Fiber Ingredients Food Applications and Health Benefits 1420043846

FIBER
INGREDIENTS
Food Applications
and Health Benefits
FIBER
INGREDIENTS
Food Applications
and Health Benefits
EDITED BY
SUSAN SUNGSOO C H O AND P R I S C I L L A SAMUEL
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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 2008050642
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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 pro-
fessionals 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 oppor-
tunities for fiber ingredients and fiber-containing foods, such as gastroin-
testinal 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 & Reg-

ulatory 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 inter-
nationally, 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 develop-
ment from Bangalore University, India.
ix
Contributors
Anne Birkett Christine E. Fastnaught

National Starch Food Innovation PhoenixAgri Research
Bridgewater, New Jersey, U.S.A. Fargo, North Dakota, U.S.A.
Jