls. Typical primary cell walls of dicotyledonous plants are composed of almost equal amounts of three types of polysaccharides: (1) pectin, rich in GalA, Gal, Ara, and Rha; (2) hemicelluloses, typically xyloglucans with minor amounts of (gluco)-mannans; and (3) cellulose. The structure of these cell walls can be summarized as three interlocking networks, namely cellulose/xyloglucans, pectin, and cell wall glycoproteins. Sugar beet cell walls differ from this blueprint in a number of key points, which will be discussed in the following. Pectins Most of the data on the structure of the constitutive polysaccharides of sugar beet cell walls and fiber deal with the pectic fraction, as it represents more than 50% of the fiber (Table 16.4) (19, 24–29). Pectin is an extremely complex polysaccharide that can be viewed as a multiblock co-biopolymer. The simplest, and the most abundant, of these blocks is homogalacturonan, an unbranched polymer of (1→4)-α-d-GalpA residues that are partly methylesterified and sometimes partly acetyl-esterified. A second major block, rhamnogalacturonan I, is mainly composed of a repeating disaccharide unit (→2)-α-l-Rhap -(1→4)-α-d-GalpA-(1→)n decorated with arabinan and (arabino)-galactan side-chains. Assemblies of RG, arabinan, and (arabino)galactan are often referred to as pectic “hairy” regions in which arabinan and (arabino)-galactan are the “hairs.” A fourth minor block, rhamnogalacturonan II, is a highly complex molecule made of a short homogalacturonan backbone with four conserved side chains consisting of 12 different monosaccharides. Sugar beet pectins have distinctive features, notably low average molar mass, high acetic acid contents, and presence of phenolic esters on their side chains. They also contain a high proportion of hairy regions, with very high Ara contents. Oosterveld et al. (29) reported that approximately 70% of the pectin in sugar beet pulp consists of hairy regions. Backbone Controlled acid hydrolysis of beet pectins (30) led to isolation of almost pure homogalacturonans. The degree of polymerization of sugar beet homogalacturonans is only slightly lower (70–100) than that of citrus or apple homogalacturonans (100–120). The Rha residues are concentrated in rhamnogalacturonans I, where they alternate with the GalA residues (31, 32). Beet pectins, with a Rha:GalA ratio > 1:10 in the cell wall, are particularly rich in Rha (Table 16.2). About 40% of the Rha residues are further substituted at position 4 by neutral sugars, mainly arabinan, side chains. Rhamnogalacturonan II, a small complex pectic polysaccharide, and its boron-cross-linked dimer, can be isolated from beet after enzymatic digestion (33).
2.2 0.5 19.9 11.1
6.4 17.8
Water 20°C Autoclave pH 5.2 121°C
5.6 28.9 7.1 27.5 13.6 2.5 28.0 5.6 35.0 19.9 —
Yield (%)
Water 20°C NH4 oxalate 1% 20°C HCl 0.05M 85°C NaOH 0.05M 4°C
Sequential Extraction Scheme
Buffer pH 4.5 20°C Buffer pH 6.5 80°C CDTA pH 4.5 20°C CDTA pH 6.5 80°C EDTA 2% 85°C HCl pH 3.0 75°C HCl pH 1.0 75°C HCl pH 3.0 95°C HCl pH 1.0 95°C NaOH 2% 45°C NaOH 0.05M 4°C
Single Extraction
Extraction Conditions
7.6 39.9
54.4 77.9 65.1 54.9
51.3 45.6 48.4 48.4 55.2 44.5 29.5 44.5 45.5 42.4 58.9
GalA
0.3 2.1
0.9 0.9 2.3 3.2
1.3 1.9 1.1 1.6 1.9 1.1 2.8 1.4 4.1 1.9 2.6
Rha (%)
7.3 26.7
8.4 1.9 10.0 12.5
10.1 16.4 8.2 14.3 33.7 11.4 29.4 15.9 3.1 8.1 20.1
Ara
Extraction Conditions and Characteristics of Sugar Beet Pectins
Table 16.4
4.0 3.9
6.5 2.4 5.9 8.1
5.1 5.5 4.6 4.8 7.3 3.3 6.8 2.7 8.5 3.7 5.5
Gal
41 70
76 60 62 8
63 52 52 55 — 94 34 83 65 — 16
DM
41 48
31 15 35 4
32 34 27 35 — 39 37 36 28 — 19
DAc
0 0.61
0.10 0.04 0.48 0.57
— — — — — 0.26 0.80 0.35 0.60 — —
FeA (%)
— —
259 57 225 181
187 70 257 100 — 454 342 351 304 — —
[] (mL/g)
29
28
24 24 24 24 25 19 19 19 19 26 27
Ref.
366 Fiber Ingredients: Food Applications and Health Benefits
Sugar Beet Fiber
367
Side Chains In beet pectins, the side chains are composed of Ara and Gal; other sugars (Xyl, Glc, Man) are present in negligible amounts (19, 28, 34, 35). Methylation analysis shows a predominant presence of arabinans with a backbone of linked α-(1→5)-Araf residues carrying ramifications predominantly on O-3. Oosterveld et al. (29) used an alkali and a combined autoclave and alkali extraction of sugar beet pulp to extract arabinans. A degree of polymerization of 130 to 170 residues was calculated for those arabinans (36). Methylation analysis and enzymatic degradation using an α-arabinofuranosidase, showed that sugar beet arabinans have a backbone of 60 to 70 residues and that more than 45% to 65% of the Ara residues are present as single unit or oligomeric side group of the arabinan main chain (29, 36). The Gal residues are mostly present as type I galactans, linear chains of β-(1→4)-linked Galp residues, but the partially methylated derivatives also indicate the presence of type II galactans (29, 34). Sugar beet type I galactans are most likely almost linear and of low degree of polymerization (34). NMR analysis of the sugar beet pectin supports the evidence of methylation analysis with presence of α-(1→5)-linked Araf residues and β-(1→4)linked Galp residues (37). Non-Sugar Substituents In sugar beet, pectin’s backbone carries both methyl esters (on the carboxylic group) and acetyl esters on the secondary alcohols. Sugar beet pectins are not very highly methylated, having a degree of methylation of about 50 to 60 (Table 16.4). The degree of acetylation of the extracted beet pectins is generally 20 to 30 (Table 16.4). Several studies about the exact location of acetyl groups on pectins have been carried out. Comparison of pectic fragments isolated after enzymatic hydrolysis of various tissues from different plant species suggests a high diversity in the degree, distribution among homogalacturonan and rhamnogalacturonan I, and location of acetyl groups. Keenan et al. (37) presented a 13C NMR study of sugar beet pectin and concluded that both of the available ring positions (O-2 and O-3) of GalA residues can be acetyl esterified. Kouwijzer et al. (38), on the basis of energy calculations, also concluded that acetyl groups at both O-2 and O-3 of GalA in the backbone of homogalacturonan and rhamnogalacturonan I are energetically favorable. In sugar beet pectins, around 75% of the acetyl groups appear to be attached to homogalacturonan (39). Only 10% of the GalA residues are present in the rhamnogalacturonan I region (30, 39, 40) so that rhamnogalacturonan I, which carries only 25% of the acetyl groups, is finally very highly acetylated (DAc ~ 60) (39). No methyl esterification was detected on sugar beet rhamnogalacturonan I (39), in agreement with studies on other plant species (41, 42). In sugar beet homogalacturonan, it was shown by mass spectrometry that (a) O-2 and O-3 acetylation are present in roughly similar amounts, (b) 2,3-di-O acetylation is absent, and (c) GalA residues that are at once O-acetyl
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Fiber Ingredients: Food Applications and Health Benefits
and methyl esterified are rare so that unsubstituted GalA residues are present in limited amounts (~10%) (39). Among dicotyledons, in species of the family Amaranthaceae, pectins carry phenolic acids (Table 16.4) (43). These include mainly ferulic acid, which represents about 0.8% of the beet cell walls, and to a lesser extent p-coumaric acid (28). In beet and spinach cell walls, ferulic acid mainly esterifies neutral sugars (Ara and Gal) of pectic side chains (28, 34, 44, 45). More precisely, ferulates are linked for about 50% to 60% to the O-2 position of Ara moieties and for 40% to 50% to the O-6 position of Gal residues (46–48). Structural analysis of longer oligosaccharides (up to DP 8) showed that the feruloyl groups are mainly linked to Ara residues of the core chain of arabinans and to Gal residues of the core chain of type I galactans (47). Recently, minor amounts of ferulic acid linked to O-5 of the Ara residues of the main core of arabinan chains were detected, indicating a potential peripheral location of some ferulic acid on pectic hairy regions (49). Feruloyl esters are not randomly distributed among the different pectic polysaccharides in the sugar beet cell wall (50). Phenolic acids are bifunctional and thus a potential cross-linking element in beet cell walls (51). Indications in favor of that role are the presence of dehydrodimers of ferulic acid in sugar beet pulp (52–57) and the possibility of cross-linking extracted beet pectins in vitro by oxidation of their feruloyl groups (53, 58–62). Distribution of Pectic Structural Elements After degradation of partly demethylated sugar beet pectin with polygalacturonase (39, 40, 63), most of the GalA (~90% of the GalA initially present in pectin) is recovered as oligogalacturonates of low degree of polymerization arising from homogalacturonans. The remaining GalA is recovered in a high molar mass fraction corresponding to hairy regions and composed mostly of neutral sugars, notably Ara, Gal, and Rha. Distribution of arabinans and galactans in the hairy regions has been studied by degradation with dilute acids (34) or specific enzymes (64, 65). Digestion by a mixture of endo-arabinase and arabinofuranosidase can lead to complete separation of the Ara while the Gal is retained with the rhamnogalacturonan I. These results indicate that galactan chains are directly linked to the backbone while arabinans might be connected through an interposed Gal unit or short galactan chain (64, 65). Extraction and Molar Mass Sugar beet cell walls contain a very low amount of readily extractable pectin (by water, buffer, or chelating agents at room temperature) even prior to the diffusion step. Though calcium is present in sugar beet in amounts sufficient to neutralize most of the non-methylated GalA (Fares et al., unpublished results), calcium cross-links do not seem to be the main mechanism holding the pectins in the beet cell wall.
Sugar Beet Fiber
369
Efficient extraction can be obtained either by heating or by alkaline treatments (i.e., demands a degradation of the pectin). Autoclaving as well as heating at pH circa 6.5 (either with buffer, EDTA, or CDTA) leads to degradation of the pectic backbone through β-elimination and therefore to extraction. This causes the presence in the extract of two populations, namely a high molar mass neutral sugars-rich fraction (analogous to the hairy regions obtained after enzymatic degradation) and a lower molar mass fraction, almost exclusively composed of GalA (24, 29, 34, 63). Hot acid treatments, comparable to those used for industrial extraction of pectins, have been studied using an experimental design (19). The type of acid used (HCl or HNO3) had no effect on the characteristics of extracted pectins. pH was shown to be the main parameter influencing extraction yield. At pH 1, degradation of the arabinan side chains took place. Depending on the extraction conditions used, intrinsic viscosity of the acid-extracted pectins varied from 172 to 493 mL/g and weight-average molar masses from 70 to 355 kDa (19). Hemicelluloses Hemicelluloses can be defined as cell wall polysaccharides that have the capacity to bind strongly to cellulose microfibrils by hydrogen bonds (66). The common structural features of hemicelluloses are a main chain with a structural resemblance to cellulose and either short side chains that result in a pipe-cleaner-shaped molecule or a different sugar interpolated in the main chain, both modifications preventing further aggregation (67). In the cell walls of land plants, three classes of polymers correspond to that definition, namely xyloglucans, heteroxylans, and mannans. In the primary cell wall of dicotyledons, the main hemicellulose is usually xyloglucan, which accounts for 15% to 20% of the dry weight of the wall. Beet cell walls have very low concentrations of the sugars that denote hemicelluloses (i.e., Xyl, Man, non-cellulosic Glc and Fuc; Table 16.3), and their hemicelluloses have been very little studied. Oosterveld (68) isolated from a 4 M NaOH extract from beet a fraction enriched in hemicelluloses, and methylation analysis of this material indicated presence of xyloglucans and mannans. Degradation by a purified endo-glucanase of this fraction allowed identification of xyloglucan oligomers, which confirmed presence, though in very low amounts, of a standard fucogalactoxyloglucan in beet cell walls. Fares et al. (69) identified fucogalactoxyloglucans and xylans in alkali extracts from sugar beet AIS. Cellulose Cellulose is the world’s most abundant naturally occurring polymer, rivalled only by chitin. Cellulose is a homopolymer of (1→4)-β-d-Glcp. The β-1,4 configuration results in a rigid and linear structure for cellulose. Cellulose chains exhibit a strong tendency to form intra- and intermolecular hydrogen
370
Fiber Ingredients: Food Applications and Health Benefits
bonds resulting in the formation of microfibrils whose length, width, and crystallinity differ much depending on the cellulose origin. Cellulose arising from primary cell walls are particularly thin (2 to 3 nm width) and of low crystallinity. This has been confirmed by solid-state NMR for beet cellulose (70). Following the initial work of Weibel (71, 72), Weibel and Myers (73), and Dinand et al. (13, 74) purified and evaluated the application potential of sugar beet cellulose. Sugar Beet Fiber Physicochemical Properties The expression “physicochemical properties” is a generic term, involving structural parameters such as particle size and shape, surface properties and porosity, as well as functional properties such as hydration and cationexchange properties of cell wall materials (75). For sugar beet fiber, some of those physicochemical properties have been studied in relation to the dietary fiber hypothesis. Hydration Properties Hydration capacities partly determine the fate of dietary fiber in the digestive tract (fermentation induction) and account for some of their physiological effects (fecal bulking of lowly fermented fiber) (76). Basically, three different parameters were defined (77): (1) swelling, “the volume occupied by a known weight of fiber under the condition used”; (2) water retention capacity (WRC), “the amount of water retained by a known weight of fiber under the condition used”; and (3) water absorption (WA), “the kinetics of water movement under defined conditions.” Beet fiber, as most of the fibers arising from dicotyledons primary cell walls, exhibits high hydration capacities, in particular compared to fibers from cereal brans. Those hydration properties fluctuate much depending on the fiber preparation and also on the conditions of measurement (Table 16.5) (9, 78–83). The major intrinsic factors affecting hydration properties are particle size and drying conditions. Drying at high temperature results in a decrease of the hydration capacities, as does a decrease in particle size (Table 16.5). Thermal or thermo-mechanical treatments increase the amount of soluble fiber in beet pulp and modify its hydration properties (Table 16.5). In addition, the measured hydration capacities are sensitive to extrinsic factors, such as the ionic strength of the hydrating solution (Table 16.5) and its ion composition. These effects are mostly visible after conversion to the H+ or Na+ form, or after saponification. Beet pulp then appears to behave as a polyelectrolyte resin. The presence of divalent cations results in a decrease in hydration capacities of deesterified beet pulp (78). A number of these effects might be masked in native beet pulp by the presence of a high calcium concentration. The conditions of hydration also play a role: The presence of shear
371
Sugar Beet Fiber Table 16.5 Hydration Properties of Different Sugar Beet Fiber Preparations Swelling (mL/g)
WA (mL/g)
WRC (mL/g)
Ref.
— — — — — —
26.6 26.5 # 22.5 23.9 — —
78 79 78 80 80 79
Beet Pulp (fiber #) in Water Native
11.0 11.5 # 25.0 17.8 32.0 32.6 #
H+-form Na+-form
Beet Pulp in Presence of Supporting Salts Native H+-form
10.0 13.4
— —
— 16.0
78
Na+-form
15.3
—
—
80 80
25.0 20.0 21.9 32.4
— — — —
24.8 20.7 18.3 —
78 78 81 81
Φ 540 µm
21.5
8.5
82
Φ 385 µm
21.4
8.8
Φ 205 µm
15.9
7.3
24.2a 12.6b 22.6a 12.0b 19.2a 9.2b
Saponified Beet Pulp in Water Native H+-form Na+-form Beet Fiber in Water
82 82
Thermomechanically Treated Pulp Extruded beet pulp Autoclaved beet pulp at 122°C at 136°C a b
14.4 (native 19.3)
—
28.2 (native 32.9)
83
20.0 (native 23.0) 21.0 (native 23.0)
— —–
35.0 (native 34.0) 38.4 (native 34.0)
9 9
Long incubation, heavy stirring. Short incubation, gentle stirring.
forces in the form of intense stirring can lead to a destructuration of the beet fiber and an increase in apparent WHC (Table 16.5). This sensitivity to the exact method and conditions of measurement explains the variability of the results.
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Fiber Ingredients: Food Applications and Health Benefits
Adsorption/Binding of Ions and Organic Molecules Sugar beet fibers behave as weak monofunctional cation-exchange resins with a cation-exchange capacity (CEC) of about 0.5 meq/g. This ion-binding capacity is due to the presence of non-methylesterified GalA residues, and the CEC is equal to the concentration of non-methylated GalA residues calculated from independent GalA and methyl groups measurements (79, 80). Beet fibers are devoid of phytic acid, the main ion-binding species in cereal fibers. In spite of the presence of acetyl groups, pectin in sugar beet fiber is able to bind divalent cations, with higher affinities than in solution (18, 80) but with the same selectivity scale: Cu ~ Pb >> Zn ~ Cd > Ni > Ca. The ability of uronic-acid- and/or phenolic-compounds-rich fibers to interact with bile acids in the small intestine has been suggested to explain their hypocholesterolemic effects. Bile acid adsorption to fibers would result in a lower re-absorption, in an increased transport toward the large intestine and, finally, in a higher excretion of bile acids (84). Recent in vitro studies showed that freeze-dried beet, sugar beet pulp, and red sugar beet fiber preparations were able to bind bile acids to a certain extent (~ 10 to 15 μmol bile acid/g of dry matter) (10, 85).
Functionality and Food Applications Extracted Polysaccharides Pectins from sugar beet do not form gels in the usual conditions (i.e., either with calcium or with high sugar concentrations and acidic conditions) (86, 87). This inability has been ascribed variously to presence of acetyl groups (88), which indeed hinders binding of ions (89), to low molar mass (16, 90) or to excessive amounts of side chains (37). Acetyl groups are the most likely candidates for these weak gelling properties. Several deesterification attempts have been made to improve the gel formation of sugar beet pectin: partial deacetylation by mild acid treatments (91), incubation with an enzyme preparation from Aspergillus niger (92), treatment with mixtures of acetyl and methyl esterases from oranges or Aspergillus niger (87, 93), treatment with mild acid, alkali, fungus methyl-esterase or plant methyl-esterase (35). All those treatments led to low-ester pectins, which gelled in the presence of Ca2+. However, sugar beet pectin is presently only produced in small amounts for specific applications where it has equal or superior properties compared with apple or citrus pectin. These applications include stabilization of flavored oil emulsions (94, 95) and stabilization of acidified drinking yogurt (96). As sugar beet pectins may form gels by an oxidative cross-linking of ferulic acid (28, 45, 61), the enzymatic gelation of sugar beet pectins in food products was studied (97). Oxidative gelation of sugar beet pectins gives a thermo-irreversible gel that is of great interest for the food industry
Sugar Beet Fiber
373
as the product can be heated while maintaining a gel structure. With 2% sugar beet pectin added, a gel was formed in luncheon meat using laccase. The cohesive gel was shown to bind the meat pieces together, thereby making the product sliceable (97). Arabinans can be extracted from isolated sugar beet pectins or directly from sugar beet pulp. Alkaline extraction at high temperature (70°C to 98°C) for 15 to 90 min followed by neutralization and ultrafiltration yields a branched arabinan (molar mass of about 50 kDa) containing around 80% of l-Ara (98). Branched arabinan exhibit surface-active properties, which make it suitable for use as an emulsifying agent. Additionally, flavor oil and fragrances may be encapsulated using arabinan (98). However, the arabinan extraction and purification cost is a clear limitation for these uses. Branched arabinan can be linearized using purified α-l-arabinofuranosidase to yield debranched arabinan (98). The debranched arabinan forms an aqueous gel, which has the properties of a fat substitute and may be used in foods (4, 98). Whole Sugar Beet Fiber Sugar beet fiber is claimed to offer nutritional benefits to consumers as well as manufacturing and functional advantages to food processors. Moisture retention, good texture, and mouthfeel are the main technical properties of the beet fibers (Fibrex®), which are proposed with a variety of particle sizes (from < 32 μm to flake; Figure 16.1) for easy blending with other ingredients. The particle size is important for applications because the ability to bind water may be affected (Table 16.5) (82) and because it may influence the texture of the product and the mouthfeel properties (99). The beet fiber also has the advantage of containing no phytic acid (a substance that may be found in cereal fiber and can tightly bind minerals) and no gluten (6). Potential applications include cereals, bakery products, pasta, processed meats, soups, and snacks. Fibrex® total volume sales are divided as follows: 55% bakery customers, 30% meat applications, and 15% health. Successful recipes have been proposed for pastries, cakes, biscuits, snack foods, pasta, and meat products. It can be used in breads as a natural improver and to maintain freshness. In biscuits, it increases the fiber content and in meat products, it may provide chewy and juicy character. Ready-to-Eat Breakfast Cereals The properties of sugar beet fiber make it a good candidate for fiber enrichment in high-fiber ready-to-eat cereals applications (99). It has been incorporated into extruded ready-to-eat cereals at high quantities (up to 40%) without affecting the mouthfeel, flavor, or color. This property can probably be ascribed to the high water-binding properties of beet fiber. Non-milled versions of the fibers or flaked versions are used in rather high amounts (up to 25%) in muesli products.
374
Fiber Ingredients: Food Applications and Health Benefits
Bakery Products Fiber-enriched breads have a large commercial success, and diverse fibers can be successfully incorporated into a large variety of bakery products, as a bulking agent and as a dietary fiber source. Cereal bran is generally used to increase the amount of dietary fiber content in breads but this addition influences the color, the taste, as well as the texture/consistency of the product. In comparison with cereal bran, sugar beet fibers are characterized by: (a) low phytate, which is of particular concern to nutritionists because of its possible adverse effects on mineral absorption (100); and (b) better water binding and retention capacity, which is of particular interest for the baking industry (101). Thereby, several research articles deal with the effect of sugar beet fibers onto yield of dough, dough mixing properties, yield of bread, bread volume, and crumb quality (11, 102–105). Up to 15% of flour replacement, beet fiber appears to provide beneficial effects on dough textural profile, especially for the prominent and suitable decrease in gumminess, and no significant adverse effects on main mechanical, surface, and extensional properties (105). An enrichment with sugar beet fiber decreases bread volume and crumb quality. In that context, less than 10% of flour replacement by sugar beet fiber is recommended (11). Sugar beet fiber is also claimed to prolong the freshness of bread. Beet fiber can also be used for the production of soft cookies or muffins for which fibers with a high water-binding capacity are required. Meat Products Beet fiber (1% to 3%) may be incorporated into meat loaves, patés, meat products, and sausages, to give a juicy character even in frozen products, and to improve the consistency or the texture, and as a fat substitute (99, 106–108).
Physiological Benefits Apparent Fermentability or Apparent Digestibility Apparent fermentability and apparent digestibility were investigated in vitro with fecal inoculate (9, 17, 109–113) or in vivo in rats (114, 115) or in pigs (116–118). All indicated a high fermentability or apparent digestibility of sugar beet fiber, in the range of 70% to 90%. GalA and Ara were virtually completely digested; Glc about 85% to 88%; only Xyl, present in small amount, was of low digestibility. It was shown in vitro that all sugars are not fermented at the same rate; Glc disappearance began more slowly than that of GalA and Ara (9, 17, 109, 110, 112). The tridimensional arrangement of the polymers within the cell wall, and thus the access of bacteria or associated enzymes to the polymers, may account for this difference (17). Process-
Sugar Beet Fiber
375
ing of fiber, such as autoclaving or chemical extraction followed by drying, influenced its fermentability (9, 17). Harsh drying conditions following pectin extraction induce the distortion and shrinking of cells and a noticeable decrease in the total pore volume, especially in the pore volume accessible to bacteria. As a result, fermentability was reduced (17). The production of short-chain fatty acid (SCFA) was analyzed in vitro (9, 17, 109, 110, 112, 113, 119) or in vivo. In the latter case, the production was deduced either from measurement of SCFA in feces or cecal digesta of animals (115) or from dynamic analysis of porto arterial differences in the concentration of SCFA and of the portal blood flow rate in pigs (120). The data confirmed the high fermentability of sugar beet fiber, especially when compared to other insoluble fibers (from cereal or legumes). Fermentation profiles, expressed as the molar percent of each of the major SCFA—acetic (C2), propionic (C3), and butyric (C4)—was characterized by a high ratio of C2 (60% to 80%) followed by C3 (11% to 23%) and then C4 (9% to 15%). In pigs, a higher level of C2 was observed compared to humans. This might be explained by the fact that the length and the capacity of the large intestine in pigs are approximately 1.5 to 3 times larger than in humans. In vitro, no alterations in the SCFA profile were observed when modulating the chemical composition and physicochemical properties of sugar beet fiber (17, 110). Transit Time and Stool Output The effect of sugar beet fiber on transit time and stool output was evaluated in healthy subjects (121), in patients complaining of chronic constipation (122), and in rats (15, 114, 123, 124). Supplementation with sugar beet fiber increased wet fecal mass and number of daily stool. More diverse were the effects on transit time and dry fecal mass. Sugar beet fiber (33 g/day) in the diet decreased transit time by 25%, as did the wheat-bran-supplemented diet (121). Both increased the number of daily stool and wet fecal mass. Weight of fecal water but not the dry fecal mass changed, while wheat bran increased both dry weight of fecal mass and fecal water. In rats, the sugar beet diet increased the fecal output, as did the other fiber diets (15, 114, 123, 124). Nyman and Asp (114), Johnson et al. (1990) (123), and Harland (15) reported both wet and dry fecal mass increase. In constipated patients, a marked decrease in severe and moderate constipation at both the 15th and 30th day of treatment with sugar beet fiber was found, with a significant increase in fecal frequency normalization (122). Moreover, fecal consistency changed from hard and semi-hard stools to soft ones. The mechanisms by which fiber influences transit time are still not fully understood. Different mechanisms have been suggested, which depend on the physical properties and fermentability of the fiber (125, 126). The fiber may act by increasing the lumen volume, depending on the amount of indigestible residue in the colon, the water-retention capacity of the residue, the stimulation of microbial growth, and the production of gas. The fiber can also reduce transit time through modulating colonic motility either by a mechan-
376
Fiber Ingredients: Food Applications and Health Benefits
ical stimulation of mechanoreceptors by the edges of the fiber particle (127), or by a chemical stimulation by the products of fermentation (125, 128), or by the release of compounds trapped by fiber such as biliary acids or fatty acids (126). In the latter case, these products can stimulate not only colon motility but also secretion. Except for stimulation of mechanoreceptors, the different mechanisms mentioned above could contribute to the effect of sugar beet fiber on transit. The increase in stool output by dietary fiber intake may have several causes (126). It could be related to the amount of excreted residue and its water-binding capacity. The increase of the bacterial mass can also contribute, since bacteria contain 80% water. Finally, the excreted water could be water not absorbed in the colon because of the short transit time or changes in colonic motility. Again, these different mechanisms can all participate in the increase of stool output. Minerals Adsorption The effect of sugar beet fiber on the absorption of zinc, iron, copper, calcium, and magnesium was investigated in humans (129–131) and rats (15, 132) and led to the same conclusions. Sugar beet fiber has no negative effect on any of the minerals studied. These studies stressed the fact that beet fiber generally has a relatively high mineral content and can therefore contribute to mineral intake. Glucose Metabolism The effects of sugar beet fiber on Glc metabolism were investigated with different objectives. The effects on fasting plasma Glc and insulin values and on Glc tolerance of sugar beet fiber intake over a period of several weeks (from 3 to 8) were studied in normal (133), normal but with high fasting cholesterol value (134), or non-insulin-dependent diabetes mellitus (NIDDM) subjects (135, 136). These parameters were regarded together with lipid parameters in order to better understand the mechanisms by which daily intake of dietary fiber can decrease the risks of cardiovascular disease. Experiments were also concerned with Glc tolerance (137–140) in healthy volunteers or pigs and focused on acute effects of fiber supplementation. No clear effect of a long-term sugar beet fiber supplementation on fasting as well as postprandial blood Glc and insulin levels has been demonstrated (Table 16.6). The source, processing, and physical form of the fiber in the diet but also the nature of the meal (amount of fiber, amount of lipids, sources of carbohydrates, etc.), the metabolic status of the subjects, and the duration of the experiment may explain these differences. Similarly, discrepancies in blood Glc and insulin responses in normal subjects to a single meal with added sugar beet fiber are recorded in the literature (Table 16.7). No clear mechanism explains the effect of sugar beet fiber on postprandial Glc level. It is well known that soluble high molar mass fiber such as oat or guar gum can significantly decrease the postprandial circulating Glc level
377
Sugar Beet Fiber Table 16.6
Chronic and Postprandial Responses of Plasma Insulin and Glucose in Volunteers Given Sugar Beet Fiber Supplements Intake (g/day/subject)
Subjects
Duration
20
Healthy
16 days
18
Healthy middle-aged with risk ischemic heart disease
3 weeks
8
NIDDM
8 weeks
40
NIDDM
8 weeks
Results
Ref.
No changes in blood fasting Glc and insulin concentrations. No effect on fasting plasma Glc and insulin Effect on postprandial parameters. Improvement in Glc response to a standardized breakfast. Blood Glc and insulin fasting or postprandial levels were not significantly affected.
133
134
135
136
Table 16.7 Postprandial Responses of Plasma Insulin and Glucose in Volunteers Given Sugar Beet Fiber Supplements Intake (g/meal)
Carbohydrate (g/meal)
Subjects
Results
Ref.
No difference in the mean blood and plasma insulin curves at any time between the control and fiber diets. An improved Glc tolerance; no change in insulin level; no decrease in postprandial insulin. Lower postprandial blood Glc and serum insulin response compared with formula without fiber. No effect on postprandial glycemic and insulinemic values. No difference in Glc absorption between sugar beet fiber and wheat bran supplemented diets.
137
20
86
Healthy male human volunteers
10
100
Healthy male human volunteers
51 (liquid formula)
Healthy male human volunteers
56
653
Pigs
114
446
Pigs
7
138
140
139
120
378
Fiber Ingredients: Food Applications and Health Benefits
by slowing the gastric emptying and/or influencing the diffusion and mixing of the intestinal contents. Sugar beet fiber is only partly soluble and it is unlikely that the soluble fiber fraction can induce a sufficient increase of the viscosity of digesta to delay starch digestion or absorption, especially in the case of a solid meal. Another mechanism suggested is by changing transit time, but, again, results in the literature are discordant. Morgan et al. (138) observed a slightly accelerated liquid gastric emptying with both sugar beet fiber and guar gum supplementation, which was unexpected. Hamberg et al. (141) and Cherbut et al. (121) found, respectively, a decreased and an increased mouth-to-cecum transit time in subjects fed with sugar beet fiber. Lipid Metabolism Sugar beet fiber, because of its significant content in water-soluble fiber, has been investigated for its effects on lipid metabolism. Studies were carried out in humans either healthy (133, 134, 142) or hypercholesterolemic (143) or with NIDMM (135, 136, 144) and in animals, pigs (145, 146) or rats (123, 147–153). Despite the fact that the dietary pattern (daily intake of dietary fiber, high-fat, low-carbohydrate diet and vice versa) and the duration of the experiments (from two to eight weeks) differed between the studies, most concluded that sugar beet fiber is hypocholesterolemic (Tables 16.8 and 16.9). In humans, it tends to reduce serum total cholesterol, and apo B levels without altering or even slightly increasing the high-density lipoprotein (HDL) cholesterol. Only some studies reported a decrease in serum triglycerides (136, 144, 147, 149). The mechanisms sustaining such effects are still not clear (154). Dietary fiber may act as hypocholesterolemic resin, which sequesters bile acids and cholesterol, with consequent interruption of the enterohepatic bile acid cycle in the small intestine (intestinal reabsorption of bile salts in humans is 96% to 98% efficient) and loss of cholesterol from increased fecal bile acid excretion. This mechanism was clearly demonstrated for viscous fiber such as guar gum and oat gum. In case of sugar beet fiber, most of the studies did not find a significant increase in fecal (124, 142, 149) and ileal (155) excretion of bile acids. These results are in agreement with those from Morgan et al. (156), who did not observe changes in concentrations of circulating postprandial bile acids in humans given an acute test meal supplemented with sugar beet fiber (10 g Betafiber per meal), contrary to guar gum or cholestyramine. In vitro data are more controversial. Morgan et al. (156) showed that the insoluble fraction of sugar beet fiber bound only small quantity of glycocholate and that no bile acids were associated with the soluble fraction. Dongowsky (10) found that cell wall material prepared from sugar beet pulp can be effective in binding bile acids (around 15 µmole/g of alcohol-insoluble material at pH 5). In a study with ileostomists (155) a decrease of 26% of ileal bile acid excretion was noted while cholesterol excretion increased by 52% with the sugar beet fiber diet. The excreted amount of cholesterol corresponded to half of the mean daily intake of cholesterol in this experiment. This pattern is
379
Sugar Beet Fiber Table 16.8 Effect of Sugar Beet Fiber on Lipid Metabolism (Human Studies) Intake (g/day/subject) 30
Subjects
Duration
Hypercholesterolemic women
2-4 weeks
8
NIDDM
8 weeks
40
NIDDM
8 weeks
18
NIDDM
6 weeks
30
Healthy volunteers
3 weeks
20
Healthy volunteers
16 days
Healthy middle-aged volunteers
3 weeks
1
Results
Ref
Significant reduction of LDL cholesterol with no change in HDL. Lower fasting blood Glc; reduction of LDL cholesterol with no change in HDL; lower fasting levels of triglycerides; improvements in Glc response to standardized breakfast. Decrease of 8% in total cholesterol when compared with the habitual diet, but no decrease compared with the low-fiber diet. Decrease of 6.2, 10.6, and 6.0% in, respectively, total cholesterol, triglycerides, and Apo B levels. Decrease of 12 and 15% in total and LDL cholesterol; small changes in HDL; significant decrease in serum triglycerides. Decrease of 4.6% in total cholesterol; decrease more marked with subject with a high habitual fat intake. Decrease of 8 and 9.6% in total and LDL cholesterol in subjects in whom fasting plasma cholesterol was above normal; no difference in HDL cholesterol.
143
135
136
144
142
133
134
380
Fiber Ingredients: Food Applications and Health Benefits
Table 16.9 Effect of Sugar Beet Fiber on Lipid Metabolism (Animal Studies) Level of Incorporation (g/kg diet)
Animals
Duration
100 g/kg semi- synthetic diet 300 g/kg fructose base diet
Rats
28 days
Rats
3 weeks
100 g/kg semi-synthetic diet
Rats
28 days
150 g/kg cholesterol free diet
Rats
14 days
100 g/kg 25% casein diet 120 g/kg semi-synthetic diet
Rats
28 days
Weaning piglets
4 weeks
100 g/kg semisynthetic diet ±0.3% cholesterol
Rats
40 days
100-220 g/kg diet
Growing pigs
Fattening period
Results
Ref.
Significant reduction of serum cholesterol, but less than that of guar gum. Decrease in plasma triglyceride and cholesterol concentration in the postprandial as well as the post-absorptive period. Depress of the liver triglyceride level in concert with decreased liver lipogenesis; no change in liver cholesterol; animal less fat. Lower circulating cholesterol, hepatic cholesterol, and circulating triacylglycerol; no change in total hepatic lipid concentrations and hepatic adipose tissue lipogenesis; reduced expression of hepatic lipoprotein A-1gene. Lower plasma total cholesterol; lower HDL cholesterol. No change in serum cholesterol and HDL cholesterol concentrations; lower fasting triacylglycerol due to reduction in VLDL synthesis. Lower plasma total cholesterol, LDL and triglycerides; decrease in HDL phospholipids and total phospholipids in cholesterol group. Diet free of cholesterol, no effect on measured parameters. Gradual increase in fiber content caused a linear decrease in total cholesterol and cholesterol fractions in blood serums; decrease in adipose tissue cholesterol.
123
147
149
150
148 145
153
146
different from the pattern generally reported for water-soluble fiber such as oat, guar gums, or pectins. The cholesterol-lowering effect of sugar beet fiber may result from its interference with the lipid absorption through alteration of the digestive processes. The reduced absorption of cholesterol results in a reduced supply to the liver, which, as a second effect, could decrease excretion of bile acids, as they are synthesized from cholesterol in the liver (155).
Sugar Beet Fiber
381
The influence of sugar beet fiber on lipid absorption may account at least for the acute postprandial effect of dietary fiber on lipemia, but the mechanisms involved have not been explored. Moreover, the extent to which the repetition of the single meal effect can lead to a new metabolic steady state in the long run remains to be further investigated. In rats fed with sugar beet fiber, hypocholesterolemia was accompanied by a reduction in hepatic cholesterol and in circulating triacylglycerol and bile acids, with no increase in bile acid fecal excretion (149). The authors pointed to another possible mechanism involving disruption of the bile acid circulation, possibly via changes in the rate of absorption patterns of triacylglycerol and its subsequent handling by circulating lipoproteins. Other mechanisms of action of dietary fiber have been suggested. Modification in hormonal status, especially insulin, could influence lipoprotein lipase activity, cholesterol, and bile acid synthesis and very low-density lipoprotein (VLDL) secretion. Only few groups (133–136) have investigated the effects of sugar beet fiber on both gastrointestinal hormones and cholesterol. Most of the authors reported no significant changes in the fasting levels of insulin. It has been suggested that the hypocholesterolemic effect of dietary fiber might also be mediated through the fermentation products, which can modify the activity of regulatory enzymes involved in hepatic cholesterol synthesis. A study in rats (148) has demonstrated that an intact cecum and colon is necessary for the fiber to be effective. One of the SCFA, propionate, has been shown in pigs and rats to significantly lower plasma and liver cholesterol concentrations and to inhibit cholesterol synthesis in isolated rat hepatocytes. However, no such effect has been reported in humans, and the role of propionate in reducing low-density lipoprotein (LDL) cholesterol levels is controversial. Hara et al. (151) showed that plasma cholesterol level decreased following ingestion of SCFA mixture simulating cecal fermentation products of sugar beet fiber. They further investigated mechanisms involved in the cholesterol-lowering effects of SCFA by feeding rats either with SCFA or sugar beet diet (152). They concluded that SCFA can decrease the hepatic cholesterol synthesis rate, which probably contributes to the lowering of plasma cholesterol level, as observed in rats fed with sugar beet fiber. It seems therefore likely that the cholesterol-lowering effect of sugar beet fiber is not dependent on increased fecal bile acid and is affected by a number of factors rather than a single mechanism. Colorectal cancer The effect of sugar beet fiber on experimentally induced colorectal cancer was mainly studied in rats (157–162). Results have been equivocal. In three studies, beet fiber reduced the incidence of precancerous lesions, aberrant crypt foci (159, 161, 162). In contrast, Thorup et al. (157, 158) reported no protective effect of sugar beet fiber at any stage of the colorectal carcinogenesis process.
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Although the contribution of dietary fiber to cancer protection is not very clear, several mechanisms by which they can be protective have been suggested. Sugar beet fiber may reduce the risk for colon carcinogenesis through enhancement of defecation and dilution of carcinogens. They can exert a protective role through decreasing the concentration of fecal bile acid. Through acidification of colonic content via fermentation, sugar beet fiber can prevent the conversion of primary bile acids to secondary bile acids, lithocholic acid and deoxycholic acid, which are considered promoters of colon cancer. Gallaher et al. (124) showed that sugar beet fiber slightly increased the total bile acid daily excretion but the fecal bile acid concentration was much lower than with the fiber-free basal diet. This concentration was even lower than with oat or rye bran diets. When compared to other sources of fiber, sugar beet fiber produced the lowest concentration of lithocholic acid. Some fibers can prevent oxidative damage to important molecules such as DNA, membrane lipids, and proteins. The mechanisms may include quenching free radical, chelating transition metal, or stimulating antioxidative enzyme systems. Antioxidant properties of sugar beet fiber were investigated in pigs (lipid peroxidase) (153) and in rats (liver antioxidant enzymes and serum enzymes) (163). Both studies concluded that sugar beet fiber has no protective role against oxidation. Sugar beet fiber significantly increased the concentration of many organic acids, especially acetate and propionate as well as butyrate. Ishizuka and Kasai (159) suggested that butyrate produced by sugar beet fiber fermentation may account for the decrease of aberrant crypt foci in 1,2 dimethylhydrazine induced aberrant crypt foci rats. Butyrate has diverse and apparent paradoxical effect on cellular proliferation, apoptosis, and differentiation. It is the primary energy source for colonic epithelium, and in an environment deficient in alternative substrate, it will paradoxically promote cell proliferation and growth and inhibit cell death. There is also some evidence that, delivered in adequate amount in the appropriate site, butyrate will protect against early colorectal carcinogenesis process (164). The mucosal epithelium has a characteristic immune system and intraepithelial lymphocytes play a role in the initial immune action against exogenous antigens. The immune response to a tumor is thought to be an early event leading to its destruction before it becomes clinically apparent (165). Ingestion of sugar beet fiber in luminal content was shown to promote an accumulation of CD8+ intraepithelial lymphocytes that participate in the elimination of abnormal epithelial cells after initiation (162). Thus, the protective effect of sugar beet fiber on colorectal carcinogenesis may be related to its capacity to stimulate the immune surveillance in the colorectal mucosa. SCFA are candidates as the mediators of this property (166). Tolerance to Sugar Beet Fiber In human studies, the daily intake varied greatly, from 7 to 40 g per subject. Generally, the fiber intake was gradually increased, in particular when large
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doses were concerned. The form under which fiber was ingested also differed: it can be included in foods (prepared dishes, bread, biscuits, chocolate bars), pressed in tablets, or mixed as a powder in water. Generally tolerance was good. Only afew studies reported cases of discomfort, abdominal cramping, and bloating or trouble with flatulence or borborygmi. This generally occurred with the largest doses. One study (144) mentioned that subjects (five of seven) found the bread and biscuits supplemented with sugar beet fiber less palatable than normal products, which led to a reduction in compliance during the last two of six weeks of sugar beet fiber supplementation. Three studies (133, 143, 144) reported an increase in energy and mean daily fat intakes during the period of sugar beet fiber supplementation. In these studies, fiber was incorporated into bread and it was suspected that the increase arose from an increased use of high-fat spread. However, no changes in subject body weight were noticed. In a subacute feeding study of male rats, sugar beet fiber at levels up to 10% was well tolerated by the animal (167). There were no reductions in food consumption and no reductions in body weight.
Safety/Toxicity Potential toxic effects of sugar beet fiber supplementation have not been extensively investigated (124, 167). Dongowski et al. (167) showed in rats that the enrichment of the diet with a sugar beet fiber preparation up to a level of 10% for four weeks did not substantially influence urinary, hematological, and serum parameters indicative of a toxic effect.
Conclusion On a wet weight basis (~ 90% humidity), 120 million tons of beet pulp are produced in the world each year and many laboratories are involved in finding new end uses to beet fiber. Beet fiber has thereby been extensively studied and has been used as a standard fiber in many functional and nutritional studies. Beet fiber has a high natural concentration of dietary fibers (~ 70%) with a particularly high soluble fiber content (~ one-third) due to its high pectin content. It exhibits a high water-holding capacity, which provides a broad application area.
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124. Gallaher, D.D., Locket, P.L, and Gallaher, C.M., Bile acid metabolism in rats fed two levels of corn oil and brans of oat, rye and barley and sugar beet fiber, J. Nutr., 122, 473, 1992. 125. Cherbut, C., Effects of short chain fatty acids on gastrointestinal motility, in Physiological and Clinical Aspects of Short Chain Fatty Acids, Cummings, J.H., Rombeau, J.L., and Sakata, T., Eds., Cambridge University Press, Cambridge, 1995, 191. 126. Cherbut, C., Fibres alimentaires: que devient l’hypotèse de Burkitt ? Etat des connaissances et questions non résolues, Cah. Nutr. Diét., 33, 95, 1998. 127. Tomlin, J. and Read, N.W., Laxative properties of plastic particles, Br. Med. J., 297, 1175, 1988. 128. Cherbut, C. et al., Short chain fatty acids modify colonic motility through nerves and polypeptide YY release in the rat, Am. J. Physiol., 275, G1415, 1998. 129. Sandström, B. et al., The effect of vegetables and beet fibre on the absorption of zinc in humans from composite meals, Br. J. Nutr., 58, 49, 1987. 130. Cossack, Z.T., Rojhani, A., and Musaiger, A.O., The effect of sugar-beet fibre supplementation for five weeks on zinc, iron, and copper status in human subjects, Eur. J. Clin. Nutr., 46, 221, 1992. 131. Coudray, C. et al., Effect of soluble or partly soluble dietary fibre supplementation on absorption and balance of calcium, magnesium, iron and zinc in healthy young men, Eur. J. Clin. Nutr., 51, 375, 1997. 132. Fairweather-Taits, S. and Wright, A.J.A., The effects of sugar-beet fibre and wheat bran on iron and zinc absorption in rats, Br. J. Nutr., 64, 547, 1990. 133. Tredger, J.A. et al., The effect of guar gum, sugar-beet fibre and wheat bran supplementation on serum lipoprotein levels in normocholesterolaemic volunteers, J. Hum. Nutr. Diet, 4, 375, 1991. 134. Frape, J. and Jones, A.M., Chronic and postprandial responses of plasma insulin, Glc and lipids in volunteers given dietary fibre supplements, Br. J. Nutr., 73, 733, 1995. 135. Hagander, B. et al., Dietary fiber decreases fasting blood Glc levels and plasma LDL concentration in non insulin-dependent diabetes mellitus patients, Am. J. Clin. Nutr., 47, 852, 1988. 136. Hagander, B. et al., Dietary fibre enrichment, blood pressure, lipoprotein profile and gut hormones in NIDDM patients, Eur. J. Clin. Nutr., 43, 35, 1989. 137. Tredger, J., Sheard, C., and Marks, V., Blood Glc and insulin levels in normal subjects following a meal with and without added sugar beet pulp, Diabetes Metabol., 7, 169, 1981. 138. Morgan, L.M. et al., The effect of soluble- and insoluble-fibre supplementation on postprandial Glc tolerance, insulin and gastric inhibitory polypeptide secretion in healthy subjects, Br. J. Nutr., 64, 103, 1990. 139. Leclère, C. et al., Influence of particle size and sources of non starch polysaccharides on postprandial glycaemia, insulinemia and triacylglycerolaemia in pigs and starch digestion in vitro, Br. J. Nutr., 70, 179, 1993. 140. Thorsdottir, I, Andersson, H., and Einarsson, S., Sugar beet fiber in formula diet reduces postprandial blood Glc serum, serum insulin and serum hydroxyproline, Eur. J. Clin. Nutr., 52, 155, 1998. 141. Hamberg, O., Rumessen, J.J., and Gudmand-Hoyer, E., Inhibition of starch absorption by dietary fibre. A comparative study of wheat bran, sugar-beet fibre, and pea fibre, Scand. J. Gastroenterol., 24, 103, 1989.
Sugar Beet Fiber
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142. Lampe, J.W. et al., Serum lipid and fecal bile acid changes with cereal, vegetable, and sugar-beet fiber feeding, Am. J. Clin. Nutr., 53, 1235, 1991. 143. Israelsson, B., Järnblad, G., and Persson, K., Serum cholesterol reduced with FibrexR, a sugar-beet fiber preparation, in Dietetics in the 90s. Role of the Dietetian/Nutritionists, Moyal, M.F., Ed., John Libbey Eurotext Ltd., 1990, 167. 144. Travis, J.S. et al., Effects of sugar beet fibre on blood Glc, serum lipids and apolipoproteins in non insulin diabetics mellitus, in Dietary Fibre — Chemical and Biological Aspects, Southgate, D.A.T., Ed., London, Royal Society of Chemistry, Special Publication n° 83, 1990, 366. 145. Frémont, L., Gozzelino, M.-T., and Bosseau, A.F., Effects of sugar beet fiber feeding on serum lipids and binding of low density lipoproteins to liver membranes in growing pigs, Am. J. Clin. Nutr., 57, 524, 1993. 146. Kreuzer M. et al., Effects of different fibre sources and fat addition on cholesterol and cholesterol-related lipids in blood serum, bile and body tissues of growing pigs, J. Anim. Physiol. Anim. Nutr., 86, 57, 2002. 147. Mazur, A. et al., Effects of dietary fermentable fiber on fatty acid synthesis and triglyceride secretion in rats fed fructose-based diet: studies with sugar beet fibre, Proc. Soc. Exp. Biol. Med., 199, 345, 1992. 148. Nishimura, N., Nishikawa, H., and Kiriyama, S., Ileorectostomy or cecectomy but not colectomy abolishes the plasma cholesterol-lowering effect of dietary beet fiber in rats, J. Nutr., 123, 12060, 1993. 149. Overton, P.D. et al., The effects of dietary sugar-beet fibre and guar gum on lipid metabolism in Wistar rats, Br. J. Nutr., 72, 385, 1994. 150. Sonoyama, K. et al., Apolipoprotein mRNA in liver and intestine of rats is affected by dietary beet fiber or cholestyramine, J. Nutr., 125, 13, 1995. 151. Hara, H. et al., Fermentation products of sugar-beet fiber by cecal bacteria lower plasma cholesterol concentration in rats, J. Nutr., 128, 688, 1998. 152. Hara, H. et al., Short chain fatty acids suppress cholesterol in rat liver and intestine. J. Nutr., 120, 942, 1999. 153. Leontowicz, M. et al., Sugar beet pulp and apple pomace dietary fibers improve lipid metabolism in rats fed cholesterol, Food Chem., 72, 73, 2001. 154. Lairon, D., Dietary fibres: effect on lipid metabolism and mechanisms of action, Eur. J. Clin. Nutr., 50, 125, 1996. 155. Langkilde, A.-M., Andersson, H., and Bosaeus, I., Sugar-beet fibre increases cholesterol and reduces bile acid excretion from the small bowel, Br. J. Nutr., 70, 757, 1993. 156. Morgan, L.M. et al., The effect of non starch polysaccharides supplementation on circulating bile acids, hormone and metabolic levels following a fat meal in human subjects, Br. J. Nutr., 70, 491, 1993. 157. Thorup, I, Meyer, O., and Kristiansen, E., Effect of a dietary fiber (beet fiber) on dimethylhydrazine-induced colon cancer in Wistar rats, Nutr. Cancer, 17, 251, 1992. 158. Thorup, I., Meyer, O., and Kristiansen, E., Influence of a dietary fiber on development of dimethylhydrazine-induced aberrant crypt foci and colon tumor incidence in Wistar rats, Nutr. Cancer, 21, 177, 1994. 159. Ishizuka, S. and Kasai, T., Suppression of the number of aberrant crypt foci of rat colorectum by ingestion of sugar beet fiber regardless of administration of anti-asialo GM1, Cancer Lett, 121, 39, 1997. 160. Ishizuka, S. et al., Ingestion of sugar beet fiber enhances irradiation-induced aberrant crypt foci in the rat colon under an apoptosis-suppressed condition, Carcinogenesis, 20, 1005, 1999.
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Fiber Ingredients: Food Applications and Health Benefits
161. Bobek, P., Galbavy, S., and Mariassyova, M., The effect of red beet (Beta vulgaris var. rubra) fiber on alimentary hypercholesterolemia and chemically induced colon carcinogenesis in rats, Nahrung, 44, 184, 2000. 162. Nagai, T. et al., Dietary sugar beet fiber prevents the increase in aberrant crypt foci induced by irradiation in the colorectum of rats treated with an immunosuppressant. J. Nutr., 130, 1682, 2000. 163. He, G. and Aoyama, Y., Effects of adding some dietary fibers to a cysteine diet on the activities of liver antioxidant enzymes and serum enzymes in rats, Biosci. Biotechnol. Biochem., 67, 617, 2003. 164. Sengupta, S., Muir, J.G., and Gibson, P.E., Does butyrate protect from colorectal cancer?, J. Gastroenterol. Hepathol., 21, 209, 2006. 165. Beverley, P., Tumour immunology, in Immunology, Roitt, I.V., Brostoff, J., and Male, D.K., Eds., Mosby-Year Book Europe, London, 1993, 17. 166. Ishizuka, S. and Tanaka, S., Modulation of CD8+ intraepithelial lymphocyte distribution by dietary fiber in the rat large intestine, Exp. Biol. Med., 227, 1017, 2002. 167. Dongowski, G., Plass, R., and Bleyl, D.W.R., Biochemical parameters of rats fed dietary fibre preparation from sugar-beet, Z. Lebensm. Unters. Forsch., A 206, 393, 1998.
17 Psyllium Seyed Ali Ziai
Contents Characteristics...................................................................................................... 393 P. psyllium L.................................................................................................. 394 P. ovata Forsk................................................................................................ 394 Chemical Constituents............................................................................... 395 Functionality and Food Application................................................................. 395 Physiological Benefits.......................................................................................... 397 Laxative Effect...................................................................................................... 397 Diverticular Disease....................................................................... 398 Irritable Bowel Syndrome.............................................................. 399 Anti-Inflammatory Effects........................................................................405 Anti-carcinogenic Effects...........................................................................405 Reducing Risk of Heart Disease............................................................... 406 Other Effects of Psyllium........................................................................... 410 In Diarrhea....................................................................................... 410 In Gallstones.................................................................................... 410 In Hemorrhoids, after Anorectal Surgery, and during Pregnancy......................................................................... 410 Safety and Toxicity............................................................................................... 410 Contraindications....................................................................................... 411 Pregnancy and Lactation........................................................................... 412 Drug Interaction.......................................................................................... 412 References............................................................................................................. 412
Characteristics Genus Plantago from the plantain family (Plantaginaceae) has about 250 species, and psyllium in pharmacopeias is a common name of the following plants: Plantago psyllium L. (Syn. P. afra L.); P. ovata Forsk. (Syn. P. ispaghula Roxb.); and P. indica L. (Syn. P. arenaria Waldst.). Plantago is a Latin word 393
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Fiber Ingredients: Food Applications and Health Benefits
which means the sole of the foot, referring to the shape of the leaf; psyllium comes from Greek and means flea, referring to the color, size, and shape of the seed (flea seed); arenaria is derived from the Latin word arena and means sand, referring to the sandy habitat of the plant. Ovata refers to the ovate shape of the leaf.1 Although true psyllium comes from the plant P. psyllium, the husk and seed of P. ovata are commonly referred to as psyllium and are used in nutraceuticals and industries. The mucilage content of P. ovata is five times more than P. exicgua Murray, and P. psyllium has more mucilage content.2 Only P. psyllium and P. ovata are cultivated. The other species have a wild distribution.2 P. psyllium L. Plantago psyllium is native to the eastern Mediterranean region where it is also cultivated (especially in France). It is an annual that is hairy and erect, with an erect-branching stem (20 to 40 cm in height); it possesses whorls of flattened linear to linear-lancolate leaves from the upper axils with flowering stalks as long as the leaves arise. It needs humid Mediterranean-like climate to grow, so in the hotter regions (e.g., India and Australia) the cultivation time is in the winter and spring. Flowers are very small with color variations of white and green. The flowering time is from March to June. Harvest time occurs when seeds, growing in bunches, are easily released by finger compression. Seed yield is 1000 kg per hectare. Seed coloration ranges from shiny brown to red or dark brown, length is from 1.3 to 2.7 mm (rarely up to 3 mm) and width is 0.6 to 1.1 mm. It is often called dark or black psyllium. Other common names are brown psyllium, French psyllium, Spanish psyllium, Semen pulicariae (Lat). Fleawort seed (Eng.), Flohsamen, Heusamen (Ger.), and Semences (granies) depules (Fr.).3–5 P. ovata Forsk Plantago ovata is found worldwide, but it is native to India, Pakistan, and Iran. Today, psyllium is widely cultivated in its countries of origin because of vast demand for its commerce and economic benefits—mainly for export— and has been adapted to Western Europe and subtropical regions. It is an annual plant covered by fine hair. The stem is short (5 to 8 cm) and often curved. The leaves are linear, slender, dentate, and bayonet shaped. Flowers are white and bloom from February to August. Seeds are oval, boat-shaped, 2 to 2.3 mm long, 1 to 1.5 mm wide, and 1 mm thick. They vary considerably in color, from pale pink to grayish brown and even reddish yellow, and are called blond psyllium. Other common names are Spogel, Ispaghula (a Persian name which means “like the ears of a horse”), Indian plantago, Isfugul, Pale psyllium, Indian psyllium (Eng.), Indische, Flohsamen, Indisches psyllium (Ger.), Ispagul (Fr.), and Isfarzeh (Per). When the seeds are placed in water, they swell rapidly and become surrounded by a colorless, transparent layer of mucilage. The taste is bland with a mucilaginous texture.3–6
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Chemical Constituents The husk of the psyllium seed is a mucilaginous hydrocolloid and forms a gel in water. It contains 10% to 30% hydrocolloid.1 This soluble fiber is composed of a soluble polysaccharide fraction which primarily contains weak acidic arabinoxylans (85%) and a neutral polysaccharide fraction. The swelling factor is >9 for the entire seed and >40 for the seed husk of Plantago ovata L.7 The polymer backbone is a xylan with 1→3 and 1→4 linkages with no apparent regularity in their distribution. The monosaccharides in this main chain are l-arabinose, d-xylose, and _-d-galacturonyl- (1→2)- l-rhamnose which are substituted on C-2 or C-3 of d-xylan.3 Solutions of the purified gum are thixotropic; the viscosity decreases as shear rate increases, a property that is of potential value.1 In an attempt to find the active fraction of psyllium seed husk, Marlett and Fischer isolated fractions of psyllium seed husk. Fraction A was an alkaliinsoluble material and non-fermentable. Fraction C, which represented 15% psyllium seed husk, was viscous and fast fermented. Fraction B, which represents about 55% of psyllium seed husk, is poor fermented and increased the stool moisture, and fecal bile acid excretion. Neither fractions A nor C altered moisture and bile acid output.8 The seeds contain fixed oil, protein, and very small amounts of iridoids such as aucubin. The major bioactive components in the seeds of psyllium are phenolic compounds (such as benzoic acid, caffeic acid, chlorogenic acid, cinnamic acid, and salicylic acid), glycosides (acetoside and isoacetoside),9 alkaloids (plantagonin, boschniakia), and amino acids (alanine, asparagine, histidine, lysine).10
Functionality and Food Application Plantago ovata is the official species in the national pharmacopeias of France, Germany, Great Britain, and the United States. Psyllium monographs also appear in the Ayurvedic Pharmacopoeia, British Herbal Pharmacopoeia, British Herbal Compendium, ESCOP Monographs, Commission E Monographs, and the German Standard License Monographs. The World Health Organization (WHO) has published a monograph on psyllium seed, covering P. afra, P. indica, P. ovata, and P. asiatica. In traditional Chinese medicine (TCM) seeds were used to treat uremia, cough, hypertension, chilling, edema (by forcing diuresis), improvement of renal function, dysuria, and constipation, as well as in eye disorders such as xerophthalmia, cataracts, eye redness, inflammation, and photosensitivity. It is also used in lung disorders. The whole plant was used for heart disease (CHF) and intoxication. Seeds were used topically to heal wounds and abscess.6,11 In East India, the seeds were used to treat dysentery, renal disease, gonorrhea, fever, and GI dysfunction as well as flu,
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Fiber Ingredients: Food Applications and Health Benefits
cough, and other respiratory diseases, especially in pediatrics. Mill-ground seeds in water were used topically in the treatment of rheumatism, gout, and skin allergies.11 In Persia seeds were used to treat dysentery and billary tract disorders in GI complaints. By mixing the seeds with water, a paste is formed that is applied directly to inflamed skin. Infusion of seeds was used to treat renal ducts mucosa inflammation and stimulation.5 Psyllium is mucilage with valuable properties such as stabilizers, suspenders, emulsifiers, and thickeners and has wide application in pharmaceuticals and other industries. Historically, the literature cites Persian scientist Rhazes (850–932 AD) as being one of the earliest tablet coaters, having used the mucilage of psyllium seeds to coat pills that had an offending taste.12 Psyllium is an excellent source of natural soluble fiber and contains experimentally eight times more soluble fiber than oat bran on a per weight basis.13 In pharmacy applications, psyllium is used as a gelling agent for preparation of emulsions and suspensions and emulsifies insoluble powders, oils, and resins. P. ovata mucilage has better suspension effects than tragacanth and methyl cellulose.4 The viscosity of psyllium mucilage dispersions is relatively unaffected between temperatures of 68oF–122oF, by pH from 2 to 10, and by salt (sodium chloride) concentrations up to 0.15 M.14 It is used as a binder in granules and tablets. It is used alone or in combination in laxatives.2,15 The husk is used as an emollient.4 It is also used in cosmetics and as an antitussive, anti-inflammatory, and an immunostimulator.15 Psyllium has also been used traditionally in food products. It is used in a type of Indian beverage. It is also used in bread, honey, marmalade, soup, or mixed with wheat flour as a thickener in the making of chocolates and jellies.6 Recent uses of psyllium are in the production of ice cream as a thickener (Merecol IC), sherbet (Merecol SH), and yogurt (Merecol Y).6 In the United States ready-to-eat (RTE) cereals have included psyllium as a component since 1989, when the FDA ruled that companies can claim that eating foods containing psyllium can reduce heart disease risk.16 Bran Buds (Kellogg’s) is one of these products. It has been reported that between 1996–2001 a total of 33 patents have been granted on various uses of psyllium husk.17 Based on use, 18 patents have been granted for use of psyllium husk in pharmaceutical/drug composition, 14 patents for use in foodstuffs, and two patents on RTE cereals.17 Seven patents were assigned to individuals and the rest to companies/corporations. The Kellogg Company has received eight patents for use of psyllium husk in preparation of pasta, dough with low cholesterol, RTE cereals, baked snacks, and pharmaceutical composition to reduce cholesterol and improve functionality. Procter & Gamble is second with patents for the use of psyllium in laxatives, food composition with improved palatability, drink composition, and treatment composition for hypercholesterolemia.17 Psyllium husk in pharmaceuticals is formulated as effervescent granules, granules, oral powder, hydrophilic mucilloid for oral suspension, and capsules.18
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Physiological Benefits Psyllium husk or seeds, defined as dietary fiber and functional fiber, are complex and non-digestible carbohydrates that can not be decomposed by human digestive enzymes in the upper alimentary tract. The physiological properties and health benefits of dietary fibers, including psyllium, are the result of the following:
1. They are substrates for fermentation. They promote microbial growth in the colon, and these microorganisms ferment to produce free fatty acids, H2, CO2, and energy. Also they change nitrogen, bile acid, and xenobiotic metabolism. By these mechanisms they are useful in treatment of constipation, diverticular disease, and colorectal cancer.
2. They have physical effects in small bowels. Because dietary fibers have gel-forming properties, they affect insulin secretion and gut hormones. Psyllium converts the small intestine into a reservoir from which nutrients are absorbed and slowly enter the circulation system. The important part that the intestine plays in this phenomenon is terminal ileum due to the increased viscosity as water is progressively removed from the luminal contents. By decreasing postprandial serum lipids and glucose, the postprandial insulin response is blunted, which affects lipids and lipoprotein synthesis.19–21 By binding to bile acids and inhibiting the enterohepatic cycle,22,23 psyllium reduces serum cholesterol.24 Psyllium and other viscous fibers, by blunting the glucose surge as well as insulin response peak, have useful health effects. Cohort studies showed that insulin surge is related to cardiovascular disease.25–28 So psyllium is useful in diabetes by controlling glycemic response and CHD by prolonging lipid absorption.
3. They have satiety and gastric emptying effects. Dietary fibers in food mixtures reinforce chewing of food and delay gastric emptying, so they will be useful in short-term appetite reduction.29,30 Enzymatic manipulation of psyllium by partially hydrolyzing it lowers its viscosity and somehow its efficacy.31–33
Laxative Effect The American College of Gastroenterology Chronic Constipation Task Force defines constipation as the following: Constipation is a symptom-based disorder with unsatisfactory defecation characterized by infrequent stools, difficult stool passage, or both present for at least three months.34
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Fiber Ingredients: Food Applications and Health Benefits
Psyllium seeds or husk contain both soluble (70% to 90%) and insoluble fiber (10%). Soluble fiber dissolves in water, forming a gel, and is fermented in the colon to a greater extent than insoluble fiber.35 Its end products are shortchain fatty acids (acetate, propionate, and butyrate) and gases (hydrogen, methane, CO2) as well as energy for growth and maintenance of colonic flora. Both of these products shorten the gut transit time and alleviate constipation. Psyllium has proved to be highly effective in the treatment of constipation and the maintenance of bowel regularity. Its stool-bulking activity principally results from the water-holding property of the resident polysaccharide, but it has a range of properties such as high non-starch polysaccharide (NSP) content, high viscosity on hydration, and, uniquely, the ability to retain some structure in the presence of significant microbial fermentation. The average increase in stool output expressed as grams of stool (wet weight) per gram of fiber fed has been studied in many experimental and clinical trials. Psyllium resulted in 4.0 g wet stool weight per gram fiber ingested, which ranked 4 on bowel habit after raw bran, fruit and vegetables, and cooked bran.29 In a systematic reviews of studies conducted from 1966 to 2003, results from 13 studies on psyllium alone or in combination with lactulose were gathered (Table 17.1). In this review, bulk or hydrophilic laxatives (psyllium, methylcellulose, bran, celandine, plantin derivatives, and aloe vera) were recommended as grade B (i.e., moderate evidence in support of the use of a modality in the treatment of constipation) and supported the use of psyllium.36 Psyllium compared to placebos37–39 or other laxatives40–43 or psyllium in combination compared to other laxatives44–46 improved stool frequency and stool consistency (Table 17.1). In one study on both healthy and chronically constipated patients, psyllium had no effect on healthy subjects but significantly increased stool frequency in constipated patients. This indicates increased regulatory function and selective activity of psyllium on constipated patients.47 One study with few patients reported decrease in transit gut time,37 so psyllium may be effective in alleviating chronic constipation. However, in those people in whom fiber aggravates their sense of abdominal distension or in whom fiber leads to incontinence (mainly in elderly subjects), a reduction in their fiber intake should be recommended.48 The usual dose is about 3.5 g one to three times daily by mouth, although higher doses have been given. It should be taken immediately after mixing in at least 150 mL water or fruit juice. The full effect may not be achieved for up to three days. Diverticular Disease Dietary fiber and psyllium have a role in diverticular disease, and a highfiber diet prevents the development of symptomatic diverticular disease and its complications.50–52 Psyllium products in the colon (short-chain fatty acids and gas) in diverticular disease patients promote laxation and reduce intra-colonic pressure resulting in reduction of pain.35
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Fiber supplement in alleviating diverticular disease was first reported by Painter.53 In a randomized placebo-controlled clinical trial, investigators used 9 g/ day psyllium or 2.3 g/day placebo on 56 diverticular disease patients for 16 weeks to evaluate symptom relief.54 They found psyllium significantly reduced straining at stool, increased wet stool weight and stool frequency, and softened the stool. Petruziello et al.55 concluded that in uncomplicated diverticular disease the optimal treatment might be an initial course of antibiotics (rifaximine) to normalize the gut flora followed by a combination of a probiotic to prevent relapse and a prebiotic (psyllium) to maintain growth of protective bacteria. Irritable Bowel Syndrome Irritable bowel syndrome (IBS) is a group of functional bowel disorders with pain and abdominal discomfort on defecation or change in bowel habit.56,57 Symptoms are constipation, diarrhea, bloating, straining, urgency, feeling of incomplete evacuation, and mucus discharge. The prevalence of IBS-type symptoms varies from 2.1% to 22% in the general population worldwide, depending on IBS definition criteria and the study design.57–61 A recent study in the United States categorized prevalence of IBS to constipation-predominant IBS (IBS-C) at 1.79%, diarrhea-predominant IBS (IBS-D) at 3%, and IBS with alternating bowel habit (IBS-A) at 9.36%, totaling 14.1% in a large community.61 Guidelines recommend symptom treatment of IBS and dietary fiber for constipation.57, 62 Several systematic reviews were made on the role of fiber on IBS.63–69 Some of them conclude no benefit of fiber in relief of symptoms, and they are useful only on IBS-C patients.63–66 A recent systematic review of 17 randomized controlled trials from 1996 –200267 involving a total of 1363 irritable bowel syndrome patients examined results separately for nine trials using soluble fiber and eight using insoluble fiber. The authors concluded that fiber in general was marginally effective in relief of global IBS symptoms (relative risk, 1.3; 95% CI, 1.19 to 1.50). Soluble fiber in particular (eight studies on psyllium and one study on calcium polycarbophil) had better results (relative risk, 1.55; 95% CI, 1.35 to 1.78), while insoluble fiber worsened the clinical outcome, with no significant difference to placebo (relative risk, 0.89; 95% CI, 0.72 to 1.11). In a meta-analysis of therapies available for IBS (literature search 1966– 2004), results from bulking agents (seven psyllium, six other fibers such as bran, corn, and calcium carbophil) showed benefit of fiber treatment in the relief of global IBS symptoms (relative risk, 1.9; 95% CI, 1.5 to 2.4).68 They categorized bulking agents, including psyllium, as grade C of recommendation (i.e., inconsistent results from inadequately controlled clinical trials or poor quality cohort studies). Adverse events were not consistently reported in most of the trials cited above, and some reported worsened abdominal pain and bloating with them.70–72
Study Design
Open, randomized and controlled crossover
Multicenter double blind crossover
Open, randomized parallel group study
Randomized double blind, crossover
Intervention
Lactoluse 30 mL/ day or Agiolax (psyllium & senna)
Lactoluse 30-60 mL/ day Agiolax (psyllium & senna) 10–20 mL/day
Lactoluse 30 mL/ day or psyllium 7g/day
Lactoluse 15 mL/ day or Agiolax (psyllium & senna) 10 mL/day
77
112
85
30
No. of Patients
Two 2-wk treatment periods with 3–5 days laxative free period before and between treatments
1-wk run in followed two 5-wk treatment periods separated by 1 wk Two 2-wk periods Agiolax or lactoluse with matching placebo with 3–5 days before and between treatments 4 wk
Duration
Summary of Clinical Trials on Laxative Effects of Psyllium36.
Table 17.1
Outcome Results
Both treatments resulted in sig. (p < 0.0001) increase in SF, SC (p = 0.027) over baseline but not between the treatment groups No sig. difference in straining and global improvement Sig. increase in SF by Agiolax than lactoluse (0.8/day vs. 0.6/day, p < 0.001) Improvement in SC (p < 0.005) and EOD (p = 0.02) by agiolax
SF was greater with the Agiolax (0.8/day) than lactoluse (0.6/day, p < 0.001), scores for SC and EOD were sig. higher for the Agiolax than for lactoluse
The Agiolax produced 4.5 BM/week (in both periods) compared with 2.2 and 1.9 per week for lactoluse
Safety Analysis
No difference in adverse effects between the treatment groups
No serious adverse effects
No difference in adverse effects
No sig. adverse effect noted
46
40
45
44
Ref.
400 Fiber Ingredients: Food Applications and Health Benefits
Open, randomized single blind controlled
Multicenter randomized placebo controlled single blind parallel
Open, multicenter randomized controlled
Psyllium (P) and psyllium with senna (PS)
Psyllium 3.6 g tid or placebo
Psyllium (P) 3.5 g/ day or another laxative (lactoluse, bisacodyl, docusate, senna, and magnesium sulfate)
224(P) 170 (other)
201
40
4 wk
2 wk
1-wk placebo and 1-wk treatment
SF increased sig. from 2.3/wk to 7/ wk with psyllium and 4.5/wk with placebo Stool consistency, sig. decreased and loose or watery stool sig. increased in psyllium group Abdominal discomfort and straining sig. decreased in the psyllium group. Sig. improvement in constipation observed by both patients and investigators GPs assessed P superior to other treatments in improving basal function and in overall effectiveness with a higher percentage of normal, well-formed stools and fewer hard stools than other laxatives P was more palatable and acceptable to patients. Incidences of soiling, diarrhea and abdominal pain were lower in the P group
Both increased stool frequency (P 3.6 BM/wk vs. PS 6.8 BM/wk p < 0.001) Both increased wet and dry stool weights Only PS increased stool moisture Both improved SC and provided a high degree of subjective relief
No sig. adverse effects
P group 3/22 cramping and gas PS group 7/22 cramping, unfavorable diarrhea, bloating, gas and nausea
(continued)
49
39
41
Psyllium 401
Single blind randomized placebo controlled with crossover
Double blind randomized placebo controlled
Multicenter randomized double blind parallel
Psyllium 10g/day or placebo
Psyllium (P) 5.1 g bid and docusate (D) 100 mg bid
Study Design
Psyllium 24 g/day or placebo
Intervention
Table 17.1 (Continued)
170
22
10
No. of Patients Duration
1-wk washout followed by 1-wk baseline (placebo) followed by 2-wk treatment
8 wk with 4-wk run in on placebo and 4-wk washout
4 wk each arm
Outcome Results Sig. decrease in gut transit time (53.9 h in placebo to 30.0 h p < 0.05) Stool weight, SC not sig. improved by P A trend in stool frequency increase in P (from 0.8 to 1.3 BM/day) SF increased sig. after 8-wk psyllium (3.8 vs. 2.9 BM/wk, p < 0.05) Subjects reported improvement in SC (3.2 vs. 3.8, p < 0.05) by psyllium EOD improvement by psyllium (pain score: 2.0 vs. 2.6 p < 0.05) colon transit unchanged Compared to baseline P increased stool water content vs. D (2.33% vs. 0.01%, p = 0.007) Stool wet weight also increased (84.9 g/BM vs. D 71.4 g/BM, p=0.04) Total stool output was higher with P (P359.9 g/wk vs. D 271.9 g/wk, p = 0.05) O'Brien rank-type score combining objective measures of constipation was higher with P (P 475.1 vs. D 403.9 p = 0.002) SF was sig. greater for P (P 3.5BM/ wk vs. D 2.9 BM/wk, p = 0.02) in treatment week 2
42
38
No sig. adverse effects
Ref. 37
Safety Analysis No sig. adverse effects
402 Fiber Ingredients: Food Applications and Health Benefits
32
50 healthy 59 chronically constipated
Open label randomized controlled crossover
Two phase
1-wk run in taking placebo then 10day treatment period with one of the M or P
Two consecutive 3-wk treatment periods
Healthy subjects: 4 g M sig. increased SF, fecal water, and fecal solids. Chronically constipated: All doses of M & P sig. increased SF, water content, and fecal solids. No increase in stool weight by both
No sig. changes in SF (C 7.20 vs. P 7.22) No difference in EOD, SC More patients seemed to favor C No difference in the incidences of abdominal camps, flatulence, or abdominal pain between the treatment and placebo periods
Not mentioned
47
43
Note: bid: Twice daily, EOD: ease on defecation, SC: stool consistency, SF: stool frequency, sig.: significant/significantly, tid: three times daily, wk: week,
Psyllium (P) 2 teaspoons/day or calcium polycarbophil (C) 2 tabs/day 1,2,or 4 g methylcellulose (M) or 3.4 g psyllium (P)
Psyllium 403
UK US
India Ireland India UK
India India
1979 1981
1982 1983 1984 1987
1987 1990
20 g 30 g
NA 2 Sachets NA 1 Sachet (5 g)
1 Sachet (5 g) 6.4 g
Dose (per day)
Note: DB: Double blind trial, O: Open trial.
Country
Year
Trials of Psyllium on Irritable Bowel Syndrome
Table 17.2
O DB
DB DB DB DB
DB DB
Study Design
2 4
3 4 NA 12
12 8
Duration (weeks)
Improved: IBS symptoms No benefit: IBS symptoms, abdominal pain, bowel habit Improved: IBS symptoms No benefit: IBS symptoms Improved: IBS symptoms Improved: IBS symptoms, constipation, Not abdominal pain Improved: IBS symptoms, abdominal pain Improved: IBS symptoms, bowel habits, Not abdominal pain
Outcome
78 72
75 76 77 71
73 74 70
Ref.
404 Fiber Ingredients: Food Applications and Health Benefits
Psyllium
405
The effect of soluble fiber on IBS–related abdominal pain was poor (relative risk, 0.67; 95% CI, 0.47 to 0.95), but on the IBS-related constipation the effect was significant (relative risk, 1.60; 95% CI, 1.06 to 2.42).67 In conclusion, fibers can be used and recommended in painless IBS-C and as an adjutant.68 Anti-Inflammatory Effects In addition to laxation, psyllium produces short-chain fatty acids such as butyrate in the colon by the colonic flora, which are taken up by colonocytes and have anti-inflammatory and anti-neoplastic effects.79 Psyllium has been reported to improve symptoms and maintain remission of ulcerative colitis.80,81 Inflammatory bowel disease (IBD) in patients can be effectively treated with prebiotics (such as psyllium) alone.82 Psyllium husk was studied in a randomized placebo-controlled trial for four months on 29 patients with ulcerative colitis.81 Grading of abdominal pain, diarrhea, loose stools, urgency, bloating, incomplete evacuation, mucus, and constipation as symptoms of ulcerative colitis showed that psyllium was significantly superior to placebo (96% vs. 24%, p < 0.001). In another trial2 105 ulcerative colitis patients in remission were randomized between psyllium seeds (10 g bid), mesalamine (500 mg tid) as standard drug, or treated with both at the same doses. After 12 months, treatment failure was 40% in the psyllium group, 35% in the mesalamine group, and 30% in the combination group with no significant differences. The authors concluded that psyllium might be as effective as mesalamin. In a recent clinical trial83 psyllium 9.9 g/day as prebiotic combined with probiotic (synbiotic) was studied in 10 patients with Crohn’s disease for about 13 months. Results showed that Crohn’s disease activity index (CDAI) was reduced (225→136, p = 0.009). CDAI in eight patients was reduced by over 70 points. The International Organization for the study of Inflammatory Bowel Disease (IOIBD) score was reduced significantly after therapy (3.5→2.1, p = 0.03). Six patients achieved remission, one had partial response, and three were non-responders. There were no adverse effects. Diarrhea and abdominal pain were also reduced significantly in the synbiotic therapy (p = 0.01, p = 0.04, respectively). They concluded that high-dose synbiotic can be safely and effectively used for the treatment of active Crohn’s disease with frequent diarrhea.82 Anti-Carcinogenic Effects The estimated new cases of colorectal cancer in 2006 in the United States were about 148,000 (about 10% of all new cases of all cancer sites), and the estimated deaths were about 55,000 (about 10% of all deaths of all cancer sites).84 For obvious reasons, there is no human intervention study with the occurrence of colorectal cancer itself as an end point.79 Specific interventions have failed to affect particular events within carcinogenesis; for example, in the
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Fiber Ingredients: Food Applications and Health Benefits
European Cancer Prevention Trial,85 665 patients with a history of colorectal adenomas were randomly assigned to calcium (2 g/day), psyllium husk (3.5 g/day), or placebo. In total, 552 patients completed the three-year follow-up period. In the calcium group 15.9% had at least one adenoma development (p = 0.16), and the figures for the psyllium husk and control groups were 29.3% and 20.2%, respectively. This study tells us that a specific intervention is unlikely to reduce the risk of adenoma recurrence in a three-year interval after colonic polypectomy and does not address the question of primary prevention.79 In the Health Professional Study conducted on 16,448 men, the findings showed that soluble fiber, but not insoluble fiber, appeared to be inversely associated with distal colonic adenoma.86 Chronic constipation is an independent risk factor for colon cancer.87 In a metaanalysis of nine case-control studies,88 the combiner OR of these studies was 1.5 (95% CI, 1.3 to 1.7), and others89 found an association between colon cancer and constipation of 4.4 (95% CI, 2.1 to 8.9) independent of dietary consumption. The molecular mechanism of anti-inflammatory and anti-carcinogenicity of psyllium and other fibers is the production of butyrate and other shortchain fatty acids in the distal colon.80,90 Butyrate is the preferred oxidative substrate for colonocytes. Butyrate is a physiological modulator of the maturation of colonic epithelial cells; thus it could reduce colon cancer risk through the mitochondrial function, arrest cell growth, induce apoptosis of colonic epithelial cells, and regulate the expression of various oncogenes.87 This molecule is absorbed by the colonocytes and interferes with the nuclear factor kappa B (NFkB)-mediated signal transduction. NFkB liberated from its inhibitory subunit kB after tumor necrosis factor-α (TNFα) binds to its extracellular receptor. Unbound NFkB subunits are then translocated to the cell nucleus where they modulate the transcription of pro-inflammatory cytokines. NFkB also inhibits apoptosis and makes tumor cells immortal.79 Butyrate at concentrations between 1 and 5 mmol/L inhibited the growth of human colon cancer cell lines and caused the phenotype of tumor cells to change to non-neoplastic tissue.91 Butyrate inhibits histone deacetylase, thus affecting expression of selected genes that control the cell cycle machinery. Histone acetylation opens the DNA strand to transcribing enzymes. This phenomenon has a key role in proliferation, differentiation, and apoptosis.79 Apoptosis was increased by incubation of adenoma and carcinoma cells with butyrate.92 Reducing Risk of Heart Disease Cardiovascular disease is the major cause of mortality in most developed countries. Atherosclerosis of the vessels, especially the coronary vessels, causes malfunction of the heart and manifests itself as coronary heart disease (CHD). CHD may represent itself as angina pectoris or MI. The major risk factors are hypertension, hyperlipidemia, and smoking, as well as diabetes. Other conditions such as fat intake, lack of physical activity, stress, and
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genetic susceptibility are also involved. Therefore, CHD is a multifactorial disease and diet itself is one of the factors contributing to the risk of CHD. Fiber is only one of the many dietary components that affect risk.29 An association between CHD and dietary fiber was suggested in the 1950s.93,94 In 1961 Keys and colleagues95 reported cholesterol-lowering effects of fiber in humans. The ability of viscous soluble fibers to lower serum cholesterol has been recognized for more than a quarter of a century. One hour after a fat meal (30 to 60 g fat) postprandial lipemia (almost triacylglycerols) rose and remained high for 5 to 8 hours.96 It is now realized that high postprandial lipemia is a characteristic metabolic abnormality of a number of lifestylerelated conditions that are associated with both increased morbidity (such as hypertriglyceridemia, metabolic syndrome, obesity, and type 2 diabetes) and mortality, especially from cardiovascular disease.96–101 The most comprehensive report on dietary fiber and coronary heart disease, which included a pooled analysis of 11 major studies investigating 336,244 individuals (91,058 men and 245,186 women), 2,506,581 follow-up years, 5249 cardiac events, and 2011 deaths, noted that soluble fiber had stronger effects than insoluble fibers. The average fiber consumption was about 19 g/day in men and 17 g/day in women. The relative risk for 10 g/day soluble fiber was 0.72 for all events and 0.46 for death, and for insoluble fibers these figures were 0.9 for all events and 0.80 for deaths.102 Thus soluble fiber is associated with a 30% reduction in CHD risk per 10 g/day increment in consumption. It is known that about 50% of cholesterol is obtained from food and 50% is synthesized in the body. Reduction of lipid absorption and increasing cholesterol turnover may help to control and treat hyperlipidemia as well as CHD. Psyllium husk as a hydrogel acts by these two mentioned mechanisms. The intestinal lumen is the primary site of action of psyllium.103 Psyllium, by interruption of enterohepatic circulation of bile acids,104 alters hepatic cholesterol homeostasis. The body synthesizes bile acids from cholesterol in the liver.105 Decreased absorption of bile acids in the GI tract induces new bile acids synthesis in the liver and in turn decreases hepatic cholesterol pool. LDL, as the rich source of cholesterol in the bloodstream, is absorbed by the up-regulating LDL-cholesterol receptors on the liver cells surface.106,107 Soluble fibers also physically disrupt the intra-luminal formation of micelles, which may reduce cholesterol absorption and bile acid reabsorption.108,109 Hepatic cholesterol 7-α-hydroxylase (CYP7) (the rate limiting enzyme in the bile acid synthesis pathway), is up-regulated following dietary soluble fiber intake.106,110 HMGCOA reductase and CYP7 are up-regulated by psyllium.111 Psyllium intake caused cholesterol-ester transfer protein (CETP) activity to decrease, which may contribute to the hypocholesterolemic effect of psyllium.111 In hamsters, decreases in hepatic cholesterol have been related to lower rates of hepatic apo B secretion.112 Increased plasma propionate concentration in rats inhibits fatty acid synthesis and therefore decreases VLDL secretion resulting in lowering plasma LDL cholesterol.113 In one study in rats, investigators found that psyllium improved the serum lipid profile by decreasing transfatty acid absorption, especially hypercholesterolemic effect. Hydrogena-
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Fiber Ingredients: Food Applications and Health Benefits
tion of vegetable oils transforms them from a liquid to a semi-solid state (margarine) and converts some cis double-bound to transconfiguration. This transformation produces trans-fatty acids which, though unsaturated, are structurally similar to saturated fatty acids.114 Both human and animal studies showed the hypocholesterolemic properties of psyllium and other soluble fibers.104,106,115,116 The U.S. Food and Drug Administration (FDA), following the Nutrition, Labeling and Education Act, has ruled that labels on certain foods containing soluble fiber from psyllium seed husk, such as certain breakfast cereals, may claim that these foods, as part of a diet low in saturated fat and cholesterol, may reduce the risk of CHD.16 This claim was based on scientific evidence and FDA-evaluated placebo-controlled studies that tested an intake of 10.2 g of psyllium (about 7 g of soluble fiber) per day.117,118 Now psyllium is one of the top 10 functional foods. The National Heart, Lung, and Blood Institute (NHLBI) of the National Institute of Health (NIH) in the third report of the National Cholesterol Education Program (NCEP) adult treatment panel III (ATP III) recommended increasing viscous fiber in the diet. On average, an increase in viscous fiber of 5 to 10 g/day is accompanied by an approximately 5% reduction in LDL cholesterol.117,119 Even higher intakes of 10 to 25 g/day can be beneficial. Soluble (viscous) fiber instead of insoluble fiber reduces LDL cholesterol levels.120 For the management of hypercholesterolemia the recommended dose is about 3.5 g in at least 150 mL water twice daily by mouth. A higher dose of 5.25 g twice daily may be given for the initial two or three months of treatment if necessary. Some investigators reported that soluble fiber such as psyllium produces a reduction in HDL cholesterol,121 and other reviews reported little, no, or inconsistent effect on HDL cholesterol.122,123 Strategies such as the reduction of dietary fat with an increase in fiber consumption are less costly and may bring about reductions comparable to the use of drugs.22,124 Psyllium, along with reduced doses of a bile-acid binding resin, has been given in the treatment of hyperlipidemia, which is reported to be effective and better tolerated than full doses of the resin alone.125 There are several meta-analyses on hypocholesterolemic effects of psyllium.126–128 Anderson et al. conducted meta-analyses on the cholesterol-lowering effect of psyllium.126 Authors analyzed the results from eight studies on 384 and 272 subjects who received psyllium or cellulose placebo, respectively. In all studies 10.2 g/day psyllium was used as an adjuvant to a low-fat diet for more than eight weeks. All subjects had mild to moderate hypercholesterolemia with a pretreatment dietary lead-in period of more than eight weeks (AHA step I diet). They also analyzed the safety and adverse events associated with psyllium from pooled data of 19 clinical studies (807 subjects on psyllium and 476 on placebo) ranging from six weeks to six months. They concluded that 10.2 g psyllium husk per day could lower serum total cholesterol by 4% (P < 0.0001) and LDL cholesterol by 7% (p < 0.0001) and the ratio of apolipoprotein (apo) B to apo A-I by 6% (p < 0.05) relative to placebo in subjects with low-fat diet and had no effect on HDL and TG.126 The incidence of adverse effects was also
Psyllium
409
similar between psyllium and placebo groups. Symptoms involving the digestive system (e.g., flatulence, abdominal pain, diarrhea, constipation, dyspepsia, or nausea) were the most commonly reported for both the psyllium and placebo groups.126 Reductions of more than 15% for serum total cholesterol concentrations and of more than 20% for serum LDL-cholesterol concentration have been reported for hypercholesterolemic patients eating a typical high-fat American diet.22,109 Olson et al.128 conducted a meta-analysis of 12 studies on the hypocholesterolemic effects of psyllium-enriched cereals in hypercholesterolemic subjects (209 patients in psyllium group) with a low-fat diet. In a meta-analysis of 67 controlled dietary studies,127 the authors found that for each gram of soluble fiber from oats, psyllium, pectin, or guar gum, total cholesterol concentrations decreased by 1.42, 1.10, 2.69, and 1.13 mg/dL respectively. Similarly, LDL-cholesterol levels were decreased by 1.23, 1.11, 1.96, and 1.20 mg/dl respectively. In a recent randomized double-blind crossover study on 33 hypercholesterolemic patients, subjects received either two test cookies containing psyllium + plant strols (PSY+PS) or placebo cookies for one month with a three-week washout period between treatments. Intake of PSY+PS decreased LDL-1 and LDL-2 and increased the LDL peak size and LDL receptors significantly. Also, colesteryl ester transfer, protein activity, and prevalence of LDL pattern B were reduced significantly. They concluded that hypocholesterolemic action of PSY and PS was in part due to modifications in the intravascular processing of lipoproteins and LDL receptor– mediated uptake.129 Since then, there have been many clinical trials on hypocholesterolemic and hypoglycemic effects of psyllium. The cholesterol-lowering effects of psyllium are less controversial.108,130 Trowel is one who first identified a link between fiber and diabetes,131,132 and Jenkins and colleagues published the first experimental evidence on fiber-modulating effects on blood glucose and insulin response.133 Psyllium, by decreasing both gastric emptying and small intestine motility and by viscousing the content of the small intestine, reduced glucose absorption and reduced postprandial glucose concentrations.133 Based on this effect the recommendations for the diabetic diet have changed from a low-carbohydrate, high-fat, high-protein diet to one moderately low in fat and high in starch and NSP.134,135 Diabetes is a chronic condition and needs maintenance therapy with chronic use of medications, and fibers as functional foods could be formulated best for long-term compliance. The principal controversy in psyllium consumption in diabetes is not about the efficacy but compliance.136 Meta-analysis showed that psyllium can reduce blood glucose by 29%,137,138 and it is postulated that soluble sources of NSP which formed gels were most effective in this context.139 In fact, 40% of patients with type 2 diabetes have hyperlipidemia and an additional 23% have hypertriglyceridemia with increase in LDL cholesterol levels.140–142 Psyllium has controversial effects on triglycerides in diabetic patients.108,109,143–146 Psyllium effects on the improvement of glucose and lipid levels were not explained by weight loss or reduced food intake.143,144
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Fiber Ingredients: Food Applications and Health Benefits
Other Effects of Psyllium Psyllium as a hydrocolloid has some benefits in pharmaceuticals. It is used successfully in the production of sustained released gastro-retentive dosage forms, which enable prolonged and continuous input of drugs to the upper parts of the gastrointestinal tract (stomach and small intestine) and improves the bioavailability of medications such as ofloxacin that are characterized by a narrow absorption window.147 Indeed psyllium prolongs the gastric retention time of the drug delivery system and has pharmacokinetic advantages like maintenance of constant therapeutic levels over a prolonged period and thus reduction in fluctuation in therapeutic levels.1,148 In Diarrhea It has been reported that psyllium has useful effects to help patients with diarrhea.149,150 Psyllium improves fecal consistency and viscosity in subjects with experimentally induced secretory diarrhea.151,152 The water-holding capacity of feces increased by daily psyllium intake.153 Psyllium also ameliorates diarrhea induced by enterotoxigenic E. coli.154 Conversely, psyllium has been shown to delay gastric emptying and reduce the acceleration of colonic transit.155 In Gallstones Gallstones, with a high prevalence in Western countries, is the most common and expensive digestive disease.156 It is found that 80% of gallstones found in patients have cholesterol as their major component.157 In dogs, fiber supplementation of a lithogenic diet reduced cholesterol gallstone formation by reducing the cholesterol saturation index.158 Seven different epidemiological studies have shown a negative association between fiber intake and gall bladder stones.159 In Hemorrhoids, after Anorectal Surgery, and during Pregnancy Psyllium is used when excessive straining of stool must be avoided, for example following anorectal surgery,160 in the management of hemorrhoids,161,162 or during pregnancy.163
Safety and Toxicity Psyllium has been marketed for more than 60 years in the United States, Europe, and Canada and has an excellent safety record. The safety of psyllium has been documented by other scientific groups, including the FDA.164
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411
The adverse effects of psyllium have been relatively uncommon; however, because of increased bulk, patients who consume psyllium commonly experience abdominal distension, pressures, and discomfort. They may also experience abdominal pain, nausea, vomiting, cramping, loss of appetite, and faintness. Esophageal or intestinal obstruction may develop. In order to prevent obstructive problems, the patient must increase water intake to two full glasses with each dose and should take psyllium immediately before going to bed.165 Hypersensitivity reactions have been reported.166–171 In most patients, sensitization was thought to have occurred during occupational exposure. The plant products may cause specific IgE–mediated sensitization and development of allergic rhinitis, conjunctivitis, and asthma, and oral intake has caused anaphylaxis.172–176 When psyllium is mixed or poured, fine dust particles are readily dispersed into the air and can then be inhaled and cause sensitization. Workers in pharmaceutical firms that manufacture the drug and health care workers dispensing it are at particular risk for hypersensitivity reaction. In one survey of 130 pharmaceutical workers, the prevalence rates of occupational asthma and IgE sensitization were found to be 3.6% and 27.9% respectively.177 Oral intake of psyllium seems to be less likely to induce sensitization. However, prior sensitization may be associated with severe allergic reactions.171 To avoid sensitization, healthcare workers should use face masks and work under fume hoods when mixing and dispensing psyllium products. And it is better to use granulated compared to finely powdered formulations. Many in vitro studies suggest that certain types of dietary fibers decrease the amount of dietary calcium available for absorption. But Lucia and Kunkel showed that there was virtually no binding of exogenous calcium by sources of cellulose, methylcellulose, or psyllium,178 and there is even evidence that prebiotics may have effects in the small intestine, particularly in enhancing calcium absorption.179,180 Psyllium has no effect on vitamin absorption.6 The seed contains a pigment that may be toxic to the kidneys, but this has been removed from most commercial preparations. In traditional medicine, seeds containing mucilaginous husk after swelling in water should be swallowed, with no chewing or crushing because of potential toxic chemicals that may be present in the seeds. Cases with psyllium adverse events have been reviewed recently.181 Contraindications Psyllium should be avoided in patients who have difficulty swallowing. Bulk laxatives should not be given to patients with pre-existing fecal impaction, intestinal obstruction, or colonic atony. Psyllium, as a nonprescription laxative, should not be recommended for children below six years of age, according to FDA-approved labeling.182
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Fiber Ingredients: Food Applications and Health Benefits
Pregnancy and Lactation In usual doses psyllium use does not have any restrictions in pregnancy and lactation. Pregnancy category B. Drug Interaction Ispaghula has interaction of relatively little significance with iron salts.183 Psyllium may diminish absorption of orally administrated drugs because of its mucilage content. In a case report a 47-year-old woman who took lithium citrate and had a constant blood level (0.53 mmol/L) of the drug started to consume 1 teaspoon ispaghula husk in water twice daily. Then she increased her lithium dose to 10 mL twice daily, but five days after this dosage increase, her lithium concentration decreased to 0.40 mmol/L. Three days later ispaghula was discontinued. Four days subsequently, lithium concentration reached to 0.76 mmol/L.184 In an experiment psyllium increased the extent of ethinylestradiol absorption but the rate of absorption decreased.185 So patients should be advised to separate psyllium intake from the administration of oral medication by at least two hours in order to avoid impairment of the absorption of the medications.
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161. Alonso-Coello, P., Guyatt, G., Heels-Ansdell, D., Johanson, J. F., Lopez-Yarto, M., Mills, E., and Zhou, Q., Laxatives for the treatment of hemorrhoids, Cochrane Database Syst Rev CD004649, 2005. 162. Alonso-Coello, P., Mills, E., Heels-Ansdell, D., Lopez-Yarto, M., Zhou, Q., Johanson, J. F., and Guyatt, G., Fiber for the treatment of hemorrhoids complications: a systematic review and meta-analysis, Am J Gastroenterol 101 (1), 2006. 163. Morgan, C., Constipation during pregnancy. Fiber and fluid are keys to selfmanagement, Adv Nurse Pract 9 (10), 57–8, 2001. 164. FDA, Food labeling: health claims; soluble fiber from certain foods and coronary heart disease: final rule, Federal Register, 1998, 8103–21. 165. Deglin, J. H. and Vallerand, A. H., Davis’s Drug Guide for Nurses, 7th ed., Philadelphia, 2000. 166. Busse, W. W. and Schoenwetter, W. F., Asthma from psyllium in laxative manufacture, Ann Intern Med 83 (3), 2–61, 1975. 167. Gross, R., Acute bronchospasm associated with inhalation of psyllium hydrophilic mucilloid, Jama 241 (15), 1573–4, 1979. 168. Suhonen, R., Kantola, I., and Bjorksten, F., Anaphylactic shock due to ingestion of psyllium laxative, Allergy 3 (5), 1983. 169. Zaloga, G. P., Hierlwimmer, U. R., and Engler, R. J., Anaphylaxis following psyllium ingestion, J Allergy Clin Immunol 74 (1), 79–80, 1984. 170. Kaplan, M. J., Anaphylactic reaction to “Heartwise,” N Engl J Med 323 (15), 1072–3. 171. Lantner, R. R., Espiritu, B. R., Zumerchik, P., and Tobin, M. C., Anaphylaxis following ingestion of a psyllium-containing cereal, Jama 264 (19), 2534–6, 1990. 172. Malo, J. L., Cartier, A., L’Archeveque, J., Ghezzo, H., Lagier, F., Trudeau, C., and Dolovich, J., Prevalence of occupational asthma and immunologic sensitization to psyllium among health personnel in chronic care hospitals, Am Rev Respir Dis 142 (6 Pt 1), 1359–66, 1990. 173. Marks, G. B., Salome, C. M., and Woolcock, A. J., Asthma and allergy associated with occupational exposure to ispaghula and senna products in a pharmaceutical work force, Am Rev Respir Dis 144 (5), 1065–9, 1991. 174. Helin, T. and Makinen-Kiljunen, S., Occupational asthma and rhinoconjunctivitis caused by senna, Allergy 51 (3), 181–4, 1996. 175. Khalili, B., Bardana, E. J., Jr., and Yunginger, J. W., Psyllium-associated anaphylaxis and death: a case report and review of the literature, Ann Allergy Asthma Immunol 91 (6), 579–84, 2003. 176. McConnochie, K., Edwards, J. H., and Fifield, R., Ispaghula sensitization in workers manufacturing a bulk laxative, Clin Exp Allergy 20 (2), 199–202, 1990. 177. Bardy, J. D., Malo, J. L., Seguin, P., Ghezzo, H., Desjardins, J., Dolovich, J., and Cartier, A., Occupational asthma and IgE sensitization in a pharmaceutical company processing psyllium, Am Rev Respir Dis 135 (5), 1033–8, 1987. 178. Luccia, B. H. and Kunkel, M. E., In vitro availability of calcium from sources of cellulose, methylcellulose, and psyllium, Food Chemistry 77, 139–146, 2002. 179. Schrezenmeir, J. and de Vrese, M., Probiotics, prebiotics, and synbiotics— approaching a definition, Am J Clin Nutr 73 (2 Suppl), 361S–364S, 2001. 180. Cummings, J. H. and Macfarlane, G. T., Gastrointestinal effects of prebiotics, Br J Nutr 87 Suppl 2, S145–51, 2002. 181. Pittler, M. H., Schmidt, K., and Ernst, E., Adverse events of herbal food supplements for body weight reduction: systematic review, Obes Rev 6 (2), 93–111, 2005.
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182. Pray, W. S., Nonprescription Product Therapeutics, Williams & Willkins, Baltimore, 1999. 183. Harkness, R. and Bratman, S., Mosby’s Handbook of Drug-Herb and Drug-Supplement Interactions, Mosby, St. Louis, 2003. 184. Perlman, B. B., Interaction between lithium salts and ispaghula husk, Lancet 335 (86), 1990. 185. Garcia, J. J., Fernandez, N., Diez, M. J., Sahagun, A., Gonzalez, A., Alonso, M. L., Prieto, C., Calle, A. P., and Sierra, M., Influence of two dietary fibers in the oral bioavailability and other pharmacokinetic parameters of ethinyloestradiol, Contraception 62 (5), 253–7, 2000.
Section IV
New Development
18 Fruit Fibers Jürgen Fischer
Contents Definition and Origin of Fruit Fibers................................................................ 427 Application of Fruit Fibers to Food Products...................................................430 Physiological Benefits of Fruit Fibers................................................................ 432 References............................................................................................................. 435
Definition and Origin of Fruit Fibers The term dietary fiber [1] has been coined for organic components of plants that cannot be degraded by human alimentary enzymes and thus remain unabsorbed in the small intestine. Following the studies of Trowell and coworkers [2] on the connection between dietary fiber intake and occurrence of diseases in modern civilization, fibers are no longer regarded as superfluous for nutrition, and attempts are being made to increase their amount in food. Traditionally parts of plants (roots, tubers, leaves, fruits, seeds) rich in protein, carbohydrate, and fat have been chosen for human consumption and in addition, fiber-depleted raw materials have been selected due to sensory reasons [3]. The main part of dietary fiber in our diet comes from cell walls of fruits, vegetables, grain, legumes, and cereals [4]. The cell walls are very complex networks of different non-starch polymers, structural proteins, and phenolic substances [5–7]. Nearly all components of the cell wall belong to the group of dietary fibers. The most abundant non-starch polymers of the plant cell walls are cellulose, hemicellulose, pectin, and lignin. According to the solubility in water, we distinguish soluble from insoluble dietary fiber. The complex, native cell wall material is primarily insoluble in water and has a fibrous structure. The composition of this intrinsic cell wall material can vary among different plants and depends on the biological function of the plant organs and tissues. The composition undergoes changes during the plant’s life. Even within the same cell, changes occur during maturation [7]. In general, the content of cellulose and lignin strongly depends on the matu427
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Fiber Ingredients: Food Applications and Health Benefits
Table 18.1 Composition of Edible Parts of Fruits
Fruit
Water (%)
Available Carbohydrates
Apple Apricot Mango Strawberry Pineapple Orange Plum Peach
85.3 85.3 82.0 89.5 85.3 86.7 83.7 87.5
12.4 9.4 12.8 6.5 13.1 9.2 11.4 9.4
Protein
Fat
Dietary Fiber
Water Binding of Dietary Fiber
0.3 0.9 0.6 0.8 0.5 1.0 0.6 0.8
0.4 0.1 0.5 0.4 0.2 0.2 0.2 0.1
2.3 2.0 1.7 2.0 1.4 2.2 1.7 1.7
31.5 37.5 40.3 41.1 51.2 34.7 42.2 45.5
Source: Souci-Fachmann-Kraut, Food Composition and Nutrition Tables 1989/90, and theoretical water binding of dietary fiber.
ration of a plant and increases with the need of a tissue for structural stabilization [8]. The highest dietary fiber content in edible parts of plants is located in the outer regions of grains, fruits, or vegetables, due to their excellent protective function. In fruits, the reproduction organs of plants that contain one or more seeds (including the embryo), the parenchyma tissue is the main cell type. These cells have comparably thin walls but are highly vacuolated [5, 6] and can stabilize a tissue with very high water content. Two facts are responsible for this high functionality: the morphological structure and the higher ratio of pectin and hemicellulose versus cellulose. For example, in quince [9] the same cellulose content was found in flesh and core tissue but a three times higher pectin content in flesh. Table 18.1 gives an overview on the composition of some fruits. The fat and protein contents are in general lower than 1% and the sugar content is in the range of 6% to 13%. Because the cell wall material (= dietary fiber) is responsible for moisture control (and the texture) a theoretical water-binding capacity can be determined for the dietary fiber. A value of 1 has been considered for sugar and protein. Raw material to produce fruit fiber is available in large quantities and is more or less a by-product of the processing of fruits to juice or puree [9–14]. The industrial residue is dried, to some extent purified or processed, and milled to a defined grain size [15]. For example the production of apple juice is accompanied by the accumulation of about 20% pomace [16]. Usually, the pomace is dried immediately after processing of the fruit. This by-product consists of skin, seeds, core, and mainly the cell wall material of flesh (parenchymal tissue). It has an average content of about 60% dietary fiber and 12% available sugars. The soluble fiber content is approximately 20%, being mainly pectin.
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In the case of citrus processing [11] of juices and essential oils, the remaining materials such as peels, pulp, and seeds account for 40% to 60% of the fruits. These by-products are used to produce secondary products such as candied peels, pectin, or (peel and/or pulp) fiber. Depending on the tissue, commercial dietary fiber with different properties can be produced. For example, the total dietary fiber content is 9.6% in orange peels, 9.7% in the membranes, and 11% in juice sacs and the water content is 69%, 81%, and 84%, respectively [17]. Hence, the total dietary fiber content of seeds is 14.6% but their water content is only 48%. This is caused by the different biological need. Protection versus moisture control is reflected by the high cellulose/ lignin fraction of 68% in contrast to only 42% in the other tissues. Although by-products of fruit processing exist in large amounts [18], the commercial production of fruit fibers is limited to small amounts since by-products are mostly used in the feed industry. Fresh fruit tissue after squeezing is not stable against enzymatic degradation and is very sensitive to microbiological spoilage. In addition, fruit ripening is mostly governed by cell wall degradation, which is responsible for softening. With over-softening, the production of fiber is economically not of interest. Therefore, a drying process soon after fruit processing is necessary (this happens naturally in case of cereal bran or legume hulls during ripening). But the drying process is expensive due to the high and stable water binding of fruit-derived cell wall material and in addition it is difficult to preserve the beneficial functionality, the high water-binding capacity [19]. This property strongly depends on the maintenance of the cell wall architecture [19–21]. The term material with cellular structure (MCS) was chosen for powdered products that can be rehydrated to suspensions that have nearly equal properties as fresh cell wall material [22, 23]. Disintegration of the cell clusters is helpful to remove water-soluble substances during preparation but must not destroy the cell wall structure. This is accompanied by lower water-binding properties [24]. In this respect, powdered cell wall material from apples was described with water-binding capacities of more than 30 g/g. Such values are in the range of the theoretical values shown in Table 18.1. The way of rehydration plays an important role in the water-binding properties of fruit fibers. Intensive stirring or shear forces lead to enhanced binding properties [25, 26]. In recent years fruit fiber–producing companies have focused on obtaining products with a high water-binding property, closer to those in fresh fruits. A comparison of this key property of commercially available fruit fibers can be seen in Figure 18.1. All values are determined under the same conditions to generate comparable results. As a matter of a wide range of different methods [27] to characterize the interaction with water (water binding, holding, swelling), as well as a strong influence of the rehydration conditions, it is impossible to compare literature data and values of company brochures. Due to the different ultra structure, the water-binding properties of fruit fibers are higher than that of cereal-based fiber. Raw materials like cereal bran or husks form a rigid cellulose coat [28] to protect the germ and should not bind water at all, a biological need. Chemical activation is necessary to increase
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Fiber Ingredients: Food Applications and Health Benefits
Water Binding (g water/g Fiber)
25 20 15 10 5
r
Q
Pl us
Ci tr
us
ul p A
ng eP ra O
Fi
be Fi
be
r
r on m Le
sic as Cl
sic
A pp le F
Fi
ib
be
er
r be Fi
Cl as
at he W
er ib aF Pe
W
he
at
Br
(H ul ls)
an
0
Figure 18.1 Water binding of commercial dietary fibers using a centrifugation method: 1 g dietary fibers is dispersed in 60 g water at 20°C, soaked for 24 h, and centrifuged at 3000 x g for 10 min. The bound water is determined by weight measurement after discarding the supernatant.
the water-binding properties as is done to produce, for example, CMC, MC, or HPMC. Finally, the natural high functionality is the main advantage of fruit fiber and reason for the positive image. It derives from succulent and attractive-to-eat plant material which has ever been a normal part of human nutrition. Application of Fruit Fibers to Food Products “Fiber is of interest to product designers for not only its nutritional value but for its versatility as a functional ingredient” [29]. Indeed, the old conceptions, especially that insoluble fiber has been related with a rough mouthfeel, slowly disappear and are replaced by multiple technological benefits [3, 30, 31]. In the past, the use of insoluble fruit fiber was limited to semi-dry applications such as bread or bars [32–35]. Nowadays, products are available with improved rehydration properties and are accompanied with a better water uptake, the fibrous material is becoming softer and can be applied even for oil/water emulsions without the formation of a sandy or grainy character [31, 36–38]. As in fruits or fruit-based products, the cell wall matrix is the principal structural component [5, 22] and the water-binding properties of fruit fiber can be used to control the texture and the rheological behavior of food thereof. Without a doubt, the key property of fruit fiber is the hydration. Hydration summarizes the ability to swell, bind water, enhance the viscosity, and prevent syneresis (see Table 18.2). Especially those fruit fibers that are produced
431
Fruit Fibers Table 18.2 Applications of Fruit Fibers to Calorie Reduced Food Low Fat o/w emulsions (mayonnaise-like) Replacement of modified starch Creamy, fat-like consistency even below 10% fat Pseudo-elastic flow behavior Spreads Stabilization of fat-reduced margarines Replacement of nuts or beans Replacement of starch or milk powders Liver Sausage and Pâté Mimic fat Improved succulence Improved consistency Replacement of cereal-based binders Frankfurter Sausage Improved succulence Enhance shelf life (less syneresis) Improved bite Sponge Cake and Muffins Improved succulence Replacement of flour and/or fat Stabilization of shape
carefully without collapse of the cell wall architecture [21] are able to swell in a very short time and form a sponge-like network. This matrix is able to immobilize water to a high degree. Scanning electron micrographs (see Figure 18.3) visualize the mechanism responsible for the superior water binding. It is mainly the cell architecture and to a smaller extent the chemical composition with the relatively high content of pectin substances. The high water-binding is a technological as well as a physiological benefit [39]. However, dietary fibers with a high functionality (in respect to water binding) are typically used at a relatively low usage level to perform a specific function and then, only consequentially, add fiber at a low level. In most cases the level will not be high enough for fulfilling a fiber claim as suggested by the authorities. Nevertheless they are advantageous to be used in low-fat or low-calorie products [40, 41]. Some applications of fruit fibers to food products are shown in Table 18.2. The use in baked products has a long history, especially for apple fibers [42–44]. But why use fruit fibers in sausages, sauces and dressings, or in ice cream? On the whole, meat products are far from being regarded as sources of dietary fiber. However, the high functionality and sensory improvement of some fruit fibers opened the doors to this new field [45–48]. Especially in boiled sausages, the addition of 3% dietary fiber in low-fat products is easy
432
Fiber Ingredients: Food Applications and Health Benefits
to achieve with a fiber ingredient with high water-binding capacity. A 20% fat-reduced product just by using only lean meat would be dry and very firm. Better results are achieved by keeping the protein at the same level and binding the water with fiber. A similar principle is applied to a successful production of low-fat varieties of baked products, such as brownies, which originally have a high fat content [25, 33, 49, 52]. It is also possible to produce low-fat mayonnaise, low-fat margarine, fresh cheese, or even ice cream without reduction of creaminess or mouthfeel. A prerequisite for such application is that the fiber can be rehydrated in a way that the grainy structure completely disappears (which is a result of cell wall collapse during production [21]). In some products the fruit fibers should be rehydrated by using intensive stirring or shear treatment [25, 51, 52] to achieve the best results. Figure 18.4 shows the rheological behavior of a low-fat o/w emulsion. Citrus fiber, dispersed in water, creates a very high yield point and can be used after this treatment similar to the known starchy slurry. The pseudo-plastic properties allow the use in products with typical shear thinning such as mayonnaise or salad dressing.
Physiological Benefits of Fruit Fibers As listed in Table 18.1, fruits consist mainly of water and are low in fat. Many studies reveal that fruits (and vegetables) are a very important part of a healthy diet [53–55] as fruits are rich in vitamins, minerals, secondary plant substances such as flavonoids, and dietary fiber. The last is definitely the difference (or what is lacking) between juice and whole fruit. The only components that may be considered as less healthy are carbohydrates, mainly sugars. According to a recent WHO report [53] “benefits of fruits and vegetables cannot be ascribed to a single mix of nutrients and bioactive substances” but as a food group they contribute to cardiovascular health. The daily intake of 400 to 500 grams of fruits and vegetables is recommended to reduce the risk of coronary heart disease, stroke, and high blood pressure through the variety of phytonutrients, potassium, and fiber they contain. These recommendations [54–55] are broadly known as 5-a-day (eat 5 or more portions of fruits or vegetables per day), and the concept is used as a strong marketing tool. Furthermore, convincing evidence exists on the positive effect of dietary fiber and energy diluted food, such as fruits and vegetables on obesity [56]. Some reports focus more on subcategories of fruits such as citrus [57]. Although much work has been done to point out the advantages of fruits in a diet, studies focusing on fruit fibers (in the sense of complex cell matrix
433
Fruit Fibers
and not an isolated fraction like pectin) are rare. Some work has been done on the bulking effects of fruit fibers [58, 59]. This effect can be considered as beneficial to prevent constipation, a major health problem mainly for elderly women. Responsible for a high bulking effect is the good water binding of fruit fiber, which is stable during the passage through the intestine and the relative filigree morphological structure that provides bacteria in the large bowel with good growth conditions. Figure 18.2 shows results of a comparative study of different commercial fruit fibers. Additionally some integral parts of fruit fibers are metabolized by desirable bacteria and with that have a prebiotic nature. A few studies have been published concerning the link between the general health benefit of fruits and their dietary fiber content. An Italian study [60] supports the hypothesis that the dietary fibers in fruits (and vegetables but not cereal) are one of the beneficial components that protects against laryngeal cancer. A Harvard research group [61] analyzed whether the source of dietary fiber has an influence on the reduction of heart disease risk by pooling results from more than 91,000 men and 245,000 women. In this study the strongest protective effect against coronary heart disease caused deaths with a reduction in risk of 30% was with fruit fiber and 25% for cereal fiber for each 10 grams per day. From all the data it is obvious that fruit fibers add a benefit to foodstuff either by the fiber itself or the secondary effect of energy dilution. Additional studies are required to demonstrate a specific effect when added to a specific foodstuff. Nevertheless, all data suggest that the consumption of fruit, fiber, and phytonutrients thereof can be generally regarded as beneficial, a fact that is reflected in the existence of general health claims for fiber-containing fruits in the United States [62]. Low Viscosity Apple Pectin (Herbapekt SF 50) Citrus Fiber (Herbacel AQ Plus) Apple Fiber (Herbacel AQ Plus) Wheat Bran Apple Fiber (Herbacel Classic 01) 0
20
40
60 80 Faecal Bulking Index
100
120
140
Figure 18.2 Faecal Bulking Index (FBI) (according to [63]) reflects non-digested food matter, hindgut bacterial biomass, and the water-holding capacity of the whole. Reference was 12.5% wheat bran (100) to the normal diet (bases = 0).
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Fiber Ingredients: Food Applications and Health Benefits
2 mm
200 µm Herbacel AQ Plus Citrus Fiber powder
2 mm
200 µm Herbacel AQ Plus Citrus Fiber, 2% powder soaked in water for 24 h
Figure 18.3 Scanning electron micrographs of citrus fiber in powdered form and after swelling in distilled water at 20°C for 20 h.
435
Fruit Fibers 40 6% Starch 1,8% Starch + 1,2% Citrus fiber
Viscosity (Pa s)
30
20
10
0
0
10
20
30
40
50
60
70
80
90
100
Shear Rate (1/s)
Ingredients Water Vegetable Oil Modified Waxy Maize Citrus Fiber (Herbacel AQ Plus ) Vinegar (5% acid) Egg Yolk Sugar Mustard Salt Lemon Juice Spices
“Starch” [%] 68 9 6 0 6 3 3 2 1,5 1 0,5
“Starch + Citrus Fiber” [%] 71,0 9 1,8 1,2 6 3 3 2 1,5 1 0,5
Figure 18.4 Flow behavior of low-fat mayonnaise on basis of starch versus starch and citrus fiber.
References
1. Hipsley, E.H., Dietary “fibre” and pregnancy toxaemia, Brit. Medical Journal, 2, 420, 1953 2. Trowell, H., Burkitt, D. and Heaton, K., Dietary Fibre – Fibre Depleted Foods and Diseases. Academic Press, London 1985 3. Meuser, F., Technological aspects of dietary fibre in Advanced Dietary Fibre Technology, McCleary and Prosky, Eds., Blackwell Science, Oxford, 2001, chap 23 4. Selvendran, R.R., Steven, B.J.H., and DuPont, M.S., Dietary fibre: chemistry, analysis and properties. Adv. Food Res., 31, 117, 1987 5. Waldron, K.W., Parker, M.L., and Smith, A.C., Plant cell walls and food quality, Comprehensive reviews in food science and food safety, IFT 2003 vol 2
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6. MacDougall, A.J. and Selvendran, R.R., Chemistry, architecture, and composition of dietary fiber from plant cell walls; Handbook of Dietary Fiber, Cho and Dreher, eds., Marcel Dekker, New York, 2001, chap 19 7. Pena, M.J., Vergara, C.E., and Carpita, N.C. The structure and architecture of plant cell walls define dietary fibre composition and the texture of foods, in Advanced dietary Fibre Technology, McCleary and Prosky, Eds., Blackwell Science, Oxford, 2001, chap 5 8. Selvendran, R.R., Dietary fibre in foods: amount and type, Physico-chemical properties of dietary fibre and effect of processing on micronutrient availability, Proceeding of a workshop, COST 92 Amado, Barry and Frolich, eds., Commission of the European Communities, Luxemburg 1993 9. Thomas, M. et al., Characterisation of dietary fibre and cell-wall polysaccharides from different tissue zones and entire fruit of Chaenomeles japonica, Poster at 1st International Conference on Dietary Fibre, Dublin 2000 10. Martin-Cabrejas, M.A. et al., By-products of food industries as source of dietary fibre, Physico-chemical properties of dietary fibre and effect of processing on micronutrient availability, Proceeding of a workshop, COST 92 Amado, Barry and Frolich, eds., Commission of the European Communities, Luxemburg 1993 11. Licandro, G. and Odio, C.E, Citrus by-products in Citrus, Dugo & DiGiacomo Eds., Taylor & Francis, London 2002, chap. 11 12. Larrauri, J.A, New approaches in the preparation of high dietary fibre powders from fruit by-products, Trends in Food Science and Technology, 10, 3, 1999 13. Martin-Cabrejas, M.A. et al., Dietary fibre content of Pear and Kiwi pomace, J. Food Chem., 43, 662, 1995 14. Valiente, C. et al., Grape pomace as a potential food fibre, J. Food Science 60, 818, 1995 15. Walter, R.H. et al., Edible fibre from Apple pomace, J. Food Science, 50, 747, 1985 16. Arrigoni, E. et al.. Chemical composition and physical properties of modified dietary fibre sources, Food Hydrocolloids, 1, 57, 1986 17. Braddock, R.J. and Graumlich, T.R., Composition of fibre from citrus peel, membranes, juice vesicles and seeds, Lebensm. Wiss. Technol. 14, 229, 1980 18. Dongowski, G. and Bock, W., Rohstoffressourcen für die Herstellung von pektinhaltigen Ballaststoffen und Ballaststoffpräparate, in Aktuelle Aspekte der Ballaststofforschung, Schulze and Bock, Eds., Behr’s Verlag Hamburg, 1993, chap 4 19. Bock, W. and Ohm, G., Einfluss der gewachsenen Struktur auf die Wasserbindungskapazität ausgewählter Obst und Gemüsepräparate, Food/Nahrung Vol. 27, 205, 1983 20. Kunzek, H. and Dongowski, G, Der Einfluß des mechanolytischen Abbaus von Obst- und Gemüsetrockenpräperaten auf die Bestimmung des Wasserbindevermögens unter Verwendung verschiedener Methoden, Lebensm. Ind., 38, 77, 1991 21. Kunzek, H., Krabbert, R., Gloyna, D., Aspects of material science in food processing: changes in plant cell walls of fruits and vegetables, Z. Lebensm. Unters. Forsch. A, 208, 233, 1999 22. Krabbert, R., Herrmuth, K., Kunzek, H., Wasserbindekapazität und Makrostruktur von Apfelgewebepartikeln, Z. Lebensm. Unters. Forsch., 197, 219, 1993 23. Müller, S. and Kunzek, H., Material properties of processed fruits and vegetables, Z. Lebensm. Unters. Forsch. A, 206, 264, 1998 24. Kunzek, H. et al., Einsatz der Druckhomogenisierung zur Herstellung von zellstrukturiertem Apfelmaterial, Z. Lebensm. Unters. Forsch., 198, 239, 1994
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25. Fischer, J., Functional properties of Herbacel AQ Plus fruit fibres, Poster at 1st International Conference on Dietary Fibre, Dublin 2000 26. Vetter, S., Kunzek, H., Senge, B., The influence of the pre-treatment of apple cell wall samples on their functional properties Eur. Food Res. Technol., 212, 630, 2001 27. Chen, J.V., Piva, M., Labuza, T.P., Evaluation of waterbinding capacity (WBC) of food fiber sources, J. Food Science, 49, 59, 1984 28. Canadian Harvest, Fiber Facts, Company brochure, USA 29. Bahr, P., New ways to apply fiber; foodproductdesign.com / archive / 1996 / 1096DE.html 30. Amado, R., Physio-chemical properties related to type of dietary fibre, PhysicoChemical Properties of Dietary Fibre and Effect of Processing on Micronutrient availability Amado, Barry and Frolich, eds., Commission of the European Communities 1993 31. Endress, H.U., and Fischer, J., Fibers and Fibre Blends for Individual Needs: a physiological and technological approach, in Advanced Dietary Fibre Technology, McCleary and Prosky, Eds., Blackwell Science, Oxford, 2001, chap 26 32. Miller, E., Lassbeck, A., and Bender, M., Apple – the fruit for more than one application, Food Tech Europe, 88, 1995 33. Fischer, J. Dietary fibres—Ingredients for sweet and bakery goods, Zucker und Suesswarenwirtschaft, 10, 20, 2001 34. Bender, M., Citrusfaser, Food Tech M, October 1996 35. Duxbury, D.D., Apple fibre powder yields higher pectin, moisture retention, Food Processing, November 1987 36. Fischer, J., Improved fruit fibres for modern food processing, Food Ingredients and Analysis, May/June, 2001 37. Figuerola, F., et al., Fibre concentrates from apple pomace and citrus peels as potential fibre source for food enrichment, Food Chem, 91, 395, 2005 38. Fischer, J., Fibres in Ice cream, Inter-Ice 2000, International Symposium, Solingen, May 2000 39. Schneeman, B.O., Dietary fibre and gastrointestinal function, in Advanced dietary Fibre Technology, McCleary and Prosky, Eds., Blackwell Science, Oxford, 2001, chap 14 40. Sandrou, D.K., and Arvanitoyannis, I.S., Low-fat/calorie foods: Current state and perspective, Critical Rev. Food Sci Nutr, 40:427, 2000. 41. Fischer, J., Dietary fibres, no.1 ingredients for calorie reduction, Wellness Foods Europe, April/May 2004 42. Bollinger, H., Ballaststoffe – Eigenschaften und ihre Anwendungsmöglichkeiten, Suesswaren, 7-8, 384, 1990 43. Bollinger, H., Calorie-reduced snacks, Food Marketing Technol, April 1993 44. Hanneforth, U., and Brack, G., Apfelballaststoffe: Eigenschaften und Eignung für die Verarbeitung in Feinen Backwaren, Brot und Backwaren, 3, 1991 45. Perez-Alvarez, J.A. et al., Effect of citrus fibre (albedo) incorporation in cooked pork sausages, IFT Annual Meeting, 2001 46. Fischer, J., Leichter Ballast, Lebensmitteltechnik 6, 2001 47. Garcia, M.L. et al., Utilisation of cereal and fruit fibres in low fat dry fermented sausages; Meat Science, Vol. 60, issue 3, 227, 2002 48. Garcia, M.l, Caeres, E., and Selgas, M.D., Utilisation of fruit fibres in conventional and reduced-fat cooked sausages, J. Sci Food Agricul
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49. Köz, P., Boyacioglu, D., Özcelik, B., Development of a functional Turkish dessert: Dietetic and diabetic baklava, IFT Annual Meeting, Las Vegas 2004 50. Hughes, K., Reduced fat with pulp fibre, Prepared Food, January 2007 51. Fischer, J., Fruit fibres to count down the calories, Innov Food Technol, November 2005 52. Auffret, A. et al., Effect of grinding and experimental conditions on the measurement of hydration properties of dietary fibres, Lebensmittel-Wissen Technol, Vol 27, No 2, 166, 1994 53. WHO/FAO Expert consultation on diet, nutrition and the prevention of chronic diseases, WHO Technical Report Series 916, Geneva 2003 54. US Department of Health and Human Service, Healthy people 2000, National Health Promotion and disease prevention objectives, DHHS Publ. 91-50212 Washington DC, 1991 55. Bazzano, L.A., Dietary intake of fruit and vegetables and risk of diabetes mellitus and cardiovascular diseases, Background paper for the joint FAO/WHO Workshop on fruit and vegetables for health, 1-3 Sept. 2004 in Kobe, Japan, WHO 2005 56. Ludwig, D.S. et al.. Dietary fibre, weight gain, and cardiovascular disease risk factors in young adults, JAMA, Vol. 282, No. 16, 1999 57. Baghurst, K., The health benefits of Citrus fruits, CSIRO Health Science and Nutrition, Report to Horticulture Australia Ltd, Project No. CT01037, June 2003 58. Bravo, L., Saura-Calixto, F., and Goni, I., Effects of dietary fibre and tannins from apple pulp on the composition of faeces in rats, Brit. J. Nutr, 67:463, 1992 59. Bird, A.R. and Topping, D.L.. CSIRO Human Nutrition PTI/FITA report, June 1999 60. Pelucchi, C. et al., Fibre intake and laryngeal cancer risk, Anals Oncol, 14, 162, 2003 61. Pereira, M.A. et al., Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies, Arch Internal Med, 164:370, 2004 62. U.S. Food and Drug Administration, Health claims 21 CFR 101.76, 21 CFR 101.77 and 21 CFR 101.78, www.cfsan.fda.gov, 2004 63. Monro, J., Faecal bulking index and wheat bran equivalents for dietary management of distal colonic bulk, Poster at 1st International Conference on Dietary Fibre, Dublin 2000
19 Aleurone Flour: A Novel Wheat Ingredient Rich in Fermentable Fiber, Micronutrients, and Bioavailable Folate Michael Fenech, Peter Clifton, Manny Noakes, and David Topping
Contents Characteristics...................................................................................................... 439 Functionality, Physiological Benefits, and Food Applications......................440 In Vitro and Rat in Vivo Studies.................................................................442 Bioavailability and Bioefficacy of Folate from Aleurone Flour: Human Studies................................................................................443 Safety and Toxicity............................................................................................... 451 Summary............................................................................................................... 451 Acknowledgments............................................................................................... 452 References............................................................................................................. 452
Characteristics Wheat aleurone flour (ALF) is a novel food product or ingredient made from the aleurone layer of cells in the wheat grain (Figure 19.1). ALF has the potential to make an important contribution to optimal nutrition because it contains significant amounts of naturally occurring nutrients including (a) minerals such as magnesium, calcium, iron, and zinc, (b) dietary fiber, (c) protein, (d) antioxidant phenolic compounds, and (e) B vitamins including folate (Tables 19.1 and 19.2) [1–3]. The aleurone cells, together with the germ, contain the wheat grain’s essential nutrients required for the growth and development of the embryo [4, 5]. Because the bran fraction of wheat contains the aleurone layer of cells, the phytochemicals, vitamins, minerals, fiber, and protein in aleurone cells are lost when wheat grain is refined to make white flour. Consequently, in recent years there has been an interest in devising novel milling technologies to purify the aleurone fraction of the wheat grain 439
440
Fiber Ingredients: Food Applications and Health Benefits
Pericarp seed coat
Aleurone
Pericarp seed coat
Aleurone Endosperm
20 µm
PTR84_01097
Endosperm
Figure 19.1 Diagram showing structure of the wheat grain and the spatial relationship of the aleurone layer relative to pericarp seed coat and the endosperm.
and make it available for human consumption. A unique and commercially viable milling process was initially developed by Goodman Fielder Pty. Ltd. (Australia) that enabled the isolation of the aleurone cell layer and at the same time split the cell walls to release the contents of these cells [6, 7]. Another method of extraction of aleurone cells from wheat bran was developed by Buhler AG and patented (patent WO 02/15711). A schematic representation of the isolation of aleurone is shown in Figure 19.2. The sheared aleurone cells together with a small amount of wheat germ have been formulated into the novel aleurone flour (i.e., ALF). ALF has been available commercially internationally since the mid-1990s and is sold widely as a major ingredient of bread and other cereal products such as pasta.
Functionality, Physiological Benefits, and Food Applications Despite the high nutritional value of ALF, only its contribution to folate status, in terms of bioavailability and bioefficacy, has been adequately studied in human feeding studies. However, before reviewing current knowledge in this area, results from in vitro studies on antioxidant properties and animal studies on fermentation and colon cancer prevention will be briefly discussed.
441
Aleurone Flour Table 19.1 Wheat Aleurone Micronutrient Compositiona Constituent
Unitb
Crude Protein Crude Fat Water insoluble dietary fiber Water soluble dietary fiber Crude Ash Phosphorous Potassium Magnesium Calcium Iron Zinc Sodium Vitamins B1 (Thiamin) B2 (Riboflavin) B6 (Pyridoxine) Niacin Folic acid Pantothenic Acid E (DL-α-tocopherol) Phytic Acid (inositol 4,5,6 triphosphate) a b c
Contentb
g/100 g g/100 g g/100 g g/100 g g/100 g g/Kg g/Kg g/Kg mg/Kg mg/Kg mg/Kg mg/Kg
20.8 5.7c 43.0 4.1 11.3 25.4 22.5 10.3 930 260 139 21
mg/100 g mg/100 g mg/100 g mg/100 g μg/100 g mg/100 g mg/100 g g/100 g
1.4 0.2 1.3 32.9 158.0 4.9 1.2 8.4
Data from Earling et al. [3] (analyses performed by Buhler laboratory, 2004). Dry matter basis. 66% polyunsaturated, 18% monounsaturated, 16% saturated fat.
Table 19.2 Proximate Analysis of Wheat Bran Flour and Aleurone Flour1 Wheat Bran Flour (g/100 g)
Aleurone Flour (g/100 g)
Total Starch Total Dietary Fiber Total Fat Total Protein Total Free Sugars Total Ash Total Moisture
21.6 31.6 5.2 17.8 6.2 3.5 10.4
36.5 15.4 6.5 23.6 7.2 4.1 5.1
Sum Total
96.3
98.4
Constituent
Note: Values are means of duplicate analyses. Source: Data from Fenech et al. [1].
442
Fiber Ingredients: Food Applications and Health Benefits Pericarp Seedcoat (Pericarp Seedcoat Flour)
Wheat Grain
Wheat Bran (Wheat Bran Flour)
Starchy Endosperm (White Flour)
Aleurone Cells and Germ (Aleurone Flour)
Figure 19.2 A schematic diagram showing the key steps in the isolation of wheat bran and aleurone flour.
In Vitro and Rat in Vivo Studies Zhou et al. [8] compared Swiss red wheat grain, bran, aleurone, and micronized aleurone for their free-radical scavenging properties against 2,2-diphenyl-1-picrylhydrazyl radical, radical cation ABTS*+ and peroxide radical anion O(2)*–, oxygen radical absorbance capacity (ORAC), chelating capacity, total phenolic content (TPC), and phenolic acid composition. Their results showed that micronized aleurone had the greatest antioxidant activities, TPC, and concentrations of all identified phenolic acids (p-OH Benzoic acid, vanillic acid, syringic acid, coumaric acid, and ferulic acid), suggesting the potential of postharvesting treatment on antioxidant activities and availability of TPC and phenolic acids. Aleurone was particularly rich in ferulic acid, which was present at a concentration of 373 μg/g. Ferulic acid has been shown to protect against colon cancer and colitis in rat models of these diseases [9, 10]. Cheng et al. [11] studied the comparative effects of dietary wheat bran and its components aleurone and pericarp-seed coat on volatile fatty acid concentrations in the rat. In this study adult male rats were fed on diets containing 100 g dietary fiber/kg either as alpha-cellulose or wheat bran or the pericarp-seed coat or aleurone layers prepared from that bran by sequential milling and air elutriation and electrostatic separation. After 10 days, concentrations of total volatile fatty acids (VFA) in cecal fluid were significantly different between diet groups with aleurone greater than wheat bran greater than pericarp-seed coat greater than cellulose. This ranking reflected the ease of fermentation of fiber polysaccharides by colonic bacteria, which also
Aleurone Flour
443
resulted in a considerably higher fecal bacterial mass in the aleurone group. The diet based on aleurone gave a relatively higher proportion of propionate but with both pericarp-seed coat and wheat bran the contribution of butyrate was raised. VFA concentrations in hepatic portal venous plasma were proportional to cecal concentrations with very high (greater than 3 mM) values being recorded in the aleurone group. McIntosh et al. [12] described a study showing that wheat aleurone flour (ALF) increases butyrate concentration and reduces colon adenoma burden in Sprague-Dawley rats induced using azoxymethane (AOM). ALF at 33 g/100 g of diet increased the weight of feces and produced significantly higher concentrations in the cecum of the shortchain fatty acid butyrate (P < 0.001) than did no fiber (NF) and ALF added at only 10 g/100 g. Cecal and fecal pH were both significantly lower in the ALF treatments relative to control and no fiber treatments (P < 0.001). There were 43% fewer colon adenomas in the ALF treatment groups relative to control (P = 0.06). The results of these studies suggest that ALF flour has potential to modify fermentation in the bowel environment in a way that could promote prevention of colon cancer. It is also possible that these effects may be partly mediated via the role of phenolic compounds such as ferulic acid in bowel fermentation and as colon cancer protective agents via antioxidant and anti-inflammatory mechanisms [9, 10]. These effects need to be verified in human studies. Bioavailability and Bioefficacy of Folate from Aleurone Flour: Human Studies One of the most notable features of the composition of ALF is the high level of folate present at a concentration between 340 and 515 µg/100 g wet weight [1, 2]. This natural level of folate is higher than that observed in wheat bran, fruits, and vegetables (usually between 20 μg/100 g and 200 μg/100 g wet) [13, 14] and is comparable to folate/folic acid levels in fortified flour and cereal that provide 50% RDI per serving (assuming an RDI of 400 µg and a serving size of 40 g wet weight) [15]. Folate plays an important role in the prevention of neural tube defects in the fetus [16, 17]. There is also increasing evidence that an above average intake of folate may help reduce plasma homocysteine, a risk factor for cardiovascular disease [18, 19] and DNA damage, a risk factor for cancer [20, 21]. There is some concern that eating foods that are naturally rich in folate may not provide for a large enough and reliable intake of folate required to prevent spina bifida [22]. Therefore, it is important to identify novel natural rich sources of folate and to test that dietary strategies based on such foods may be effective for the optimization of tissue folate in the general population. To assess the potential of ALF as a source of folate it is first necessary to measure bioavailability by determining how much folate actually appears in the blood after ingesting foods rich in this ingredient. To achieve this we performed a randomized, controlled intervention trial to compare the change in plasma folate after consumption of (a) a cereal made from ALF, (b) a cereal
444
Fiber Ingredients: Food Applications and Health Benefits
made from wheat bran (WB) and (c) a tablet containing 0.5 mg folic acid that was taken together with WB cereal [1]. Sixteen healthy volunteers, eight males and eight females, aged between 20 and 50 years, were recruited to the study. Volunteers who were supplementing their diet with folic acid, and/ or who were deficient in plasma vitamin B12 (<150 pmol/L) were excluded from the study. The design of the study was a randomized controlled trial with a crossover consisting of three intervention rounds: (1) in the first round each volunteer was randomly assigned to the ALF cereal or the 0.5 mg folic acid tablet (Sigma Pharmaceuticals, Victoria, Australia) with WB cereal, (2) in the second round all volunteers were given WB cereal only, and (3) in the third round there was a crossover either to ALF cereal or 0.5 mg folic acid tablet with WB cereal. The WB cereal was given as a low-folate control, and the 0.5 mg folic acid tablet with WB cereal was given as a high-folate positive control against which the ALF cereal could be compared. The tablet was given together with WB cereal to provide a dietary background identical to the low-folate control. The WB cereal was 100% extruded wheat bran and the ALF cereal contained 90% aleurone flour and 10% waxy maize starch. It was estimated, by microscopic image analysis, that 45% of the aleurone flour consisted of aleurone cell contents (i.e., cytoplasm, nucleoplasm, and organelles) with the remainder (55%) consisting of aleurone cell walls. The WB cereal and the ALF cereal were prepared by Goodman Fielder Milling and Baking Pty. Ltd. (Summerhill, NSW, Australia). There was a period of seven days between each intervention round to allow sufficient time for plasma folate to return back to baseline before the next round. On the day prior to each intervention round volunteers were required to refrain from drinking alcohol and to fast overnight. On the following morning volunteers donated a fasted blood sample after which they ate 100 g of cereal with 250 mL fresh milk (containing 1.5 g/100 g fat) over a period of 30 min. The folic acid tablet was taken while the WB cereal was being ingested. Further blood samples were collected at 1 h, 2 h, 4 h, and 7 h after commencing cereal intake. During the course of the day volunteers were provided with light snacks that were poor in folate (as estimated from food composition tables [23]) and they were not allowed to eat any other foods. The level of folate in the milk was 0.6 μg/L. The texture and color of the ALF and WB cereal were clearly different but the volunteers were not informed which of the cereals was made from ALF. Proximate analyses of the aleurone and wheat bran flour indicated a higher starch and protein content and a lower fiber content in aleurone flour when compared to wheat bran flour (Table 19.2). The total folate level per 100 g in the WB cereal and the ALF cereal was 94 ± 4 μg (n = 2) and 515 ± 7 ug (n = 2) respectively; the folic acid in each tablet was 526 ± 24 μg (n = 3). The proportion of folate in the tablet, ALF cereal, and WB cereal that could be detected by microbiological assay without prior treatment with folate conjugase was 100%, 81%, and 32% respectively, which indicates that folate in ALF has a low level of polyglutamation. The latter could be due to release of endog-
445
Aleurone Flour 30
WB cereal
Plasma Folate, nmol/L
ALF cereal 0.5mg folic acid + WB cereal
25
20
15
10
0
1
5 6 2 3 4 Time Relative to Cereal Intake, h
7
8
Figure 19.3 Change in plasma folate following ingestion of WB cereal, ALF cereal, and 0.5 mg folic acid with WB cereal. Results represent the mean ± SEM, n = 16 (8 males, 8 females combined). The ANOVA P values for the change in plasma folate with time for the WB cereal, ALF cereal, and 0.5 mg folic acid with WB cereal were 0.1139, < 0.0001, < 0.0001, respectively.
enous conjugases subsequent to aleurone cell shearing during the milling and purification process. The results for plasma folate at each time-point for each intervention round are shown graphically in Figure 19.3. The plasma folate data during the WB cereal intervention round clearly showed only a minimal increment in the vitamin level during the course of the intervention; the increment achieved statistical significance in the male group only. In contrast plasma folate following 0.5 mg folic acid tablet with WB cereal increased significantly in both males and females (P = 0.003 and P = 0.002, respectively); the combined results showed a sharp increase in plasma folate during the first 2 h, from a mean baseline level of 13.4 nmol/L to a peak at 2 h of 23.0 nmol/L, and a subsequent steady decline down to baseline during the next 5 h (Figure 19.3). The increase in plasma folate following consumption of ALF cereal was also statistically significant in both males and females (P = 0.0001 for both genders) and appeared to be of the same magnitude to that observed for the 0.5 mg folic acid supplement with WB cereal, with a steady increase in plasma folate during the first 2 h from a baseline of 13.9 nmol/L to a peak at 2 h of 23.5 nmol/L and a decline down to baseline by 7 h (Figure 19.3). However, the time response following ALF cereal showed significant increments in plasma folate at 2 h and 4 h after ingestion of the cereal, which suggested a slower rate of appearance of folate into the plasma compared to the results for the folic acid tablet with WB cereal, which showed significant increments in plasma folate at 1 h and 2 h following ingestion. ANOVA analysis of the combined male and female data showed that the observed increments in plasma folate following intake of ALF cereal or folic acid tablet with WB
446
Fiber Ingredients: Food Applications and Health Benefits
cereal were highly statistically significant (P<0.0001); however there was no change following ingestion of WB cereal. The results from this study on breakfast cereal made from aleurone flour showed quite clearly that this natural source of folate can make a significant difference to blood folate concentration. Of main interest was (a) the much greater capacity for ALF cereal, relative to WB cereal, to increase plasma levels of folate and (b) that the increase in plasma folate following ingestion of 100 g of ALF cereal was the same as that observed following intake of 500 μg synthetic folic acid with 100 g WB cereal. These results suggest that inclusion of foods made from wheat aleurone flour in the diet can be considered as an alternative important strategy for increasing folate intake in the general population. Although the results from this initial short-term feeding study indicated that ALF cereal is an important source of folate, long-term studies are required to establish the extent to which folate from aleurone flour may reduce plasma homocysteine (a biomarker of bioefficacy) and increase the level of red cell folate, which is considered to be a more reliable biomarker of tissue folate stores and bioavailability. We, therefore, performed a long-term (16 weeks), randomized controlled intervention to (a) verify the incremental effect of ALF ingestion on plasma folate concentration and (b) determine whether moderate ALF intake can also substantially increase red blood cell (RBC) folate and reduce plasma homocyst(e)ine to an extent that is close to the maximum effect produced by taking a folic acid supplement greater than 500 μg per day [2]. Volunteers were recruited by advertising the study in local newspapers without providing payment for participation. A total of 235 volunteers (mainly Caucasian) aged 20 to 70 years were screened initially for their plasma homocyst(e)ine, RBC folate, and plasma vitamin B12 concentration. We included those in the highest 50th percentile for plasma homocyst(e)ine and the lowest 50th percentile for RBC folate. We excluded volunteers (a) with low levels of plasma vitamin B12 (<150 pmol/L) and/or (b) who were taking folate and vitamin B12 supplements above Australian recommended dietary intake (RDI) levels (i.e., >200 μg/d folic acid, >2 μg/d vitamin B12), and/or (c) who were epileptic and on anti-convulsant therapy and/or (d) those with a past or present history of cancer or pernicious anaemia. Of the initial 235 volunteers screened only 79 met the selection criteria described above and these individuals were invited to participate in the study. The design of the study was a randomized controlled intervention in a freeliving middle-aged healthy population, comparing the effect of high-folate bread made with aleurone flour (ALF) to that of a low-folate bread made with pericarp-seed coat flour (PCS) and to that of a folic acid tablet (FA) given with the low-folate PCS bread. The appearance and texture of the ALF and PCS breads were similar. Volunteers were assigned to the three dietary groups using a randomized block design based on screening plasma homocyst(e)ine concentration. The dietary groups were:
447
Aleurone Flour ALF group: ALF bread + placebo tablet PCS group: PCS bread + placebo tablet (low-folate control group) FA group:
PCS bread + folic acid tablet (high-folate control)
The breads (supplied by Goodman Fielder Milling and Baking Ltd., Summerhill, Sydney, NSW Australia) were balanced for starch and fiber content and were kept stored frozen at –20oC until required. ALF bread contained 38.5 g aleurone flour and 20.1 g of white flour per 100 g (wet weight) in comparison to PCS bread, which contained 11.3 g of pericarp-seed coat flour and 57.6 g white flour per 100 g (wet weight). The folate content (mean ± SEM of triplicate measurements) of ALF bread and PCS bread was 340 (±9) µg per 100 g (wet weight) and 112 (±15) µg per 100 g (wet weight) respectively. The folate content of PCS flour and white flour relative to aleurone flour was 24% and 3%, respectively. Using the latter figures and the relative amounts of different types of flour in the ALF and PCS breads we estimated (a) that in ALF bread 98.5% of the folate originated from aleurone flour and 1.5% from white flour and (b) that in PCS bread 61.8% of the folate content was due to the pericarp-seed coat flour and 38.2% was contributed by white flour. The ALF and PCS breads were cut into 70 g (wet weight) slices, which contained approximately 238 μg and 78 μg folate per slice, respectively. ALF and PCS breads were similar with regard to content of protein (10.5, 7.8 g/100 g wet weight), starch (26.6, 31.0 g/100 g wet weight), total dietary fiber (7.2, 7.0 g/100 g wet weight), and sugars (4.2, 4.3 g/100 g wet weight), respectively. Folic acid (mean of duplicate measurements) in the folic acid tablet and the placebo tablet was 640 μg and 26 μg folic acid, respectively. Volunteers were requested to (a) eat 2.5 slices (175 g wet weight) of the provided bread per day and (b) ingest one tablet per day of the tablets provided. They were also asked to keep to their customary diet and to refrain from ingesting folic acid supplements or foods that were supplemented with folic acid. The dose of the folic acid supplement in the tablet was chosen to produce a maximum effect on lowering of plasma homocyst(e)ine [24, 25]. The level of ALF or PCS flour in bread and the amount of bread eaten per day was the maximum possible without compromising palatability and compliance during the intervention. We chose PCS bread as the low-folate control to balance for starch and fiber content and thus minimize the possible effect of differences in bowel fermentation on folate status [26]. The low level of folic acid in the placebo tablet was unintended and caused by contamination with folic acid during formulation of the tablets. The intervention was of 16 weeks duration to maximize the detection of RBC folate changes because RBCs have a life-span of 120 days [27]. Blood samples were collected just before the start of the intervention and at 28-day intervals thereafter. RBC and plasma folate, plasma homocyst(e)ine, and vitamin B12 were measured at each time-point. The number of participants who completed every phase of the intervention was 25, 25, and 18 for the ALF, PCS, and FA groups, respectively. The
448
Fiber Ingredients: Food Applications and Health Benefits
Table 19.3 Daily Folate Intake (μg) from Supplied Tablets and Bread and Other Dietary Sources during the Long-Term (16-week) Intervention (arithmetic mean, 95% CI in parentheses) PCS group N = 25
ALF group N = 25
FA group N = 18
ANOVA Pa
Tabletsb 25 (24, 26)a 25 (25, 26)a 633 (625, 641)b < 0.0001 b a Bread 198 (182, 215) 590 (533, 647) 186 (167, 206)b < 0.0001 Other dietary 213 (175, 250) 220 (188, 253) 239 (203, 275) 0.4749 sources Total 436 (393, 478)b 836 (769, 903)a 1059 (1028, 1090)c < 0.0001 a Values not sharing the same superscript letter are significantly different from each other. b Values for tablets represent folic acid content. Source: Data from Fenech et al. [2].
dietary record data showed high compliance in tablet consumption in all groups (> 95%). Mean consumption rate of the supplied breads averaged between 2.4 and 2.5 slices per day (i.e., 167 to 178 g wet weight), and fruit, vegetable, breakfast cereal, and flesh food consumption was similar between groups. Using the dietary record and compliance data it was possible to estimate consumption of folate in the study groups (Table 19.3). Total daily folate intake in the ALF group (836 μg) was significantly lower than that in the FA group (1059 μg) but significantly greater than that in the PCS group (436 μg) (ANOVA P < 0.0001). Folate from the ALF bread contributed 70% of the folate intake in the ALF group. It was evident that dietary sources other than the supplied bread and tablets provided a significant proportion of the dietary folate (between 238 μg and 245 μg of total) in the three groups. Estimated folate intake from the dietary record was significantly correlated with plasma homocyst(e)ine (R = –0.55, P < 0.0001), plasma folate (R = 0.69, P < 0.0001), and red cell folate (R = 0.64, P < 0.0001) measured at the end of the intervention. There was no change in plasma folate levels in the PCS group during the course of the intervention. However, significant increments in plasma folate occurred in the ALF and FA groups at 4 weeks and subsequent sampling times with mean plasma folate levels increasing from 12.9 nmol/L and 17.5 nmol/L at baseline to 27.1 nmol/L and 40.1 nmol/L at 16 weeks, respectively. The percentage change in plasma folate at 16 weeks (adjusted for baseline level) (Figure 19.4a) in the ALF and FA groups was significantly elevated relative to the PCS group (P < 0.0001) and the increments observed in the FA group was 1.7 times greater than that observed for the ALF group (P < 0.0001). There was a 16% increment in RBC folate at 16 weeks (relative to baseline) in the PCS group during the course of the intervention (ANOVA P = 0.081). The increments in RBC folate in the ALF and FA groups were much greater achieving significant increases by 12 weeks of 50.9% and 79.2% relative to baseline, respectively (Figure 19.4b). The increment differences observed at 16 weeks between groups were statistically significant for
449
Aleurone Flour ANOVA P < 0.0001 c
FA
b
ALF
a
PCS 0
25
50
75 100 125 150 175 200 225
% Plasma Folate Change Relative to Baseline (a)
ANOVA P < 0.0001 c
FA
b
ALF
a
PCS
0 10 20 30 40 50 60 70 80 90 100 110 % RBC Folate Change Relative to Baseline (b)
ANOVA P = 0.0034 FA
ALF
b
b
a
PCS –40
–30
–20
–10
% Plasma Homocyst(e)ine Change Relative to Baseline (c)
0
Figure 19.4 Percentage change in (a) plasma folate, (b) RBC folate and (c) plasma homocyst(e)ine at 16 weeks relative to baseline. Percentage change was adjusted for baseline value. Mean values that do not share a common letter are significantly different from each other. FA, ALF, and PCS refer to the treatment groups. FA group: PCS bread + folic acid tablet (high folate control, N = 18); ALF group: ALF bread + placebo tablet (N = 25); PCS group: PCS bread + placebo tablet (low folate control, N = 25).
450
Fiber Ingredients: Food Applications and Health Benefits
all comparisons (Figure 19.4b). Significant reductions in plasma homocyst(e)ine were observed in the ALF group and the FA group only. The maximum homocyst(e)ine reduction in the ALF group from 9.1 μmol/L (at baseline) down to 6.8 μmol/L was observed at 8 weeks. In the FA group homocyst(e)ine was reduced from 8.1 μmol/L (at baseline) down to a minimum of 6.0 μmol/L at 16 weeks. A comparison of change in plasma homocyst(e)ine (adjusted for baseline level) showed that there was no significant difference between the ALF group and the FA group at 16 weeks (Figure 19.4c). The results from this study show for the first time that moderate intake of ALF is an effective strategy for raising red cell folate and lowering plasma homocyst(e)ine in individuals who were selected for their relatively low red cell folate and relatively high plasma homocyst(e)ine. Due to the relatively large differences between additional natural folate intake from bread in the ALF group relative to the FA group (i.e., 404 μg/d) and the additional folic acid intake from the tablet in the FA group (608 μg/d) and because intakes of folic acid > 400 μg/d are likely to maximize the homocyst(e)ine-lowering effect [25], it was not possible to calculate accurately the bioavailability and bioefficacy of ALF. Nevertheless it is evident that a relatively small daily intake of ALF bread (containing approximately 67 g ALF) can produce a homocyst(e)ine-lowering effect that is of a similar magnitude as that produced by a high dose folic acid tablet supplement, which suggests that natural folate in ALF has a high level of bioavailability and bioefficacy. The maximum mean decline in plasma homocyst(e)ine achieved in this intervention in the ALF group (–2.3 μmol/L) with a mean baseline of 9.1 μmol/L is greater than that obtained in a previous study with men aged 50 to 70 years (–0.8 μmol/L) with an initial mean plasma homocyst(e)ine of 9.3 μmol/L who were given 700 μg folic acid for two months followed by a further 2 months with 2000 μg folic acid and comparable to the reduction in young adults (aged 18 to 32 years) (–2.7 μmol/l) with an initial plasma homocyst(e)ine of 9.4 μmol/l given 7 μg vitamin B12 with 700 μg folic acid for three months [28, 29]. A meta-analysis of 12 clinical trials with folic acid involving 1114 people estimated that supplementation with 500 to 5000 μg/d folic acid should reduce plasma homocyst(e)ine by 23% in subjects who had 12 nmol/L folate and 12 μmol/L homocyst(e)ine in plasma before treatment [30]. Subjects in the ALF group in our study had an additional natural folate intake level of 404 μg/d from ALF, a pre-intervention plasma folate of 12.9 nmol/L, a plasma homocyst(e)ine of 9.1 μmol/L, and a 25% reduction (adjusted for baseline) in plasma homocyst(e)ine which is similar to the estimated effect for 500 to 5000 μg/d folic acid in the meta-analysis. Mandatory fortification of flour with folic acid has proven to be an effective and reliable method of preventing folate deficiency and possibly diseases caused by folate deficiency such as neural tube defects [31]. It is clear from the results of our study that ALF has the potential to be a practical alternative to folic acid fortification, which may be useful in those countries in which folic acid fortification is either not mandatory or is prohibited and for those sections of the community who may have a preference to eating natural sources
Aleurone Flour
451
of folate. ALF is also a rich source of a wide range of vitamins, minerals, and amino acids required for cell growth and maintenance that may provide additional health benefits to that provided by fortification with only folic acid [4, 32]. A direct comparison of ALF bread and bread made with folic acid–fortified flour is required to determine the relative performance of ALF bread for optimizing folate status as well as other measures of health status such as immune response and genome stability. These studies should also take into consideration the possibility of inter-individual differences in deconjugation and absorption of polyglutamated folate and the variation in folate content in ALF depending on cultivar, field conditions, and method of preparation. In conclusion, it is evident from the results of this study that ALF is a good source of bioavailable folate that can, at moderate intake levels, increase tissue folate and reduce plasma homocyst(e)ine substantially in humans. Although the studies shown used ALF in cereal and bread, it is evident that ALF can be readily included in other food preparations such as hamburger buns, pizza crust, muffins, pie crust, and pasta [3].
Safety and Toxicity There are, at this point in time, no reported cases of adverse reactions to intake of ALF. The folate studies, which are the only published human intervention studies with ALF, involved 16 adults in the short-term intervention and 79 adults in the long-term (16-week) study with daily intakes of aleurone flour equivalent to 90 g and 67 g ALF, respectively. In neither of these studies was there any evidence of toxicity. Unpublished data from the longterm study showed a reduction in DNA damage in lymphocytes measured using the cytokinesis-block micronucleus assay, which suggested a protective effect against chromosomal DNA damage. The puro-indoles PINA and PINB, which are strongly concentrated in the aleurone layer of wheat grain, have been shown to have antibacterial activity [33]; whether ALF at very high doses has any antibacterial activity or any detrimental effect on bowel bacterial populations remains unknown. The safe upper limit of ALF consumption has not been determined yet.
Summary In summary, aleurone flour has a strong potential as an important ingredient in functional foods from the baking industry because of its high micronutrient density as well as high fermentable fiber content. The bioavailability and bioefficacy of nutrients in aleurone flour deserve further attention as it
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likely that the health benefits of this important wheat fraction have yet to be fully realized. The possibility of extracting and using aleurone from other grains also needs to be investigated.
Acknowledgments Goodman Fielder Milling and Baking Pty. Ltd. (Sydney, Australia) are gratefully acknowledged for providing the cereal products and breads used in the folate studies. We would like to thank Josephine Rinaldi, Felicia Bulman, and Carolyn Salisbury for performing the blood folate measurements; Rodney Trimble for sample processing, total dietary fiber and free sugar measurements; Sylvia Usher for the total starch measurements; Caroline Cook for the total fat measurements; Ben Brinkman for performing the plasma homocyst(e)ine assays; Ben Scherer and Peter Royle for the nitrogen measurements. Rosemary McArthur and Clare Aitken are acknowledged for their important role in blood collections and blood sample preparation for analysis, respectively. Anne McGuffin and Kay Pender arranged appointments for the volunteers at the clinic, coordinated the supply of bread and tablets, and ensured that the food records were completed as required. Dr. Tony Bird is gratefully acknowledged for providing valuable advice regarding the composition data of the breads. Dr. Jayashree Arcot (University of New South Wales) is thanked for her assistance in measuring folate in the bread using the tri-enzyme method. Blackmore’s Ltd. is thanked for providing the tablets. Nick Stenvert and Wendy Morgan are duly acknowledged for their advice during the planning stages of the folate studies.
References
1. Fenech M, Noakes M, and Clifton P, Topping D (1999) Aleurone flour is a rich source of bioavailable folate in humans. J. Nutr. 129:1114–1119. 2. Fenech M, Noakes M, Clifton P, and Topping D (2005) Aleurone flour increases red cell folate and lowers plasma homocyst(e)ine in humans. Brit. J. Nutr. 93(3):353–60. 3. Earling J, Atwell B, and von Reding W (2005) Wheat aleurone. Am. Inst. Baking Tech. Bull. 28(7):1–11. 4. Clysedale FM (1994) Optimising the diet with whole grains. Crit. Rev. Food Sci. Nutr. 34:453–471. 5. Saxelby C, and Venn-Brown U (1980) The structure and composition of the wheat grain. In The Role of Australian Flour and Bread in Health and Nutrition. Glenburn Pty. Ltd., Chatswood Australia, pp. 37–41.
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6. Stenvert N (1995) New high fibre bread — Farrer’s Gold. Food Australia 47(10):462–463. 7. Stenvert N (1997) Novel natural products from grain fractionation. In Cereals — Novel Uses and Processes, Cambell GM, Webb C, and McKee SL, eds., Plenum Press, New York, 241–245. 8. Zhou K, Laux JJ, and Yu L (2004) Comparison of Swiss red wheat grain and fractions for their antioxidant properties. J. Agric. Food Chem. 52(5):1118–23. 9. Dong WG, Liu SP, Yu BP, Wu DF, Luo HS, and Yu JP (2003) Ameliorative effects of sodium ferulate on experimental colitis and their mechanisms in rats. World J. Gastroenterol. 9(11):2533–8. 10. Kawabata K, Yamamoto T, Hara A, Shimizu M, Yamada Y, Matsunaga K, Tanaka T, and Mori H (2000) Modifying effects of ferulic acid on azoxymethaneinduced colon carcinogenesis in F344 rats. Cancer Lett. 157(1):15–21. 11. Cheng BQ, Trimble RP, Illman RJ, Stone BA, and Topping DL (1987) Comparative effects of dietary wheat bran and its morphological components (aleurone and pericarp-seed coat) on volatile fatty acid concentrations in the rat. Br. J. Nutr., 57:69–76. 12. McIntosh GH, Royle PJ, and Pointing G (2001) Wheat aleurone flour increases cecal beta-glucuronidase activity and butyrate concentration and reduces colon adenoma burden in azoxymethane-treated rats. J. Nutr. 131(1):127–31. 13. Bailey LB (1995) Folate requirements and dietary recommendations. In: Folate in Health and Disease, Bialey L.B. ed., Marcel Dekker, New York, 123–151. 14. Subar AF, Block G., and James LD (1989) Folate intake and food sources in the U.S. population. Am. J. Clin. Nutr. 50:508–516. 15. Crane CT, Wilson DB, Cook DA, Lewis CJ, Yetley EA, and Rader JI (1995) Evaluating food fortification options: General principles revisited with folic acid. Am. J. Pub. Health 85: 660–666. 16. Czeizel AE, and Dudas I (1992) Prevention of first occurrence of neural tube defects by periconceptional vitamin supplementation. N. Engl. J. Med. 327:32–35. 17. MRC Vitamin Study Research Group (1991). Prevention of neural tube defects: results from the Medical Research Council Vitamin Study. Lancet 338:131–137. 18. Boushey CJ, Beresford SA, Omenn GS, and Motulsky AG (1995) A quantitative assessment of plasma homocyst(e)ine as a risk factor for vascular disease: probable benefits of increasing folic acid intakes. J. Am. Med. Assoc. 274:1049–1057. 19. Kang SS, Wong PWK, and Malinow MR (1992) Hyperhomocyst(e)inemia as a risk factor for occlusive vascular disease. Annu. Rev. Nutr. 12:279–298. 20. Blount BC, Mack MM, Wehr CM, MacGregor JT, Hiatt RA, Wang G, Wickramasinghe SN, Everson RB, and Ames BN (1997) Folate deficiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal damage. Proc. Natl. Acad. Sci. 94:3290–3295. 21. Fenech M (2001) The role of folic acid and vitamin B12 in genomic stability of human cells. Mutation Res. 475:56–67. 22. Cuskelly GJ, McNulty 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. 23. Holland B, Welch AA, Unwin ID, Buss DH, Paul AA, and Southgate DAT (1995) McCance and Widdowson’s: The Composition of Foods (5th Ed.) Xerox Ventura Publisher, UK.
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24. Rydlewicz A, Simpson JA, Taylor RJ, Bond CM, and Golden MHM (2002) The effect of folic acid supplementation on plasma homocysteine in an elderly population. Q. J. Med. 95:27–35. 25. van Oort FVA, Melse-Boonstra A, and Brouwer IA (2003) Folic acid and plasma homocysteine reduction in older adults: a dose-finding study. Am. J. Clin. Nutr. 77:1318–1323. 26. Rong N, Selhub J, Goldin BR, and Rosenberg IH (1991) Bacterially synthesized folate in rat large intestine is incorporated into host tissue folyl polyglutamates. J. Nutr. 121:1955–1959. 27. Cooper RA, and Jandl JH (1972) Destruction of erythrocytes. In Haematology, Williams WJ, Beutler E, Erslev AJ, and Rundles RW (Eds.), McGraw-Hill Book Company, New York, 178–191. 28. Fenech M, Dreosti IE, and Rinaldi JR (1997) Folate, vitamin B12, homocyst(e)ine status and chromosome damage rate in lymphocytes of older men. Carcinogenesis 18(7):1329–1336. 29. Fenech M, Aitken C, and Rinaldi J (1998) Folate, vitamin B12, homocysteine status and DNA damage in young Australian adults. Carcinogenesis 19(7):1163–1171. 30. Homocyst(e)ine Lowering Trialists’ Collaboration. (1998) Lowering blood homocyst(e)ine with folic acid based supplements: meta-analysis of randomised trials. BMJ 316:894–898. 31. Honein MA, Paulozzi LJ, Mathews TJ, Erickson JD, and Wong LY (2001) Impact of folic acid fortification of the U.S. food supply on the occurrence of neural tube defects. JAMA 285:2981–2986. 32. Hinton JJ, Peers FG, and Shaw B (1953). The B vitamins in wheat — the unique aleurone layer. Nature 172 (4387):993–995. 33. Capparelli R, Amoroso MG, Palumbo D, Iannaccone M, Faleri C, and Cresti M (2005). Two plant puroindoles colocalise in wheat seed and in vitro synergistically fight against pathogens. Plant Mol. Biol. 58(6):857–867.
Appendix: Suppliers of Dietary Fiber Ingredients
Sponsors The editors wish to acknowledge a generous sponsorship from the following companies:
Dow Chemical: cellulose, hydroxypropylmethyl cellulose JRS USA: oat fiber, bamboo fiber, wheat fiber and other Vitacel line Roquette America: Nutriose (resistant maltodextrin) Wacker Chemical: Alpha-cyclodextrin
Alpha Cyclodextrin Wacker Chemical: CAVAMAX® W6 Alpha Cyclodextrin: Wacker Chemicals is the global leader in cyclodextrin products. All CAVAMAX® cyclodextrins are FDA notified GRAS. CAVAMAX® W6 is a colorless natural dietary fiber. It is heat stable even under acidic conditions and stable in carbonated beverages. With a viscosity like sucrose, a neutral taste, and no browning effect it can be used even in complex food systems. CAVAMAX W6 also lowers the glycemic index of starch containing food. www.wacker.com E-mail:
[email protected] Physical address: 3301 Sutton Road, Adrian, MI 49221-9397, USA Phone number & contact information–sales: From North America: Call +1 517 264 8671 Fax +1 517 264 8795 Aleurone Cargill: GrainwiseTM: The isolated aleurone layer of wheat bran, a concentrated source of vitamins, minerals, and fiber www.horizonmilling.com/products/products_GWwheataleurone. shtml E-mail:
[email protected] Physical address: 15407 McGinty Road W. MS 61, Wayzata MN 55391 455
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North America: Call 1-800-742-4506 Fax 1-952-742-4050 Cellulose, Hydroxymethylpropyl Cellulose (HMPC, Soluble Cellulose) Dow Chemical FORTEFIBER™ soluble dietary fiber from cellulose FORTEFIBER™ HB Plus (Medium Viscosity) FORTEFIBER™ HB Ultra (High Viscosity): The products have been shown to help maintain healthy levels of cholesterol, blood glucose, and insulin. www.fortefiber.com E-mail:
[email protected] Physical address: 1650 N. Swede Rd, Larkin 100, Midland, Mi 48674, USA Phone number & contact information–sales: From North America: Call 1-800-488-5430 Fax 1-989-638-9836 From Europe, India, Africa and the Middle East: Toll-free +800 3 694 6367* Toll-free for Italy +800 783 82 Call +32 3 450 2240 Fax +32 3 450 2815 From Latin America: Call +55 11 5188 9222 Fax +55 11 5188 9749 From the Pacific: Toll-free call 800 7776 7776** Toll-free fax 800 7779 7779 Call +60 3 79583392 Fax +60 3 7958 5598 Cellulose International Fiber Corporation: Alpha-cel, Keycel, and QualFlo International Fiber Corporation 50 Bridge Street North Tonawanda, New York 14120
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www.ifcfiber.com;
[email protected] Phone: 1-888-698-1936 or +1-716-693-4040 Fax: +1-716-693-3528 Jean-Dominique Verstreken B-9140 Temse Belgium Tel: +32-3-7111636 Fax: +32-3-7713399
[email protected] Tom Yu Shanghai, 200040 China Tel: +86-21-6249-6576 Fax: +86-21-6249-4459
[email protected] SunOpta Ingredients Group T: 781-276-5118 F: 781-276-5101 Corn Bran Cargill: MaizeWise™ Corn Bran Products MW80 - 80% Total Dietary Fiber Corn Bran MW60 - 60% Total Dietary Fiber Corn Bran and Cooked Corn Bran Description/Application MaizeWise™ corn bran is an insoluble fiber that can dramatically boost dietary fiber at low to moderate inclusion rates, while providing minimal impact to flavor, texture, color, and processing characteristics. Contact Information Bryan Wurscher Commercial Manager Cargill Dry Corn Ingredients Tel: 1 952 742 2518 Fax: 1 952 742 4573 website: www.cargilldci.com
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Gum Arabic (Acacia gum) Colloïdes Naturels International FORTEFIBER™ and its organic-certified versions, FIBREGUM™ BIO & FIBREGUM™ BIO L, are all-natural soluble dietary fibers (guaranteed 90% minimum level) from Acacia Gum. Website address: www.cniworld.com E-mail:
[email protected] France 129 Chemin de Croisset - BP 4151 - 76723 Rouen cedex 3 Ph: +33 (0) 2.32.83.18.18 Fax: +33 (0) 2.32.83.19.19 U.S.A. Colloïdes Naturels, Inc 1140 US Highway 22 East, Center Point IV, Suite 102 Bridgewater, NJ 08807 Ph: +1.908.707.9400 Fax: +1.908.707.9405 Brazil Colloïdes Naturels Brasil Comercial Ltda. Av. Pompéia, 2289 – Sumarézinho - CEP 05023-001 Sao Paulo-SP Ph/Fax: +55.11.3862.2028 Mexico Colloïdes Naturels de Mexico, S.A. de C.V. 20, Calle Magdalena Col. del Valle - C.P. 03100 Mexico D.F. Ph: +52.55.55.36.83.83 Fax: +52.55.55.43.41.45 United Kingdom Colloïdes Naturels, UK Ltd The Triangle Business Centre - Exchange Square - M4 3TR - Manchester Ph: +44 (0) 161.838.5744 Fax: +44 (0) 161.838.5746 Inulin/Fructo-oligosaccharides Orafti BENEO™ L60/L85/L95/P95 (Oligofructose) BENEO™ ST/GR/ST-Gel (Inulin) BENEO™ HP/HP-Gel/HPX (long-chain inulin)
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BENEO™ HSI (high-soluble inulin) BENEO™ Synergy1 (Oligofructose-enriched inulin): The products are prebiotic dietary fibers and have been shown to contribute to gut health, better calcium absorption and immunity. Website address BENEO:
[email protected] www.orafti.com E-mail:
[email protected] Headquarters ORAFTI Active Food Ingredients Aandorenstraat, 1 3300 Tienen Belgium Call + 32 16 801 301 Fax + 32 16 801 308 US Office Corporate Office 2740 Route 10 West, Suite 205 Morris Plains, NJ 07950 USA Call + 1 973 867 2140 Fax + 1 973 867 2141 Sensus Frutafit® and Frutalose® inulin and oligofructose from the chicory root Frutafit® HD (Highly Dispersable) Frutafit® IQ (Instant Quality) Frutafit® TEX! (Texturizing) Frutafit® CLR (Highly Soluble) Frutalose® L90 (Sweet Liquid Fiber) Head Office Sensus Operations C.V P.0. Box 1308 4700 BH Roosendaal The Netherlands Phone: +31 165 582 578 Fax: +31 165 567 796 E-mail:
[email protected] www.sensus.nl
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North American Office Sensus America, Inc. 1 Deer Park Dr., Suite J Monmouth Junction, NJ 08852 Phone: 1-646-452-6150; 1-866-456-8872 Fax: 1-646-452-6150 E-mail:
[email protected] www.sensus.us Cargill Oliggo-Fiber™ Instant (Native) Oliggo-Fiber™ XL (Fat mimetic properties) Oliggo-Fiber™ F97 (High solubility) www.cargill.com E-mail:
[email protected] Physical address: 15407 McGinty Road West, Wayzata, MN 55391 Oat Beta Glucan Foodfiles www.foodfiles.com E-mail:
[email protected] Physical address: Neulaniementie 2 L 6, FI-70210 Kuopio, FINLAND Phone number & contact information: Call + 358 – 17 – 288 1270 Fax + 358 – 17 – 288 1269 ConAgra Foods, Inc. Nutrition Center of Excellence Six ConAgra Drive, 6-475 Omaha, NE 68102 402-595-7688 Oat Fiber JRS (J. RETTENMAIER & SÖHNE) Vitacel® Oat Fibers: Vitacel® Oat Fibers are available in a variety of grades suitable for use in meat, bakery, cereal and beverage applications for fiber fortification, calorie reduction and structural enhancement.
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Website address: www.jrsusa.com www.jrs.de E-mail:
[email protected] Contact for USA & Canada J. Rettenmaier USA LP 16369 US Highway 131 Schoolcraft, MI 49087 Phone: (269) 679 2340 Toll Free: (877) 895 4099 Fax: (269) 679 2364 Contact outside USA and Canada J. RETTENMAIER & SÖHNE GmbH + Co. KG Holzmühle 1 D-73494 Rosenberg (Germany) Tel.: ++49 - (0) 79 67 - 1 52-0 Fax: ++49 - (0) 79 67 - 1 52-2 22 Partially Hydrolyzed Guar Gum (PHGG) Taiyo International, Inc. SUNFIBER® soluble dietary fiber SUNFIBER® R (regular) SUNFIBER® AG (agglomerated): Sunfiber® has been clinically shown to maintain digestive health and micro-flora balance, lower glycemic index, improve mineral absorption, inhibit gas production and control symptoms of IBS. www.taiyointernational.com and www.sunfiber.com E-mail:
[email protected] Physical address: 5960 Golden Hills Drive, Minneapolis, MN 55416 North America: Taiyo International, Inc. 5960 Golden Hills Drive Minneapolis, MN 55416 Call 1-763-398-3003 Fax 1-763-398-3007
[email protected] From Europe: Call +49-711-779-8291 Fax +49-711-779-8292
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Japan: Call +81-593-47-5427 Fax +81-593-47-5438 Latin America: Call 1-763-398-3003 Fax 1-763-398-3007 China: Tel: 86-21-6876-6828 Fax: 86-21-6876-6830 Korea: Tel: 82-2-571-7588 Fax: 82-2-571-7589 Pectin Herbstreith & Fox KG Pektin-Fabrik Neuenbuerg Turnstrasse 37 D-75305 Neuenbuerg/Germany
[email protected] http://www.herbstreith-fox.de Phone: +49 7082 7913 0 Fax: +49 7082 20281 Resistant Maltodextrin Editors feel that Nutriose and Fibersol-2 share a similar chemical structure and physicochemical properties. Both ingredients can be categorized into resistant maltodextrin. Roquette: Nutriose www.Roquette.com Roquette Frères Corporate headquarters 62080 LESTREM Cedex Tel: + 33 3 21 63 36 00 Fax: + 33 3 21 63 38 50 ROQUETTE AMERICA Inc. 1417 Exchange Street
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P.O. Box 6647 KEOKUK. IA 52632–6647 Phone: (1) 319 524 5757 Fax: (1) 319 526 2345 ROQUETTE JAPAN K.K. Tokyo Head Office 2F, Kasuga Business Center Building 1-15-15 Nishikata Bunkyo-Ku, TOKYO 113-0024 Phone: +81 3 38301510 IP phone +81 350 5514 9041 Fax: +81 3 38301525 E-mail:
[email protected] Matsutani Chemical : Fibersol®-2 Fibersol®-2 (dietary fiber ≥90%) Fibersol®-2H (hydrogenated Fibersol®-2, available in Asia-Pacific region) Fibersol®-2 is a soluble dietary fiber that helps promote intestinal regularity and healthy levels of blood glucose, insulin, and triglyceride. Website address: www.matsutani.com Physical address: Matsutani Chemical Industry Co., Ltd. 5-3 Kita-itami, Itami, Hyogo 664-8508 Phone number: +81-72-771-2013 Fax number: +81-72-771-7447 E-mail address:
[email protected] Resistant Starch National Starch Hi Maize 5 in 1 fiber and Novelose Benefits range from weight management, glycemic (blood sugar) management, energy management, and digestive health. More than 40 studies in humans using natural Hi-maize and Novelose provide a high level of confidence that the benefits are reliable and real. National Starch and Chemical Company 10 Finderne Ave Bridgewater, NJ 08807 1-800-743-6343
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UK, Ireland, Nordic Europe Dagmar Krappe Gruener Deich 110 20097 Hamburg, Germany Tel: +49 (0) 40-23915-0 Australia 7 – 9 Stanton Road Seven Hills, Sydney NSW 2147, Australia Tel: +61 2-9624-6022 Germany Colloïdes Naturels International GmbH Walter-Kolb-Str. 9-11 - D - 60594 Frankfurt am Main Ph: +49 (0) 69.96.21.76.18 Fax: +49 (0) 69.96.21.76.19 Russia ZAO “Colloïdes Naturels Vostok” (Stroikomtech) - 11, Kravchenko Str. - 119 415 Moscow Ph: +7.495.935.9510 Fax: +7.495.131.2609 Japan Colloïdes Naturels Japan Inc. Miseki Bldg, 2F - Uguisudani-cho 18-1 - Shibuya-Ku - Tokyo 150-0032 Ph: +81.3.3463.6511 Fax: +81.3.3463.6522 China Colloïdes Naturels International 2/F Mayfair Tower - 83 Fu Min Road - Shanghai 200040 Ph: +86.21.6132.7186/6132.7187 Fax: +86.21.6132.7199 Sugar Beet Fiber Danisco and IFC Fibrex
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Other Fibers: Bamboo Fiber, Sugar Cane Fiber, and Cottonseed Fiber JRS: Vitacel line International Fiber Corporation: JustFiber® line including cottonseed fiber, white wheat fiber and bamboo fiber Becky Finn North Tonawanda, NY 14120 U.S.A. Tel: +1-888-698-1936 Fax: +1-716-693-3528
[email protected] www.ifcfiber.com Soy Fiber The Solae Company USA PO Box 88940 St. Louis, MO 63188 Local: (314)659-3000 Phone: (800)325-7108 Europe Solae Europe S.A. 2, chemin du Pavillon CH-1218 Le Grand-Saconnex Geneva Switzerland Tel.: + 41 22 717 6420 Fax: +41 22 717 6401
Index
A Abdominal pain partially hydrolyzed guar gum, 96 psyllium, 405, 409 Abscesses, 395 Absorption, 27–29 Acacia gum bakery products, 130 beverages, 129 breakfast cereals, extruded, 130 cereal bars, 130 characteristics, 121–123 cholesterol, 127–128 confectionery, 130–131 constipation, 125–126 defined, 121–122 diarrhea, 125–126 extruded snacks and breakfast cereals, 130 food product applications, 128–131 health benefits, 125–128 hypoglycemic effect, 127–128 metabolism, 123 nitrogen excretion, 126–127 nutritional aspects, 123–125 prebiotic effect, 123–125 safety, 122–123 snacks, extruded, 130 suppliers, 458 tolerance, 123 Acesulfame K, 75 Acetate, 91, see also Short-chain fatty acids (SCFA) Acetic acids, 91, see also Short-chain fatty acids (SCFA) Acetobacter xylinum, 271 Acidic conditions acacia gum, 129 inulin, 46 Nutriose soluble fiber, 35 Activated Barley, 336 Acute intestinal infections, 148–149
Acute postprandial glycemic responses, 86–87 Adamii studies, 277 Adequate intake, vii Adverse effects partially hydrolyzed guar gum, 107–108 psyllium, 411 Aerated desserts, 55 Aftertaste, 45 Agama-Acevedo studies, 208 Ahotupa, Vasankari and, studies, 179 Ahrens, Scholz and, studies, 102 Aitken, Clare, 452 Alam studies, 87, 89, 91, 93–94 Aleurone flour, 442 Aleurone flour (ALF) characteristics, 439–440 folate levels, 443–451 food applications, 440–451 functionality, 440–451 fundamentals, 451–452 human studies, 443–451 physiological benefits, 440–451 rat studies, 442–443 safety, 451 suppliers, 455–456 toxicity, 451 Alginates, 54, 81 Allergies, 396 Alles studies, 237 Alpha-cell, 456–457 Alpha-cyclodextrin (α-CD) characteristics, 9–10 food applications, 11 functionality, 11 fundamentals, 14–15 physiological benefits, 11–13 safety and toxicity, 13–14 suppliers, 455 Aman studies, 286, 336 American Heart Association Step 1 diet, 89 467
468 Ames studies, 333, 336 Amino acids, 313 Analysis polydextrose, 184 resistant starch, 216–217, 222–223 Anderson studies, 250, 254, 257, 408 Animal studies, see also specific animal barley fiber, 337, 342, 346–347 guar gum, 82 hydroxypropylmethylcellulose, 270 partially hydrolyzed guar gum, 104 psyllium, 408 resistant starch, 222, 238 rice bran, 315–316 Annison and Topping studies, 206, 208 Annison studies, 208 Anorectal surgery, 410 Antibacterial activity, 451 Anti-caking effect, 110 Anticarcinogenic properties and effects partially hydrolyzed guar gum, 108 psyllium, 405–406 Anti-inflammatory effects, 405, see also Inflammation Anti-neoplastic effects, 405 Antioxidation aleurone flour, 439 partially hydrolyzed guar gum, 110 sugar beet fiber, 382 Antitussive effects, 396 AOAC methods definition of fiber, 2 pectin, 136 polydextrose, 184 resistant maltodextrin, 75–76 resistant starch, 222–223 sugar beet fiber, 363 Apoptosis psyllium, 406 resistant starch, 231 Appearance, 36 Appetite modulation, see also Satiety guar gum, 82 inulin, 51–52 polydextrose, 183 Apple fiber, 430 Apple juice fruit fiber, 428 oat beta-glucan, 286
Index Apple pectin cholesterol reduction, 151 sources, 140–141 texture, 157 Approved health claims, see Health claims AQ Plus citrus fiber, 430 Arabinogalactan, 94 Arcot, Jayashree, 452 Arginine levels, 105 Aro studies, 98 Arteriosclerosis, 142 Artificial sweeteners, 110 Artiss studies, 12 Aruga studies, 106 Asp, Nyman and, studies, 375 Asparagus, 43 Aspartame, 75 Aspergillus niger partially hydrolyzed guar gum, 84 sugar beet fiber, 372 Asp studies, 209 Atherosclerosis, 149–150 Auerbach studies, 175, 183, 197 Available calories, 237, see also Caloric value Avicel, 271 Ayano studies, 312
B Bacterial adaptation, 91, see also specific type Bacterial biomass acacia gum, 124 inulin, 47, 48 polydextrose, 178 resistant starch, 227 Bacterial overgrowth, 107–108 Bacteroides spp. acacia gum, 124 Nutriose soluble fiber, 33 pectin, 142 resistant maltodextrin, 65, 67 resistant starch, 230 Bacteroides ovatus, 142 Bacteroides succinogenes, 265 Bacteroides thetaiotaomicron, 143 Bacteroidetes spp., 34
Index Baik and Czuchajowska studies, 331–332 Bakery products and applications acacia gum, 130 aleurone flour, 451 alpha-cyclodextrin, 11 barley fiber, 332–335 fruit fiber, 431–432 guar gum, 81 inulin, 50, 54 Nutriose soluble fiber, 28, 35, 36, 37 oat beta-glucan, 287, 289, 292 oat fiber, 250, 252–253 partially hydrolyzed guar gum, 109–110 pectin, 159 polydextrose, 187, 189, 194 sugar beet fiber, 373–374, 383 Baltes, Stumm and, studies, 175 Bamboo fiber, 465 Bananas (green), 149 Baray studies, 121–131 Barley fiber bakery products, 332–334 beta-glucan extracts, 334–335 blood pressure, 344 cancer, 344–345 cardiovascular disease, 338–342 characteristics, 323–329 digestion, 337 extrusion, 329–332 food applications, 329–337 functionality, 329–337 glucose response, 342–344 immune response, 344–345 insulin response, 342–344 meats, 334 miscellaneous, 336–337 physiological benefits, 337–345 safety, 346–347 toxicity, 346–347 Barley oil, 342 Barliv Barley Betafiber, 335 Basman studies, 333 Beauty supplementation, 103–104 Becker, Siddhuraju and, studies, 209 Bednar studies, 209 Beef, beef patties, and beef burgers barley fiber, 334 cellulose, 271 oat fiber, 253
469 polydextrose, 195 Beer studies, 287, 293 Beet fiber, see Sugar beet fiber Behall and Howe studies, 237 Behall studies, 234, 237, 338, 343–344 Benefits, physiological alpha-cyclodextrin, 11–13 Nutriose soluble fiber, 28–29 Beneo appetite and food intake modulation, 52 suppliers, 458–459 Berglund studies, 331, 333 Beringer and Wenger studies, 51 Berry studies, 217, 254 Betafiber, 378 Beta-glucan extracts, see also Oat betaglucan barley fiber, 334–335 characteristics, 284 Beverages acacia gum, 129 barley fiber, 335–336 cellulose, 271 Nutriose soluble fiber, 28, 37 oat beta-glucan, 287 partially hydrolyzed guar gum, 92, 98–99, 110 pectin, 158–159 polydextrose, 193, 195 psyllium, 396 resistant starch, 216 Bhatty, Vasanthan and, studies, 329 Bhatty studies, 326, 328, 332 Bifidobacteria spp. acacia gum, 123–124 inulin, 49–50, 52 partially hydrolyzed guar gum, 95–96 pectin, 143 polydextrose, 182 resistant starch, 230 Bifidobacteria adolescensis, 124 Bifidobacteria longum, 124 Bifidobacterium spp. barley fiber, 337 partially hydrolyzed guar gum, 95 pectin, 142, 144 resistant maltodextrin, 65, 67 Bifidobacterium angulatum, 144
470 Bifidobacterium bifidum, 144 Bifidobacterium infantis, 144 Bifidobacterium pseudolongum, 143 Bifidogenic effect, 49 Bile acids cellulose, 267 guar gum, 82 oat beta-glucan, 293 partially hydrolyzed guar gum, 88–89 pectin, 149, 151 psyllium, 395, 397, 407, 408 rice bran, 316 rice bran oil, 312–313 sugar beet fiber, 372, 376, 378, 382 Binders/extenders, 252 Binders (tablets) acacia gum, 131 cellulose, 271 polydextrose, 196 Bingham studies, 1 Biorklund studies, 338, 343 Bird studies, 227, 230, 452 Birkett studies, 205–239 Birkitt studies, 266 Biscuits, see also Bakery products and applications barley fiber, 332, 333–334 Nutriose soluble fiber, 28 sugar beet fiber, 373, 383 Bjorck, Liljeberg and, studies, 342 Björklund studies, 287, 293, 296 Blake studies, 89 Blanchet studies, 86 Bloating alpha-cyclodextrin, 13, 14 barley fiber, 346 Nutriose soluble fiber, 25, 28 partially hydrolyzed guar gum, 86, 92, 96 Blockages, 107 Blood cholesterol concentration levels, see Cholesterol Blood glucose, see Glucose metabolism and response Blood lipids, see Lipid metabolism Blood pressure barley fiber, 344 psyllium, 395 Bodner studies, 249–259
Index Body composition, 238 Body fat alpha-cyclodextrin, 12–13 resistant maltodextrin, 71–72 Body weight, see also Weight management and control hydroxypropylmethylcellulose, 270 inulin, 48 partially hydrolyzed guar gum, 89 Bologna barley fiber, 334 oat fiber, 253–254 Bond studies, 334 Bone mineral content inulin, 52–53 polydextrose, 182 Borborygmi, 383 Bosscher studies, 41–55 Bourquin studies, 258 Bowel function, see also Intestinal regularity; Stools partially hydrolyzed guar gum, 93 polydextrose, 178 resistant maltodextrin, 65 Braaten studies, 293, 296 Bran Buds, 396 Breads, see also Bakery products and applications aleurone flour, 440, 446–451 barley fiber, 332, 333, 335, 343, 346 inulin, 50 Nutriose soluble fiber, 28, 36 oat beta-glucan, 287, 289, 289, 292, 296 oat fiber, 253 partially hydrolyzed guar gum, 98–99 psyllium, 396 resistant starch, 208, 234 sugar beet fiber, 373–374, 383 Breakfast cereals acacia gum, 130 aleurone flour, 444–446 barley fiber, 329 inulin, 54 oat beta-glucan, 286, 296 Breath freshener, 11 Brennan, Symons and, studies, 334 Brewer’s spent grain (BSG), 342 Brinkman, Ben, 452 Brouns studies, 5
471
Index Brownies, 431–432, see also Bakery products and applications Brown studies, 206–210, 216, 230–231, 234, 288 BSG, see Brewer’s spent grain (BSG) Buckley studies, 9–15 Bulking effect barley fiber, 331 inulin, 48–49 sugar beet fiber, 374 Bulking ingredient cellulose, 271 inulin, 45 Bulman, Felicia, 452 Buns, see also Bakery products and applications aleurone flour, 451 oat beta-glucan, 289 Burdock and Flamm studies, 184 Burgers, see Beef, beef patties, and beef burgers Burkitt and Trowell studies, 1–2 Burkitt studies, 2 Butyrate, see also Short-chain fatty acids (SCFA) aleurone flour, 443 partially hydrolyzed guar gum, 91 psyllium, 406 resistant starch, 230 sugar beet fiber, 382 Butyric acid, see Short-chain fatty acids (SCFA) Butyrivibrio fibrisolvens, 143 Byrnes studies, 236
C Cadmium barley fiber, 347 pectin, 146 Cakes, see also Bakery products and applications polydextrose, 187 sugar beet fiber, 373 Calcium aleurone flour, 439 barley fiber, 346–347 cellulose, 277 inulin, 53
oat beta-glucan, 298 partially hydrolyzed guar gum, 102–103 pectin, 139, 145, 147 polydextrose, 182 psyllium, 411 sugar beet fiber, 376 Caloric value acacia gum, 123 inulin, 47 Nutriose soluble fiber, 34–35 partially hydrolyzed guar gum, 107 polydextrose, 183 resistant maltodextrin, 75 resistant starch, 237 Calorie-reduced foods, see Low-calorie products Calories, available, 237 Calvert studies, 100 Cameron studies, 250, 257–258 Cancer alpha-cyclodextrin, 12 approved health claims, 3 barley fiber, 344–345 inulin, 52 pectin, 154–156 sugar beet fiber, 381–382 Candida albicans, 50 Canine studies, see Dog studies Capsules, 159 Carbohydrates alpha-cyclodextrin, 11 cellulose functionality, 267, 269 resistant starch comparison, 229 Carcinogenesis, 266 Cardiovascular disease, see also Coronary heart disease; Heart disease aleurone flour, 443 alpha-cyclodextrin, 11, 12 barley fiber, 338–342 psyllium, 406–409 Carrageen gum, 81 Carriers, 11 Caseinate replacement, 54 Cashman, Kennefick and, studies, 347 Cataracts, 395 Cat studies, 266 Cattle studies, 257, 258 Cavallero studies, 343
472 CAVAMAX W6, 455 Cecal enlargement, 14 Celiac disease barley fiber, 347 oat beta-glucan, 298 Cell proliferation, 266 Cellulose blood glucose, 268 carbohydrates, 267, 269 carcinogenesis, 266 cell proliferation, 266 characteristics, 263–264 constipation, 264–265 dilution effect, 266 fats, 267 fermentation, 265 flow behavior, 275–276 food applications, 271–272 functionality, 264–271 gastric emptying blood glucose, 268 hydroxypropylmethylcellulose, 270–271 insulin, 268 intestines, water absorption, 269–270 large intestine fermentation, 265 mixing-in behavior, 272–275 nutrients interrelationship, 276 oat fiber, 251 peristalsis, 275 physiological benefits, 270–271, 272–276 proteins, 270 psyllium comparison, 411 resistant starch, 232 safety, 277 segmentation, 276 stool output, 264–265 sugar beet fiber, 369–370 suppliers, 456–457 technology, 277 water absorption, intestines, 269–270 Ceolus, 271 Cereal products acacia gum, 130 aleurone flour, 440 barley fiber, 335 cellulose, 271 fruit fiber, 429 inulin, 54 Nutriose soluble fiber, 36
Index oat beta-glucan, 289 oat fiber, 251 pectin, 159 psyllium, 396 resistant starch, 209 sugar beet fiber, 373–374 Cereals aleurone flour, 444–446 oat beta-glucan, 286, 289, 290–291, 296 sugar beet fiber, 373 Cergen, 288 Champ studies, 217, 222 Characteristics acacia gum, 121–123 aleurone flour, 439–440 alpha-cyclodextrin, 9–10 barley fiber, 323–329 cellulose, 263–264 oat beta-glucan, 283–284 oat fiber, 252 psyllium, 393–395 sugar beet fiber, 361–372 Cheese and cheese products, see also Dairy products cellulose, 271 inulin, 54 pectin, 158 Chemically modified starch, 210, 216 Chemical properties and structure inulin, 42, 45–46 pectin, 136–138 psyllium, 395 resistant starch, 206 Cheng studies, 442 Cherbut studies, 378 Chicken products, 334 Chicks and chicken studies cellulose, 272, 275 oat fiber, 255, 256 partially hydrolyzed guar gum, 103 rice bran, 313–314 Chicory, 43, 45 Chilling, 395, see also Freezing Chiu, Henley and, studies, 208–209 Chiu studies, 208–209 Cho and Prosky studies, 2 Chocolate confectionery polydextrose, 194 Chocolate products, 383 Choe studies, 178
Index Cholera toxin, 125 Cholesterol, see also Lipid metabolism; Triglyceride levels acacia gum, 127–128 alpha-cyclodextrin, 13 barley fiber, 337–338 guar gum, 82 hydroxypropylmethylcellulose, 270 inulin, 48 oat beta-glucan, 289, 293 partially hydrolyzed guar gum, 85, 88–90 pectin, 150–152 polydextrose, 178–179 psyllium, 407, 409 resistant maltodextrin, 70–71 rice bran, 309–315, 312 rice bran oil, 310, 312–313 sugar beet fiber, 378, 381 viscous dietary fiber, 20 Cholestyramine, 378 Cho studies, 1–5, 249–259 Chromatography inulin, 44 Nutriose soluble fiber, 21 Chromium, 146 Cichorium intybus, 45 Cigar wrappers, 81 Cihan studies, 108 Citracel, 100 Citrobacter spp., 148 Citrus pectin cancer, 155–156 sources, 140–141, 429 texture, 157 Ciukanu and Kerek studies, 176 Classification, resistant starch, 206–208 Clifton studies, 439–452 Clostridia spp., 49 Clostridium spp., 124 Clostridium butyricum inulin, 50 resistant starch, 230 Clostridium difficile, 50 Clostridium lochhradii, 265 Clostridium perfringens inulin, 52 Nutriose soluble fiber, 31, 34 Coates studies, 9–15 Cobalt, 146
473 Coffee, 11 Cold-stage scanning electron microscopy (CryoSEM), 189–190 Colitis, 442 Colon cancer, see also Colorectal cancer aleurone flour, 442–443 pectin, 154 psyllium, 406 resistant starch, 231 Colonic cell health, 231 Colonic motility cellulose, 265 sugar beet fiber, 376 Colon tumorigenesis, 265 Colorectal cancer, see also Colon cancer alpha-cyclodextrin, 11 polydextrose, 181 psyllium, 405–406 resistant starch, 231 sugar beet fiber, 381–382 Colors alpha-cyclodextrin, 11 barley fiber, 335–336 Commercial developments and applications partially hydrolyzed guar gum, 109–110 resistant starch, 209–210, 216 Compositae spp., 43 Composition Nutriose soluble fiber, 27 rice bran, 307–308 sugar beet fiber, 362–364 Condiments, 159, see also specific type Confectionery acacia gum, 130–131 alpha-cyclodextrin, 11 Nutriose soluble fiber, 36, 37 partially hydrolyzed guar gum, 110 pectin, 158 polydextrose, 189, 193–194 Constipation, see also Intestinal regularity; Stools acacia gum, 125–126 cellulose, 264 cellulose functionality, 264–265 fruit fiber, 434 inulin, 48
474
partially hydrolyzed guar gum, 86, 90–93 psyllium, 395, 398, 409 Continuing Survey of Food Intakes by Individuals, ix Contraindications, psyllium, 411 Conventional fibers barley fiber, 323–347 cellulose, 263–277 oat beta-glucan, 283–298 oat fiber (oat hull), 249–259 psyllium, 393–412 rice bran, 305–318 sugar beet fiber, 359–383 Cook, Caroline, 452 Cookies, see also Bakery products and applications barley fiber, 333 Nutriose soluble fiber, 28 oat beta-glucan, 287, 289 oat fiber, 251, 252, 253 partially hydrolyzed guar gum, 110 polydextrose, 187 sugar beet fiber, 374 Copper barley fiber, 347 cellulose, 277 pectin, 145–147 sugar beet fiber, 376 Corn bran oat fiber comparison, 249 rice bran comparison, 312 suppliers, 457 Corn flakes, 335 Cornstarch, 81 Coronary heart disease, see also Cardiovascular disease; Heart disease approved health claims, 3 fruit fiber, 434–435 Cosmetics, 81 Cottonseed fiber, 465 Cough, 395, 396 Cow’s milk, 293 Cow studies, 257, 258 Crackers, 252, see also Bakery products and applications Craig studies, 175, 197 Cramping, 92 Cream cheese, 54
Index Creatinine, 126 Crispiness inulin, 54 oat fiber, 252 polydextrose, 186 Crohn’s disease inulin, 50 psyllium, 405 CryoSEM, see Cold-stage scanning electron microscopy (CryoSEM) Cultured dairy products, 194 Culture protagonist, 228 Cummings studies, 178, 237 Cyamopsis tetragonolobus, 83 α-cyclodextrin, see Alpha-cyclodextrin (α-CD) Cynomolgus monkey studies, 313 Czuchajowska, Baik and, studies, 331–332
D Daas studies, 84 Dahlia, 43, 45 Dairy desserts, 54 Dairy drinks, 195, see also Beverages Dairy products, see also Cheese and cheese products; Milk and milk products barley fiber, 335 guar gum, 81 inulin, 46, 54 Nutriose soluble fiber, 28, 36, 37 oat beta-glucan, 293 oat fiber, 254 partially hydrolyzed guar gum, 109 pectin, 158 resistant starch, 216 Dalidowicz, Wendy, 240 Danisco Sweeteners, 175 DASH Study Group, 344 Davidson, Peters and, studies, 87 Davidson studies, 288 Dea and Madden studies, 363 De Cassia Freitas studies, 103 Delaney studies, 346 Delessert, Benjamin, 360 Demark-Wahnefried studies, 289
475
Index De Mateo Silleras, Mijan de la Torre and, studies, 91 Den Hond studies, 230 Desserts, frozen inulin, 46, 54 oat fiber, 250, 254 Detection methods, resistant starch, 220–221 Detoxification, 127 Developments aleurone flour, 439–452 fruit fibers, 427–435 DeVries studies, 222 Dextrin, indigestible, 94 Diabetes, see also Glucose metabolism and response; Glycemic management and response alpha-cyclodextrin, 12 inulin, 50–51 oat fiber, 257 partially hydrolyzed guar gum, 86–87 potential health claim, 4 psyllium, 397, 407, 409 resistant maltodextrin, 70 resistant starch, 234, 236 sugar beet fiber, 376, 378 Diarrhea, see also Intestinal issues; Intestinal regularity acacia gum, 125–126 alpha-cyclodextrin, 13, 14 inulin, 50, 54 Nutriose soluble fiber, 25, 27, 28 oat fiber, 255 partially hydrolyzed guar gum, 86, 89–94, 102 pectin, 148 psyllium, 405, 409–410 resistant maltodextrin, 65 resistant starch, 232 Diet and food, resistant starch, 208–209 Dietary Approaches to Stop Hypertension (DASH) Study Group, 344 Dietary fiber approved health claims, 3 defined, x–xi, 2, 20 historical developments, 19–20 intake, global levels, 1–2 mean intake, x
Nutriose soluble fiber, 22–25 potential health claim, 4 potential structure function claims, 4–5 recommended daily amounts, vii, x, 1, 398, 433–434 sources of in diet, ix stool softening, 53 Dietary gums, 80–81, see also Partially hydrolyzed guar gum (PHGG) Dietary supplements, 11, see also Vitamins; specific types Digestible carbohydrates, 229 Digestion and digestive tract function barley fiber, 337 Nutriose soluble fiber, 28–29 resistant maltodextrin, 68 resistant starch, 227–232 sugar beet fiber, 374–375 Dikeman studies, 81 Dilution effect, 266 Dinand studies, 370 Direct methods, resistant starch, 217 Diverticular disease partially hydrolyzed guar gum, 97 psyllium, 398–399 DNA protection, 451 Dog studies alpha-cyclodextrin, 9, 14 cellulose, 265–266 partially hydrolyzed guar gum, 103 psyllium, 410 Dongowski studies, 383 Dongowsky studies, 378 Dougherty studies, 249–250, 253 Dressings cellulose, 271 fruit fiber, 431–432 guar gum, 81 partially hydrolyzed guar gum, 109 Drinks and beverages, 293, 294 Drug delivery systems, 410 Drug interaction, 412 Dry food mixes, 11 Dry-substance conditions, 46 Dumping syndrome, 148 Dysentery, 395, 396 Dyspepsia, 409 Dysuria, 395
476
Index
E Edema, 395 Electrolyte balance acacia gum, 125 partially hydrolyzed guar gum, 90, 96 Electronic speakers, 272 Ellis studies, 82 Embryonic safety, 13–14 Emollient effects, 396 Emulsions dietary gums, 81 fruit fiber, 432 inulin, 46 pectin, 159 psyllium, 396 Endress studies, 135–159 Energy contribution, 183 Energy partitioning, 238–239 Englyst’s classification, 10 Englyst’s method, 222 Englyst studies, 216–217, 222 Enteral nutrition formula and feeding guar gum, 82–83 oat fiber, 256 partially hydrolyzed guar gum, 86, 87, 93, 102, 107–108 pectin, 148 resistant maltodextrin, 68 Enterobacter spp., 148 Entner-Doudoroff pathway, 143 Escherichia spp., 230 Escherichia coli inulin, 49 partially hydrolyzed guar gum, 106 pectin, 142–143 psyllium, 410 Eubacteria spp., 230 Eubacterium, 337 Evans studies, 82 Extensible products, 287 Extracted polysaccharides, 372–373 Extruded snacks and breakfast cereals, see also Cereal products acacia gum, 130 inulin, 54 Nutriose soluble fiber, 36 oat beta-glucan, 286, 296
sugar beet fiber, 373 Extrusion barley fiber, 329–332 resistant starch, 209 rice bran, 312 Eye disorders, 395
F Falk, Sundberg and, studies, 329 Fares studies, 363, 368–369 Fässler studies, 222 Fastnaught studies, 323–347 Fat-free products oat fiber, 253–254 pectin, 158 Fat mass, 48 Fat metabolism, 70–71 Fats barley fiber, 334–335, 337 cellulose functionality, 267 gums as mimetics, 81 pectin, 147 polydextrose, 179 Fatty acids, 407–408 Favier studies, 88 Fecal issues, see Constipation; Diarrhea; Intestinal issues; Stools Feeding tubes, see Enteral nutrition formula and feeding Fenech studies, 439–452 Fermentation acacia gum, 123 aleurone flour, 443 alpha-cyclodextrin, 9, 10, 11 cellulose functionality, 265 inulin, 47, 49, 53 Nutriose soluble fiber, 20, 25, 27, 33 oat beta-glucan, 298 oat fiber, 258 partially hydrolyzed guar gum, 92, 94, 107, 108 pectin, 142–143 polydextrose, 182 psyllium, 397 resistant maltodextrin, 66, 67–68 resistant starch, 227, 230, 232 sugar beet fiber, 374–375, 382 Fernandez-Garcia studies, 254
477
Index Fetal safety, 13–14 Fever, 395 Fiber content, see Dietary fiber; Total dietary fiber (TDF) Fibersol-2 resistant maltodextrin body fat ratio decreases, 71–72 bowel movements, 65 cholesterol levels, 70–71 digestive tract function maintenance, 68 fat metabolism, 70–71 food applications, 74–75 fundamentals, 61–64 gastrointestinal functions, 64–68 historical developments, 61–63 intestinal environments, 65–68 measuring method, total dietary fiber, 75 physiological effects, 64–72 postprandial blood glucose level attenuation, 69–70 prebiotic effects, 65, 67 production, 63–64 resistant starch, 216 safety applications, 72, 74 short-chain fatty acids, 67–68 sugar metabolism, 70–71 suppliers, 462–463 triglyceride levels, 70–71 Fibregum, 123–124, 128, 458, see also Acacia gum Fibrex, 361, 373, see also Sugar beet fiber Film-coating agents dietary gums, 81 polydextrose, 196 psyllium, 396 Filter paper, 272 Finocchiaro studies, 205–239 Firmness, 109 Fischer, Marlett and, studies, 395 Fischer studies, 427–435 Fish oil supplementation, 150 Fish studies, 345 Flamm, Burdock and, studies, 184 Flatbreads, 332 Flatulence alpha-cyclodextrin, 13 barley fiber, 346 inulin, 53–54 Nutriose soluble fiber, 25, 27, 28
partially hydrolyzed guar gum, 92, 93, 96 psyllium, 409 sugar beet fiber, 383 Flavors alpha-cyclodextrin, 11 inulin, 54 partially hydrolyzed guar gum, 109 Flood studies, 184 Flow behavior, 275–276 Flu, 395 Foams inulin, 46, 55 partially hydrolyzed guar gum, 109–110 Foehse studies, 331 Folate levels, 440–451 Food and food product applications acacia gum, 128–131 aleurone flour, 440–451 alpha-cyclodextrin, 11 barley fiber, 329–337, 346 cellulose, 271–272 fruit fibers, 430–432 inulin, 54–55 Nutriose soluble fiber, 35–36 oat beta-glucan, 287–293 oat fiber, 252–254 pectin, 156–159 polydextrose, 193–196 psyllium, 395–396 resistant maltodextrin, 74–75 resistant starch, 224 rice bran, 308 sugar beet fiber, 372–374, 383 Food characteristics, effects on, 287 Food grade specifications, 85 Food intake modulation, 51–52 Food matrix, inclusion in, 28 Forsberg studies, 336 FORTEFIBER products, 456, 458 Fouache studies, 207–208, 216 Fox studies, 336 Franck studies, 41–55 Frankfurters, 253–254 Freezing, see also Chilling barley fiber, 335 oat beta-glucan, 287 Fried products, 36 Frozen products
478 inulin, 54 Nutriose soluble fiber, 36 oat fiber, 250, 254 polydextrose, 194 Fructooligosaccharides (FOS) acacia gum comparison, 124–125 resistant starch, 232 suppliers, 458–460 Fruit fibers food product applications, 430–432 fundamentals, 427–430 intestinal regularity, 5 physiological benefits, 433–435 Fruit fillings Nutriose soluble fiber, 36 polydextrose, 195 Fruit juices, 35 Fruits partially hydrolyzed guar gum, 110 recommended daily amounts, 433–434 Fruit spreads pectin, 157 polydextrose, 195 Frutafit products, 459–460 Frutalose products, 459–460 Fulcher, Miller and, studies, 325 Fullness, feeling of, 82, see also Satiety Functionality aleurone flour, 440–451 alpha-cyclodextrin, 11 barley fiber, 329–337 oat beta-glucan, 284–287 psyllium, 395–396 resistant starch, 224 sugar beet fiber, 372–374 Functionality, cellulose blood glucose, 268 carbohydrates, 267, 269 carcinogenesis, 266 cell proliferation, 266 constipation, 264–265 dilution effect, 266 fats, 267 fermentation, 265 gastric emptying blood glucose, 268 hydroxypropylmethylcellulose, 270–271 insulin, 268 intestines, water absorption, 269–270
Index large intestine fermentation, 265 physiological benefits, 270–271 proteins, 270 stool output, 264–265 water absorption, intestines, 269–270 Fussell studies, 93
G Galdeano and Grossmann studies, 251, 253 Galdeano studies, 253 Gallaher studies, 382 Gallstones, 410 Galvin studies, 2 Garleb studies, 257 Garlic, 43 Gases, see also Flatulence inulin, 47 partially hydrolyzed guar gum, 86 pectin, 143 resistant starch, 227 Gastric emptying cellulose functionality, 268 oat beta-glucan comparison, 297 psyllium, 397 Gastrointestinal functions, see also Intestinal issues alpha-cyclodextrin, 14 partially hydrolyzed guar gum, 89 resistant maltodextrin, 65–68 Gatlin, Jaramillo and, studies, 345 Gee studies, 82 Gelatin partially hydrolyzed guar gum comparison, 100 replacement, inulin, 54 Gelation inulin, 54 pectin, 138–139 psyllium, 397 sugar beet fiber, 372–373 Gene expressions, 48 Genotoxicity, 106 Gerbil studies, 179 Giaccari studies, 96 Giannini studies, 96 Gibson, Rastall and, studies, 96 Gibson, Wang and, studies, 182
479
Index Gibson and Roberfroid studies, 180 Gill studies, 333, 335 Glass beads, 266 Glass transition temperature (Tg), 186–187, 193 Glucagel, 288, 335 Glucose metabolism and response, see also Diabetes; Glycemic management and response barley fiber, 342–344 cellulose, 267–268 cellulose functionality, 268 oat beta-glucan, 296–297 partially hydrolyzed guar gum, 85 pectin, 152–154, 267–268 polydextrose, 179–180 psyllium, 397 resistant maltodextrin, 70–72 sugar beet fiber, 376–378 Glycemic index (GI) acacia gum, 127–128 alpha-cyclodextrin, 12 barley fiber, 342–343 CAVAMAX W6, 455 oat beta-glucan, 296 partially hydrolyzed guar gum, 97–100, 105 pectin, 153 polydextrose, 179–180 resistant starch, 232–233 Glycemic management and response, see also Diabetes; Glucose metabolism and response alpha-cyclodextrin, 12 Nutriose soluble fiber, 29 oat fiber, 250, 254–255 potential structure function claims, 5 resistant starch, 228, 232, 234–236 Golay studies, 86 Goni studies, 217 Gonorrhea, 395 Gordon and Okuma studies, 223 Gould studies, 249–250 Gout, 396 Graham studies, 100 Grainwise, 455–456 Granfeldt studies, 342 Granola bars, 251 Grape juice, 28 Green bananas, 149
Greenberg and Sellman studies, 84 Grossmann, Galdeano and, studies, 251, 253 Guar gum, see also Partially hydrolyzed guar gum (PHGG) fundamentals, 81–82 glucose effects, 269 glycemic control, 5 pectin comparison, 150–151 psyllium comparison, 409 sugar beet fiber comparison, 378 Guillon studies, 359–383 Gulliford studies, 102 Gum arabic, 458, see also Acacia gum Gu studies, 86 Gut function, effects on, 48–49 Gut microflora, 49, see also Microflora Gut well-being, 31–34
H Hagen-Poiseuille law, 269 Hallfrisch studies, 344 Hamberg studies, 378 Hamster studies cellulose, 267, 270 inulin, 48 psyllium, 407 rice bran, 309–312 Hanai studies, 337 Hara, Suzuki and, studies, 88, 105 Haralampu studies, 206, 209 Hara studies, 102, 182, 381 Harland studies, 375 Harrington studies, 346 Hashizume studies, 61–75 Hawrysh studies, 343 Hayes, Pronczuk and, studies, 179 Health benefits, see Physiological functions and benefits Health claims approved, 3 barley fiber, 323–324, 338 no-sugar(s)-added, 37 Nutriose soluble fiber, 37 potential, 4 potential structure function, 4–5 psyllium, 396, 408 resistant maltodextrin, 74
480 sugar(s)-free claims, 37 Heart disease, see also Cardiovascular disease; Coronary heart disease approved health claims, 3 psyllium, 395, 406–409 Heifer studies, 257, 258 Heijnen studies, 237 Heini studies, 100 Helianthus tuberosus, 45 Hematologic parameters, 105 Hemicelluloses oat fiber, 251 sugar beet fiber, 369 Hemodialysis, 126 Hemorrhoids, 410 Henley and Chiu studies, 28, 209 Henningsson studies, 209 Hepatic parameters, 105 Hetland and Svihus studies, 255–257 Hetland studies, 255 Heyl, Wise and, studies, 51 Higgins studies, 232, 234, 238 High amylose corn starch, see Resistant starch (RS) High-density lipoprotein (HDL), see Cholesterol; Lipid metabolism High-fiber foods, potential structure function claims, 4–5 High-intensive sweeteners, 75 High-moisture systems, 224 High-protein diet, 126 Hi-Maize products resistant starch, 210, 234 suppliers, 463–464 Hinata studies, 343 HIV-positive patients, 144 HMPC, see Hydroxymethylpropyl cellulose (HMPC) Homann studies, 93 Honey, 396 Hong studies, 345 Hordeins, 347 Hormone status, 48 Hot dogs, see Frankfurters Howe, Behall and, studies, 237 Howe studies, 9–15 Hudson studies, 333 Human studies acacia gum, 125–128
Index
aleurone flour, 443–451 barley fiber, 337–338, 346–347 cellulose, 264–265, 275, 277 fruit fiber, 434–435 guar gum, 82 hydroxypropylmethylcellulose, 270–271 inulin, 47–49 Nutriose soluble fiber, 33, 34 oat beta-glucan, 289, 293 oat fiber, 255–256, 257, 258 partially hydrolyzed guar gum, 92, 94–96, 103 pectin, 155 polydextrose, 178–179 psyllium, 407–408 resistant maltodextrin, 70 resistant starch, 222, 230, 232, 238 rice bran, 314–316 sugar beet fiber, 376 Humectant, 186, 188, see also Hydration Hunger, reduced, 51–52, see also Satiety Hydration fruit fiber, 430–431 polydextrose, 188–190 sugar beet fiber, 370–371 Hydrocolloid properties, 410 Hydroxycellulose, 100 Hydroxymethylpropyl cellulose (HMPC) glycemic control, 5 suppliers, 456 Hydroxypropylmethylcellulose (HPMC), 269, 270–271 Hygroscopicity, 131 Hylla studies, 237 Hyperglycemia, 70, see also Glycemic management and response Hyperlipidemia, see also Lipid metabolism pectin, 142 polydextrose, 179 Hypersensitivity, see Adverse effects Hypertension, see Blood pressure Hypoglycemia and hypoglycemic effects acacia gum, 127–128 pectin, 148 psyllium, 409 resistant maltodextrin, 70
481
Index
I IBS, see Irritable bowel syndrome (IBS) Ice cream fruit fiber, 431 inulin, 46 Nutriose soluble fiber, 28 psyllium, 396 Ice cream cones, 252 Ice crystals, 159 Ide studies, 88 Ikegami studies, 100 Ileal morphology, 147 Immune response, 344–345 Immunological effects, 101 Immunostimulation, 396 IMT, see Intima-media thickness (IMT) Indirect methods, resistant starch, 217 Industrial fruit preparations, 157 Industrial processing resistance, 35–36 Infection, resistance to, 49–50 Inflammation inulin, 49–50 psyllium, 395, 396 Inflammatory bowel disease (IBD) inulin, 50 psyllium, 405 Inglett, Lee and, studies, 335 Inglett studies, 251, 335 Instant teas and coffees, 11 Insulin response and insulin resistance, see also Glycemic management and response alpha-cyclodextrin, 13 barley fiber, 342–344 cellulose, 267–268 guar gum, 82 oat beta-glucan, 296 partially hydrolyzed guar gum, 86–87, 105 pectin, 149 psyllium, 397 resistant maltodextrin, 72 resistant starch, 234 sugar beet fiber, 376, 381 Intake mean intake, x recommended daily amounts, vii, x, 1, 398, 433–434 sources of in diet, ix
Intestinal helminth infections, 250, 259 Intestinal issues acceptability, inulin, 53–54 acute infections, pectin, 148–149 bowel function, polydextrose, 178 environments, 65–68, 228, 231–232 function, resistant starch, 228 Nutriose soluble fiber, 28 psyllium, 395, 396 resistant maltodextrin, 65–68 resistant starch, 228 stool output, sugar beet fiber, 375–376 transit time, sugar beet fiber, 375–376 water absorption, cellulose, 269–270 Intestinal microflora, 94–96, see also specific type Intestinal regularity bowel movements, resistant maltodextrin, 65 diarrhea, acacia gum, 125–126 oat fiber, 250, 255–256 partially hydrolyzed guar gum, 96 potential structure function claims, 5 stool output, cellulose, 264–265 Intima-media thickness (IMT), 149 Intoxication, 395 Inulin appetite modulation, 51–52 caloric value, 47 cancer risk reduction, 52 chemical properties, 45–46 chemical structure, 42 diabetes suitability, 50–51 food applications, 54–55 food intake modulation, 51–52 fundamentals, 41–42 gut function, effects on, 48–49 gut microflora, modulation of, 49 infection, resistance to, 49–50 inflammation, resistance to, 49–50 intestinal acceptability, 53–54 lipid metabolism, improvement, 47–48 material properties, 46–47 mineral absorption increase, 52–53 native, 42 natural occurrence, 42–43 non-digestibility, 47 nutritional properties, 47–54 outlook and perspectives, 55
482
Index
physical properties, 45–46 production, 45 properties, 45–54 quantitative determination, in food, 43–44 sources, 42, 43 stability, 109 suppliers, 458–460 Ions/organic molecules, 372 Iron aleurone flour, 439 barley fiber, 346 cellulose, 277 oat beta-glucan, 298 partially hydrolyzed guar gum, 103 pectin, 145–146 psyllium, 412 sugar beet fiber, 376 Irritable bowel syndrome (IBS) partially hydrolyzed guar gum, 96–97 psyllium, 399, 404–405 Ishizuka and Kasai studies, 382 Ishizuka studies, 181 Isoleucine, 313 Iyengar studies, 208–209 Izydorczk studies, 332
J Jam, 50 Jaramillo and Gatlin studies, 345 Jaskari studies, 287 Jejunal morphology, 147 Jenkins studies, 237, 296, 409 Jerusalem artichokes, 43, 45 Jiang and Vasanthan studies, 326 Jie studies, 178, 180, 182 Johnson studies, 266, 375 Juices fruit fiber, 428 Nutriose soluble fiber, 28, 35 oat beta-glucan, 286 Juneja studies, 79–112 JustFiber products, 465
K Kabir studies, 238
Kahlon studies, 305–318 Kaolin, 266 Kapoor studies, 79–112 Karman vortex, 274 Kasai, Ishizuka and, studies, 382 Kay studies, 88 Keenan studies, 237–238, 338, 367 Kelleher studies, 265 Kellogg cereals, 396 Kendall studies, 209, 227 Kennefick and Cashman studies, 347 Keogh studies, 338 Kerek, Ciukanu and, studies, 176 Keycel, 456–457 Keys studies, 407 Kidneys, see also Renal issues acacia gum, 126 resistant maltodextrin, 71 King studies, 183 Klebsiella spp., 148 Knoblock, Ken, 197 Knuckles studies, 328, 332 Kokke studies, 1 Koksel studies, 331 Kondo studies, 89 Koujitani studies, 106 Kouwijzer studies, 367 Krüger, Chris, 197 Kulp and Ponte studies, 208 Kunkel, Lucia and, studies, 411
L Labeling, see Health claims Lachnospira multiparus, 144 Lactate, 47 Lactation, 412 Lactobacilli spp. acacia gum, 123–124 inulin, 49–50, 52 Nutriose soluble fiber, 31, 33 oat fiber, 254 polydextrose, 182 resistant starch, 230 Lactobacilli acidophilus, 144 Lactobacilli casei Shirota, 144 Lactobacilli plantarum, 144 Lactobacillus spp.
Index
partially hydrolyzed guar gum, 95–96 pectin, 142 Lactobacillus acidophilus, 345 Lairon studies, 2 Lampe studies, 91 Large intestine fermentation, see also Fermentation alpha-cyclodextrin, 9, 10, 11 cellulose functionality, 265 Large intestine morphology, 259 Larrauri studies, 361 Larrea studies, 251 Laxation partially hydrolyzed guar gum, 85, 90–94 resistant maltodextrin, 68 resistant starch, 227 Laxative effects acacia gum, 123 Nutriose soluble fiber, 27 polydextrose, 184 psyllium, 396 Laxative effects, psyllium anti-carcinogenic effects, 405–406 anti-inflammatory effects, 405 diverticular disease, 398–399 fundamentals, 397–398 heart disease risk, 406–409 irritable bowel syndrome, 399, 404–405 Lead, 146–147 Le Bihan studies, 19–37 Lee and Inglett studies, 335 Lee and Prosky studies, 2 Lee and Schwarz studies, 330 Leeks, 43 Lee studies, 223, 254, 332 Lefranc-Millot studies, 19–37 Le Leu studies, 230–231 Lemon fiber, 430 Le Quéré studies, 363 Leucine, 313 Levigne studies, 363 Lewis studies, 51 Lia studies, 337 Light bologna, 253–254 Light microscopy, 189 Lignin blocking iron absorption, 103
483 oat fiber, 251 pectin, 146 Liliacea spp., 43 Liljeberg and Bjorck studies, 342 Liljeberg-Elmstahl studies, 209 Liljeberg studies, 343 Lina studies, 14 Lindstrom studies, 4–5 Lipid metabolism, see also Cholesterol; Triglyceride levels alpha-cyclodextrin, 11 barley fiber, 338 hydroxypropylmethylcellulose, 270 inulin, 47–48 oat beta-glucan, 288–293, 295 oat fiber, 257 partially hydrolyzed guar gum, 88, 96 pectin, 142, 150–152 polydextrose, 178–180 psyllium, 407 sugar beet fiber, 378–381 Lipodystrophy, 144 Lipolysis, 265 Lipoproteins, 150 Liquid food products, 28, 37 Listeria spp., 49 Listeria monocytogenes, 50 Li studies, 343 Litesse and Litesse Ultra, 175, 179–180, 183 Lithium citrate, 412 Liu and Tsai studies, 178 Liver pectin, 141, 149 resistant maltodextrin, 71 Livesey studies, 342 Locust (carob) bean gum, 81 Lopez-Guisa studies, 255, 257 Lopez-Miranda studies, 1 Lopez studies, 232 Lorenz, Vis and, studies, 336 Low-calorie products fruit fiber, 431 resistant maltodextrin, 75 Low-density lipoprotein (LDL), see Cholesterol; Lipid metabolism Low-fat foods and products fruit fiber, 431–432 inulin, 54
484
Index
pectin, 158, 159 potential structure function claims, 4–5 Low-moisture systems, 224 Lucia and Kunkel studies, 411 Lung disorders, 395 Lyly studies, 335 Lysine, 313
M Madden, Dea and, studies, 363 Magnesium aleurone flour, 439 barley fiber, 346 cellulose, 277 oat beta-glucan, 298 partially hydrolyzed guar gum, 102 pectin, 145–146 sugar beet fiber, 376 Maize, 37 MaizeWise corn bran, 457 Maki studies, 271 Mäkivuokko, Harri, 197 Mäkivuokko studies, 182 MALDI-TOF mass spectrometry, 176 Maltodextrin replacement, 54 Manganese, 298 Manufacturing, see Production and processing Marggraf, Andreas Sigismund, 360 Market potential, rice bran, 316 Marlett and Fischer studies, 395 Marlett studies, 1, 5, 330 Marmalade, 396 Mateos studies, 255 Material properties, inulin, 46–47 Material with cellular structure (MCS), 429 Matsuoka, Tokunaga and, studies, 69 Mattes studies, 135–159 Mayonnaise, 432, see also Emulsions May studies, 124 McArthur, Rosemary, 452 McCleary and Monaghan studies, 208, 217 McCleary and Neukom studies, 84 McCleary studies, 208, 217, 222 McGuffin, Anne, 452
McIntosh studies, 345, 443 McLean Ross studies, 125 MCS, see Material with cellular structure (MCS) Measuring method barley fiber, 327 resistant maltodextrin, 75 Meat and meat products barley fiber, 334 fruit fiber, 431–432 inulin, 54 oat fiber, 250, 252 polydextrose, 189, 195 sugar beet fiber, 373–374 Medical aspects, pectin acute intestinal infections, 148–149 atherosclerosis, 149–150 cancer, 154–156 cholesterol, 150–152 dumping syndrome, 148 glucose metabolism, 152–154 intestinal infections, acute, 148–149 lipid metabolism, 150–152 short bowel syndrome, 148 short gut syndrome, 148 Medications, 410, 412, see also Pharmaceuticals Megazyme, 335 Meier studies, 91 Melting properties, 54 Mesalamine, 405 Metabolic functions, 85–104 Metabolic syndrome psyllium, 407 resistant starch, 234 Metabolism acacia gum, 123 pectin, 141–142 Metal ions, 145–147 Metamucil, 100 Methylcellulose partially hydrolyzed guar gum comparison, 94 psyllium comparison, 411 Mice studies alpha-cyclodextrin, 13–14 inulin, 50–51 partially hydrolyzed guar gum, 106 pectin, 155 resistant starch, 231
485
Index Michel studies, 124 Microcrystalline cellulose, 266–267 Microflora, see also specific type inulin, 49 partially hydrolyzed guar gum, 94–96 Mijan de la Torre and de Mateo Silleras studies, 91 Milk and milk products, see also Cheese and cheese products; Dairy products guar gum, 81 Nutriose soluble fiber, 36 partially hydrolyzed guar gum, 109 Miller and Fulcher studies, 325 Miller-Fosmore studies, 96 Minekus studies, 222 Minerals, see also specific type barley fiber, 346–347 inulin, 52–53 partially hydrolyzed guar gum, 102–103, 105 sugar beet fiber, 376 Mint sauces, 159 Misra studies, 345 Mitchell, Helen, 197 Mitsuyama studies, 337 Mixing-in behavior, 272–275 Modak studies, 345 Moisture management, 186 Molecular weight, 285 Monaghan, McCleary and, studies, 208, 217 Morgan, Wendy, 452 Morgan and Ofman studies, 328 Morgan studies, 378 Morita studies, 227, 231–232, 238, 313 Mousses, 55 Mouthfeel, 36–37 Mucin, 231 Muesli oat beta-glucan, 296 sugar beet fiber, 373 Muffins aleurone flour, 451 barley fiber, 333, 343 oat beta-glucan, 287, 289 sugar beet fiber, 374 Muir and O’Dea studies, 217 Muir studies, 237
Murakami studies, 2, 4–5 Mutagenicity alpha-cyclodextrin, 14 partially hydrolyzed guar gum, 106 Myers, Weibel and, studies, 370
N Naito studies, 101 Nakagawa studies, 178 Nakao studies, 91 Naokes studies, 439–452 Narain studies, 343 National Data Laboratory, ix National Nutrient Databank Conference, ix Natural occurrence, 42–43 Natureal, 288 Nausea alpha-cyclodextrin, 13, 14 psyllium, 409 NCEP step-1 diet, 315 Nephrotoxicity, 126 Neukom, McCleary and, studies, 84 Neural tube defects, 443 Newman and Newman studies, 324 Nichols, Chuck, 197 Nitric oxide (NO) metabolism, 125 Nitrogen excretion, 126–127 Nitrogen metabolism, 258–259 NO, see Nitric oxide (NO) metabolism Noakes studies, 289 Nondigestibility, 47 Nontraditional resistant starch, 210, 216, 218–219 Noodles, see Pasta and noodles No-sugar(s)-added claims, 37, see also Sugar(s)-free food products Novelose products, 463–464 Nugent studies, 230 Nurture 1500, 288 Nutraceutical products, 159 Nutrient interactions and interrelationships cellulose benefits, 276 resistant starch, 232 Nutrim-OB, 288 Nu-trim X, 343 Nutriose soluble fiber
486
absorption in small intestine, 28–29 caloric value, 34–35 composition of fiber, 27 description, 21–22 dietary fiber content, 22–25 digestion in small intestine, 28–29 digestive tolerance, 25, 27–28 food applications, 35–36 food matrix, inclusion in, 28 fundamentals, 19–21, 37 glycemic response, 29 gut well-being, 31–34 industrial processing resistance, 35–36 intestinal bacterial adaptation, 28 labeling, 37 mouthfeel, 36–37 physiochemical properties, 35–36 physiological benefits, 28–29 powder’s properties, 35 production, 21–22 regulation, 37 resistant starch, 216 safety, 37 sources, 37 suppliers, 462–463 taste, 36–37 technical properties, 35–36 Nutritional aspects, acacia gum, 123–125 Nutritional aspects, inulin appetite modulation, 51–52 caloric value, 47 cancer risk reduction, 52 diabetes suitability, 50–51 food intake modulation, 51–52 gut function, effects on, 48–49 gut microflora, modulation of, 49 infection, resistance to, 49–50 inflammation, resistance to, 49–50 intestinal acceptability, 53–54 lipid metabolism, improvement, 47–48 mineral absorption increase, 52–53 non-digestibility, 47 Nutritional aspects, pectin fermentation, 142–143 ileal morphology, 147 jejunal morphology, 147 metabolism of, 141–142
Index metal ions, 145–147 prebiotic nature, 143–144 toxic metals excretion, 145–147 weight management, 144–145 Nuts, 110 Nyman and Asp studies, 375
O Oat beta-glucan bakery applications, 289, 292 breads, 289, 292 cereals, 289, 290–291 characteristics, 283–284 drinks and beverages, 293, 294 food applications, 287–293 food characteristics, effects on, 287 functionality, 284–287 fundamentals, 284 glucose metabolism, 296–297 glycemic control, 5 lipid metabolism, 288–293, 295 mechanism, 293 molecular weight, 285 physiological benefits, 288–297 postprandial effects, 296–297 processing, effects on, 285–287 randomized studies, 289–293 safety, 297–298 suppliers, 460 viscosity, 284–285 Oat bran barley fiber comparison, 342, 345, 347 intestinal regularity, 5 psyllium comparison, 409 rice bran comparison, 315 sugar beet fiber comparison, 382 Oat fiber (oat hull) bakery products, 252–253 body weight, 256 characteristics, 252 fat-free frankfurters, 253–254 fermentability, 258 food applications, 252–254 frozen desserts, 254 fundamentals, 249–250 glycemic control, 254–255 intestinal regularity, 255–256
487
Index large intestine morphology, 259 light bologna, 253–254 nitrogen metabolism, 258–259 pasta shells, 252–253 pectin comparison, 150–151 pork products, 253–254 production, 250–252 serum lipids, 257 suppliers, 460–461 yogurt, 254 Oatmeal, 342 Oatrim, 288 OatsCreme, 288 OatVantage, 288 Oatwell, 288 Obesity fruit fiber, 434 pectin, 142 psyllium, 407 O’Dea, Muir and, studies, 217 Ofloxacin, 410 Ofman, Morgan and, studies, 328 Ohkuma studies, 207–208, 216 Oil replacement, 271, see also Fats Okoniewska studies, 205–239 Okubo studies, 95 Okuma, Gordon and, studies, 223 Okuma studies, 61–75 Oliggo-Fiber, 460 Oligosaccharides dietary fiber content, 22–23 introduction in foods, 20 Olson studies, 409 Onions, 43 Önning studies, 293 Oosterveld studies, 365, 369 Orafti products, 45, see also Synergy 1 Oral health, 183 Oral medication, 412, see also Medications; Pharmaceuticals Oral Rehydration Solution (ORS), 93–94 Oral rehydration solutions, 129 Orange pulp fiber, 430 Organic molecules, 372 Ostergard studies, 330 Ostman studies, 343 O’Sullivan, Geoff, 197 Outlook and perspectives, inulin, 55
P Painter studies, 399 Palacio and Rombeau studies, 102 Pancakes, 333 Pancreas, 71 Pancreatic amylase activity, 11 Pancreatic enzymes, 141–142 Paper manufacturing cellulose, 272 guar gum, 81 Parisi studies, 97 Park, Matthew R., 240 Partially hydrolyzed guar gum (PHGG) acute postprandial glycemic responses, 86–87 adverse effects, 107–108 anticarcinogenic properties, 108 beauty supplementation, 103–104 blood cholesterol concentration levels, 88–90 commercial applications, 109–110 dietary gums, 80–81 food grade specifications, 85 fundamentals, 80, 82–83, 110–112 glycemic index, 97–100 guar gum, 81–82 immunological effects, 101 insulin response, 86–87 intestinal microflora balance, 94–96 irritable bowel syndrome, 96–97 laxation improvements, 90–94 metabolic functions, 85–104 mineral absorption, 102–103 physiochemical properties, 85 physiological functions, 85–104 postprandial glycemic responses, 86–87 prebiotic effects, 94–96 processing, 83–85 regulatory status historical background, 108–109 safety issues, 104–107 satiety, 100–101 suppliers, 461–462 toxicological behavior, 104–107 weight control, 100–101 Partially methylated alditol acetates (PMAAs), 175–176 Pasta and noodles
488 aleurone flour, 440, 451 barley fiber, 331–332 cellulose, 271 oat beta-glucan, 286 oat fiber, 252–253 partially hydrolyzed guar gum, 109 pectin, 159 polydextrose, 195 sugar beet fiber, 373 Pastries, see also Bakery products and applications inulin, 50 polydextrose, 189–191, 194 sugar beet fiber, 373 Pâtés, see also Meat and meat products inulin, 54 sugar beet fiber, 374 Pawlak studies, 238 Pea fiber inulin, 52 oat fiber comparison, 258 water-binding properties, 430 Pearled barley, 325, 342 Pectin acacia gum comparison, 124 acute intestinal infections, 148–149 apple juice, 428 atherosclerosis, 149–150 bakery products, 159 barley fiber comparison, 335 beverages, 158–159 cancer, 154–156 capsules, 159 cereal products, 159 chemical structure, 136–138 cholesterol, 150–152 commercial type, 140–141 condiments, 159 confectionery articles, 158 dairy products, 158 dumping syndrome, 148 fermentation, 142–143 food product applications, 156–159 fruit spreads, 157 fundamentals, 136 glucose metabolism, 152–154, 267–268 glycemic control, 5 ileal morphology, 147 industrial fruit preparations, 157 intestinal infections, acute, 148–149
Index jejunal morphology, 147 lipid metabolism, 150–152 medical aspects, 148–156 metabolism of, 141–142 metal ions, 145–147 nutraceutical products, 159 nutritional aspects, 141–147 partially hydrolyzed guar gum, 90 physical properties, 138–140 prebiotic nature, 143–144 psyllium comparison, 409 short bowel syndrome, 148 short gut syndrome, 148 sorbet, 158–159 sources, 140 spreads, 157, 159 sugar beet fiber, 363, 365–369 suppliers, 462 technological aspects, 136–141 toxic metals excretion, 145–147 weight management, 144–145 Pediatric care, 396 Pender, Kay, 452 Peristalsis, 275 Peritoneal dialysis, 126 Persia studies, 51 Persson studies, 347 Peters and Davidson studies, 87 Petruziello studies, 399 Pharmaceuticals, see also Medications acacia gum, 131 guar gum, 81 polydextrose, 196 psyllium, 396 Phenylalanine, 313 PHGG, see Partially hydrolyzed guar gum (PHGG) pH levels, see also Prebiotic characteristics and effects acacia gum, 129 aleurone flour, 443 alpha-cyclodextrin, 10 barley fiber, 335 inulin, 46, 48 Nutriose soluble fiber, 20, 31–32, 34, 36 partially hydrolyzed guar gum, 84, 91–92, 94 pectin, 138–140, 145, 157 polydextrose, 192–193
Index resistant starch, 227 Phosphorus cellulose, 277 oat beta-glucan, 298 Photosensitivity, 395 Physical characteristics and properties inulin, 45–46 pectin, 138–140 polydextrose, 186–190 resistant starch, 211 Physiochemical properties Nutriose soluble fiber, 35–36 partially hydrolyzed guar gum, 85 sugar beet fiber, 370–372 Physiological functions and benefits acacia gum, 125–128 aleurone flour, 440–451 alpha-cyclodextrin, 11–13 barley fiber, 337–345 cellulose functionality, 270–271 fruit fibers, 433–435 Nutriose soluble fiber, 28–29 oat beta-glucan, 288–297 partially hydrolyzed guar gum, 85–104 polydextrose, 183–184 psyllium, 397 resistant maltodextrin, 64–72 sugar beet fiber, 374–383 Physiological functions and benefits, resistant starch (RS) available calories, 237 body composition, 238 colonic cell health, 231 culture protagonist, 228 digestible carbohydrates comparison, 229 digestion, 227–232 energy partitioning, 238–239 fermentation, 227, 230 fundamentals, 226–227 glycemic management, 228, 232, 234–236 intestinal environment and function, 228, 231–232 nutrient interactions, 232 prebiotic benefits, 228, 230–231 satiety hormone production, 238 tolerance, 228 weight management, 228, 237–239
489 Phytates pectin, 146 sugar beet fiber, 374 Phytic acid, 345–346 Pick studies, 289, 343 Pie crusts, 451 Pig studies cellulose, 270, 272, 275 oat fiber, 250, 255–257, 259 resistant starch, 231–232 sugar beet fiber, 375, 378, 381–382 Pi-Sunyer, Wursch and, studies, 343 Pizza crust, 451 Plantago ovata Forsk, 394, see also Psyllium Plantago psyllium, 394, see also Psyllium Plantains (green), 90 PMMAs, see Partially methylated alditol acetates (PMAAs) Poksay and Schneeman studies, 100 Polydextrose affinity for water, 188–190 analysis of, 184 baked goods, 194 beverages, 195 blood glucose responses, 179–180 blood lipids, 178–180 bowel function, 178 chocolate confectionery, 194 confectionery items, 193–194 cultured dairy products, 194 dairy drinks, 195 energy contribution, 183 as fiber, 177–180 food applications, 193–196 frozen dairy desserts, 194 fruit spreads and fruit fillings, 195 fundamentals, 174, 196 glass transition temperature, 186–187 manufacture of, 175 meat applications, 195 moisture management, 186 oral health, 183 partially hydrolyzed guar gum comparison, 94 pasta and noodles, 195 pharmaceuticals, 196 physical nature, 186–190 physiological aspects, 183–184 prebiotic properties, 180–182
490
regulatory status, 196 safety, 184 satiety, 183 specification, 177 stability, 109, 191–193 structure, 175–177 sweetness and sweetness enhancement, 185 technological functionality, 185–193 toleration, 183–184 Polysaccharides acacia gum comparison, 124 sugar beet fiber, 365–370, 372–373 Pomeranz, Szczodrak and, studies, 329 Ponte, Kulp and, studies, 208 Pork products barley fiber, 334 oat fiber, 253–254 Porridge, 346 Postage stamps, 81 Postmenopausal women, 52 Postprandial blood glucose level, see also Glucose metabolism and response cellulose, 267 guar gum, 82 partially hydrolyzed guar gum, 105 resistant maltodextrin, 69–70, 72 sugar beet fiber, 376 Postprandial effects alpha-cyclodextrin, 12 oat beta-glucan, 296–297 psyllium, 407 sugar beet fiber, 381 Postprandial glycemic responses, 86–87, see also Glycemic management and response Postprandial hypertriglyceridemia, 179 Potatoes, 208 Potential health claim, 3–4, see also Health claims Pouchitis, 50 Powder properties, 35 Prebiotic characteristics and effects acacia gum, 123–125 barley fiber, 337 fruit fiber, 434 Nutriose soluble fiber, 31 partially hydrolyzed guar gum, 94–96
Index pectin, 143–144 polydextrose, 180–182 psyllium, 411 resistant maltodextrin, 65, 67, 68 resistant starch, 228, 230–231 Pregnancy alpha-cyclodextrin, 13–14 psyllium, 410, 412 Pretzels, 252 Prevotella ruminicola, 143–144 Printing, 81 Probiotics, 52 Processed cheese, 54, see also Cheese and cheese products Processing, see Industrial processing resistance; Production and processing Proctor & Gamble, 396 Product attributes, resistant starch, 226 Production and processing guar gum, 83–85 inulin, 45 Nutriose soluble fiber, 21–22 oat beta-glucan, 285–287 oat fiber, 250–252 partially hydrolyzed guar gum, 83–85 polydextrose, 175 resistant maltodextrin, 63–64 rice bran, 305–306 sugar beet fiber, 361 Pronczuk and Hayes studies, 179 Propionate, 91, see also Short-chain fatty acids (SCFA) Propionic acids, 91, see also Short-chain fatty acids (SCFA) Prosky, Cho and, studies, 2 Prosky, Lee and, studies, 2 Prosky studies, 208, 223 Proteins aleurone flour, 439 cellulose functionality, 270 partially hydrolyzed guar gum, 107 Proteus spp., 148 Protopectin, 136 Psyllium acacia gum comparison, 124 anorectal surgery, 410 anti-carcinogenic effects, 405–406 anti-inflammatory effects, 405
491
Index
blocking iron absorption, 103 characteristics, 393–395 chemical constituents, 395 contraindications, 411 diarrhea, 410 diverticular disease, 398–399 drug delivery systems, 410 drug interaction, 412 food applications, 395–396 functionality, 395–396 gallstones, 410 glycemic control, 5 heart disease risk, 406–409 hemorrhoids, 410 hydrocolloid properties, 410 irritable bowel syndrome, 399, 404–405 lactation, 412 laxative effect, 397–410 oat beta-glucan comparison, 293 partially hydrolyzed guar gum comparison, 94, 100, 103 pectin comparison, 150–151 physiological benefits, 397 Plantago ovata Forsk, 394 Plantago psyllium, 394 pregnancy, 410, 412 resistant starch, 232 safety, 410–412 summary of, 400–403 toxicity, 410–412 Pylkas studies, 94 Pyroconversion, 21
Q QualFlo, 456–457 Quinde studies, 336
R Rabbani studies, 90 Rabbit studies alpha-cyclodextrin, 13 rice bran, 313 Raghupathy studies, 232 Raghuram studies, 315 Ralet studies, 359–383 Ramakrishna studies, 232
Ramaswamy studies, 250 Ranald studies, 9–15 Randomized studies, 289–293 Rashes, 86 Rastall and Gibson studies, 96 Rat studies acacia gum, 124–126, 129 aleurone flour, 442–443 alpha-cyclodextrin, 11–14 barley fiber, 345–346 cellulose, 265–266, 269–272, 275–277 inulin, 47–48, 51–52 Nutriose soluble fiber, 29, 32–34 oat fiber, 255, 258 partially hydrolyzed guar gum, 88, 90–91, 100–106 pectin, 142–147, 150, 154–155 polydextrose, 178, 181–182 psyllium, 407 resistant maltodextrin, 68–71 resistant starch, 231–232, 236, 238 rice bran, 312–313 sugar beet fiber, 375, 381–383 Rautonen, Nina, 197 RBO, see Rice bran oil (RBO) Read, Tomlin and, studies, 178 Ready-to-drink beverages, 216 Ready-to-eat cereals barley fiber, 330 oat beta-glucan, 289 psyllium, 396 sugar beet fiber, 373 Recommended intake, vii Reformed meat products, 189, 195, see also Meat and meat products Regulation Nutriose soluble fiber, 37 partially hydrolyzed guar gum, 108–109 polydextrose, 196 Renal issues, see also Kidneys acacia gum, 126 oat fiber, 250, 259 partially hydrolyzed guar gum, 105 psyllium, 395 Renard and Thibault studies, 363 Renard studies, 359–383 Resistant dextrin, 109, see also Nutriose soluble fiber
492 Resistant maltodextrin, see also Fibersol-2 resistant maltodextrin; Nutriose soluble fiber glycemic control, 5 suppliers, 462–463 Resistant starch (RS) alpha-cyclodextrin comparison, 10 analysis, 216–217, 222–223 available calories, 237 background, 206 barley fiber, 329 body composition, 238 chemically modified starch, 210, 216 chemistry, 206 classification, 206–208 colonic cell health, 231 commercial developments and applications, 209–210, 216 culture protagonist, 228 detection methods, 220–221 diet and food, 208–209 digestion, 227–232 energy partitioning, 238–239 fermentation, 227, 230 food applications, 224 functional properties, 224 fundamentals, 226–227, 239 glycemic control, 5 glycemic management, 228, 232, 234–236 health benefits, 226–236 high-moisture systems, 224 intestinal environment and function, 228, 231–232 low-moisture systems, 224 non-traditional form, 210, 216, 218–219 nutrient interactions, 232 physical comparisons, natural commercial, 211 prebiotic benefits, 228, 230–231 product attributes, 226 RS vs. digestible carbohydrates, 229 satiety hormone production, 238 soluble dextrins, 210, 216 sources, commercial, 212–215 suppliers, 463–464 tolerance, 228 traditional forms, 212–215
Index types, 206–207 weight management, 228, 237–239 Reynolds number, 272–276 Rhazes studies, 396 Rheumatism, 396 Rice barley similarity, 329 brown, cooking time, 316 partially hydrolyzed guar gum, 98–99 pectin, 149 resistant starch, 208 Rice bran bile acid binding, 316 chick studies, 313–314 cholesterol, 309–315 composition, 307–308 cynomolgus monkey studies, 313 food applications, 308 fundamentals, 316–318 hamster studies, 309–312 human studies, 314–315 market potential, 316 oat beta-glucan comparison, 289, 297 physiological benefits, 309–315 production, 305–306 rabbit studies, 313 rat studies, 312–313 safety, 309 whole grain recommendation, 316 Rice bran oil (RBO) cholesterol, 311, 312–313 substituting cooking oil, 315 Rice milk, 293, 308 Rinaldi, Josephine, 452 Ripsin studies, 288 Roberfroid, Gibson and, studies, 180 Roberfroid studies, 34, 47 Robertson studies, 227, 234, 333, 337 Rochat studies, 125 Roland studies, 258 Rolls studies, 183 Rombeau, Palacio and, studies, 102 Romero studies, 289 Rong studies, 312 Rose studies, 98 Roturier studies, 19–37 Royle, Peter, 452 Ruminococcus albus, 265 Rushdi studies, 93
493
Index Rye and rye products barley fiber comparison, 347 oat beta-glucan, 296 sugar beet fiber comparison, 382
S Saccharomyces cerevisiae, 36 Safety issues and applications acacia gum, 122–123 aleurone flour, 451 alpha-cyclodextrin, 13–14 barley fiber, 346–347 cellulose, 277 Nutriose soluble fiber, 37 oat beta-glucan, 297–298 partially hydrolyzed guar gum, 104–107 polydextrose, 184 psyllium, 410–412 resistant maltodextrin, 72, 74 rice bran, 309 sugar beet fiber, 383 Sajilata studies, 206–207 Saku studies, 178 Salad dressing, 432, see also Dressings Salisbury, Carolyn, 452 Salmonella spp. inulin, 49 pectin, 148 Salmonella typhimurium inulin, 50 partially hydrolyzed guar gum, 105–106 Salty goods, 36 Salyers studies, 94 Sandstrom studies, 346 Saniez-Degrave studies, 19–37 Sarkkinen studies, 283–298 Satiety, see also Appetite modulation guar gum, 82 inulin, 52 partially hydrolyzed guar gum, 100–101 polydextrose, 183 potential structure function claims, 4–5 psyllium, 397 resistant starch, 238
viscous dietary fiber, 20 Sato, Suzuki and, studies, 12 Sauces cellulose, 271 fruit fiber, 431 guar gum, 81 inulin, 46, 54 partially hydrolyzed guar gum, 109–110 pectin, 159 Sausages barley fiber, 334 fruit fiber, 431 inulin, 54 polydextrose, 195 sugar beet fiber, 374 SCFA, see Short-chain fatty acids (SCFA) Scherer, Ben, 452 Schneeman, Poksay and, studies, 100 Scholz and Ahrens studies, 102 Schwab studies, 179 Schwarz, Lee and, studies, 330 Seaweed extracts, 81 Segmentation, 276 Seib and Woo studies, 208 Sellman, Greenberg and, studies, 84 Sensitization, see Adverse effects Sepsis and septic shock, 93 Serum lipids, 257, see also Lipid metabolism Shah studies, 100 Shamai studies, 208 Shand studies, 334 Shao, Yokoyama and, studies, 344 Shi and Trzasko studies, 210 Shigella spp. inulin, 49 pectin, 148 Shimomura studies, 180 Shinnick studies, 328 Shi studies, 210 Short bowel syndrome, 148 Short-chain fatty acids (SCFA), see also Prebiotic characteristics and effects acacia gum, 124 aleurone flour, 443 alpha-cyclodextrin, 11 cellulose, 265, 269 guar gum, 82
494
inulin, 47 Nutriose soluble fiber, 27, 32, 34, 35 oat fiber, 258 partially hydrolyzed guar gum, 87, 90, 91, 94 pectin, 142–143, 147 polydextrose, 178–179 psyllium, 398, 405–406 resistant maltodextrin, 67–68, 68 resistant starch, 227, 236 sugar beet fiber, 375, 381–382 Shortcrust pastry, 189–191, see also Pastries Short gut syndrome, 148 Siddhuraju and Becker studies, 209 Skin partially hydrolyzed guar gum, 86, 103 psyllium, 396 Slimy products, 287 Snack foods acacia gum, 130 barley fiber, 336 oat beta-glucan, 286 resistant starch, 209 sugar beet fiber, 373 Snart studies, 345 Softness, 36 Soluble cellulose, 456 Soluble dextrins, 210, 216 Soluble fibers acacia gum, 121–131 alpha-cyclodextrin, 9–15 inulin, 41–55 Nutriose, 19–37 partially hydrolyzed guar gum, 79–112 pectin, 135–159 polydextrose, 173–196 resistant maltodextrin, 61–75 Sorbet, 158–159 Soups barley fiber, 329, 335, 346 inulin, 54 Nutriose soluble fiber, 37 oat beta-glucan, 287 partially hydrolyzed guar gum, 109 psyllium, 396 sugar beet fiber, 373 Soya milk
Index alpha-cyclodextrin, 11 oat beta-glucan, 293 Soy fiber, 465 Spaghetti, 332 Spapen studies, 93 Speakers, electronic, 272 Specifications, 177 Spina bifida, 443 Sponsors, 455 Sports drinks, 129, see also Beverages Spreads and spreadable products inulin, 46, 54 pectin, 157, 159 Stability barley fiber, 334 gums, 81 inulin, 46, 54, 109 partially hydrolyzed guar gum, 109–110 pectin, 159 polydextrose, 109, 191–193 psyllium, 396 resistant dextrin, 109 sugar beet fiber, 372 Staphylococcus aureus, 230 Starch replacement, 54 Steatosis, 48 Steenblock studies, 253 Stenvert, Nick, 452 Step 1 diet (AHA), 89 Stephen studies, 255 Sterilization, 20, 35 Stevia, 75 Stickiness, 131 Stool bulk alpha-cyclodextrin, 11 inulin, 48–49 Stool consistency acacia gum, 126 partially hydrolyzed guar gum, 90–91 psyllium, 398 Stool frequency cellulose, 264 inulin, 48–49 partially hydrolyzed guar gum, 91–92 polydextrose, 178 psyllium, 398, 399 Stool incontinence, 126
Index Stool output, see also Intestinal regularity cellulose functionality, 264–265 inulin, 48–49 partially hydrolyzed guar gum, 94 sugar beet fiber, 375–376 Stool softening inulin, 53–54 partially hydrolyzed guar gum, 105 polydextrose, 178 sugar beet fiber, 375 Stool straining, 399 Stool transit time cellulose, 264–265 oat fiber, 255–256 partially hydrolyzed guar gum, 90–91 polydextrose, 178 psyllium, 398 sugar beet fiber, 378 Stool weight cellulose, 264 inulin, 48–49 oat fiber, 255–256 partially hydrolyzed guar gum, 90–91 psyllium, 399 resistant starch, 227 Stowell studies, 173–196 Strauss studies, 51 Streptococcus spp., 230 Streptococcus bovis, 144 Streptococcus iniae, 345 Strontium, 146–147 Stumm and Baltes studies, 175 Sucralose, 75 Sugar beet fiber adsorption/binding of ions/organic molecules, 372 backbone, 365, 367 bakery products, 374 cellulose, 369–370 cereals, 373 characteristics, 361–372 colorectal cancer, 381–382 composition, 362–364 digestability, 374–375 extracted polysaccharides, 372–373 extraction, 368–369 fermentability, 374–375
495 food applications, 372–374 functionality, 372–374 fundamentals, 360–361, 383 glucose metabolism, 376–378 hemicelluloses, 369 hydration properties, 370–371 lipid metabolism, 378–381 meat products, 374 mineral adsorption, 376 molar mass, 368–369 non-sugar substituents, 367–368 pectin structure, 365–369 physiochemical properties, 370–372 physiological benefits, 374–383 production, 361 safety, 383 side chains, 367 stool output, 375–376 structure of polysaccharides, 365–370 tolerance, 382–383 toxicity, 383 transit time, 375–376 whole fiber, 373–374 Sugar cane fiber, 465 Sugar metabolism, see Glucose metabolism and response Sugar(s)-free food products acacia gum, 128, 130 claims, 37 Nutriose soluble fiber, 37 polydextrose, 175, 196 Sundberg and Falk studies, 329 SunFiber, 461–462, see also Partially hydrolyzed guar gum (PHGG) Sunitha studies, 313 Sunvold studies, 255–257 Suppliers acacia gum, 458 aleurone flour, 455–456 alpha—cyclodextrin, 455 bamboo fiber, 465 cellulose, 456–457 corn bran, 457 cottonseed fiber, 465 Fibersol-2, 462–463 fructo-oligosaccharides, 458–460 gum arabic, 458 hydroxymethylpropul cellulose, 456 inulin, 458–460 Nutriose soluble fiber, 462–463
496
Index
oat beta glucan, 460 oat fiber, 460–461 partially hydrolyzed guar gum, 461–462 pectin, 462 resistant maltodextrin, 462–463 resistant starch, 463–464 soluble cellulose, 456 soy fiber, 465 sugar beet fiber, 464 sugar cane fiber, 465 Surimi, 195 Suspension, 396 Suzuki and Hara studies, 88, 105 Suzuki and Sato studies, 12 Svihus, Hetland and, studies, 255–257 Sweetness and sweet products alpha-cyclodextrin, 11 inulin, 45 Nutriose soluble fiber, 36 polydextrose, 185 Symons and Brennan studies, 334 Synergy 1 cancer risk reduction, 52 fundamentals, 45 gut microflora modulation, 49 mineral absorption, 52–53 ulcerative colitis, 50 Szczodrak and Pomeranz studies, 329
T Table spreads, 46, 54, see also Spreads and spreadable products Tablet binders acacia gum, 131 pectin, 159 polydextrose, 196 Takahashi studies cellulose, 263–277 partially hydrolyzed guar gum, 88, 92, 95, 100, 103, 106 Takeno studies, 88, 90 Tapola studies, 283–298 Tappy studies, 296 Tartness, 109 Taste inulin, 54 Nutriose soluble fiber, 36–37
Tea, 11 Teacakes, 286 Technology cellulose, 277 Nutriose soluble fiber, 35–36 polydextrose, 185–193 Temelli studies, 328, 335 Temperatures acacia gum, 129 alpha-cyclodextrin, 10 barley fiber, 330 Nutriose soluble fiber, 20 pectin, 140 polydextrose, 192–193 Textiles, 81 Texture barley fiber, 334 cellulose, 271 inulin, 54 oat fiber, 251 partially hydrolyzed guar gum, 109 pectin, 156 Tg, see Glass transition temperature (Tg) Thibault, Renard and, studies, 363 Thibault studies, 359–383 Thickeners guar gum, 81 oat beta-glucan, 287 psyllium, 396 Thomsen studies, 250, 259 Thorup studies, 381 Tiihonen, Kirsti, 197 Timing of medications, 412 Tissue damage, 127 Titgemeyer studies, 258 Toden studies, 231 Tokunaga and Matsuoka studies, 69 Tolerance, see also Digestion acacia gum, 123 Nutriose soluble fiber, 25, 27–28 polydextrose, 183–184 resistant starch, 228 sugar beet fiber, 382–383 Tomato sauces, 159 Tomlin and Read studies, 178 Tooth-friendly properties, 183 Topping, Annison and, studies, 206, 208 Topping studies, 329, 439–452 Tortillas barley fiber, 333, 336
497
Index resistant starch, 208 Total dietary fiber (TDF) barley fiber, 330, 333–334 maltodextrin, 23 measuring method, 75 rice bran, 307, 309, 311, 312 Tovar studies, 207 Toxicity aleurone flour, 451 alpha-cyclodextrin, 13–14 barley fiber, 346–347 partially hydrolyzed guar gum, 100, 104–107 psyllium, 410–412 sugar beet fiber, 383 Toxic metals excretion, 145–147 Traditional resistant starch, 212–215 Tragacanth gum, 81 Transit time cellulose, 264–265 dietary fiber, 5 oat fiber, 255–256 partially hydrolyzed guar gum, 90–91 polydextrose, 178 psyllium, 398 sugar beet fiber, 375–376, 378 Treponema saccharophilum, 143 Triacylglycerides, 96 Trichuris suis, 259 Triglyceride levels, see also Cholesterol; Lipid metabolism alpha-cyclodextrin, 13 barley fiber, 338 inulin, 47–48 partially hydrolyzed guar gum, 88 pectin, 150 polydextrose, 178–179 resistant maltodextrin, 70–71 Trimble, Rodney, 452 Trinidad studies, 98 Trogh studies, 333 Trowell, Burkitt and, studies, 1–2 Trowell studies, 427 Trowel studies, 409 Tryptophan, 313 Trzasko, Shi and, studies, 210 Tsai, Liu and, studies, 178 Tsuda studies, 86
Tube-feeding formulas, see Enteral nutrition formula and feeding Tuohy studies, 95
U Udon noodles, 332 Ulcerative colitis, 50 Urea acacia gum, 126 oat fiber, 250, 259 Uremia, 395 Urine acacia gum, 126 pectin, 141 Uronic acids, 141 Usher, Sylvia, 452
V Vahouny Fiber Symposium, x Valine, 313 Vasankari and Ahotupa studies, 179 Vasanthan, Jiang and, studies, 326 Vasanthan and Bhatty studies, 329 Vegetables and vegetable juices Nutriose soluble fiber, 35 recommended daily amounts, 433–434 Veillnella spp., 49 Velazquez studies, 94 Vis and Lorenz studies, 336 Viscosity acacia gum, 128 alpha-cyclodextrin, 10 barley fiber, 335 guar gum, 82 inulin, 46 oat beta-glucan, 284–285, 298 partially hydrolyzed guar gum, 99–100 pectin, 151, 156 psyllium, 396 Vitacel Oat Fibers, 288, 460–461 Vitamins aleurone flour, 439 alpha-cyclodextrin, 11 barley fiber, 346–347 partially hydrolyzed guar gum, 107
498
Index
psyllium, 411
W Waalkens-Berendsen studies, 13 Wang and Gibson studies, 182 Wang studies, 230–231, 255–256 Watanabe studies, 102 Water absorption, intestines, 269–270, see also Hydration Water binding property, 429–430 Wattle blossom model, 122 Weaver studies, 108 Weber studies, 347 Weibel and Myers studies, 370 Weibel studies, 370 Weickert studies, 250, 254 Weight management and control, see also Body weight alpha-cyclodextrin, 12–13 oat fiber, 256 partially hydrolyzed guar gum, 100–101 pectin, 144–145 potential structure function claims, 4–5 resistant starch, 228, 237–239 Wells studies, 107–108 Wenger, Beringer and, studies, 51 Wheat, 37 Wheat bran acacia gum, 124 aleurone flour comparison, 444 barley fiber comparison, 347 intestinal regularity, 5 oat beta-glucan comparison, 289, 293, 297 oat fiber comparison, 249, 258 resistant starch, 232 rice bran comparison, 312 water-binding properties, 430 Wheat fiber, 430 Whipped cream cellulose, 271 partially hydrolyzed guar gum, 110 Whole fiber, 373–374 Whole grain recommendation, 316 Williams studies, 1
Wils studies, 19–37 Wise and Heyl studies, 51 Wisker studies, 346 Wolf studies, 208 Woo, Seib and, studies, 208 Wood studies, 286, 296, 343 Woo studies, 210 Wounds, 395 Wursch and Pi-Sunyer studies, 343
X Xerophthalmia, 395 Xylitol, 183 Xylooligosaccharides, 124
Y Yacon, 43 Yamada studies, 88, 101 Yamatoya studies, 87, 89, 92, 98 Yeast fermentation, 129 Yeast-leavened bread, 287 Yogurt, see also Dairy products barley fiber, 335 inulin, 54 Nutriose soluble fiber, 28 oat fiber, 250, 254 partially hydrolyzed guar gum, 89, 109 pectin, 158 polydextrose, 194 psyllium, 396 sugar beet fiber, 372 Yokoyama and Shao studies, 344 Yokoyama studies, 343 York studies, 175 Younes studies, 250, 258 Yu studies, 257
Z Zarling studies, 253, 255–256 Zervas and Zijlstra studies, 256, 259 Zhang studies, 1, 345 Zheng studies, 335
499
Index Zhou studies, 238, 442 Ziai studies, 393–412 Zijlstra, Zervas and, studies, 256, 259 Zinc aleurone flour, 439 barley fiber, 346–347
cellulose, 277 oat beta-glucan, 298 partially hydrolyzed guar gum comparison, 103 pectin, 145–147 sugar beet fiber, 376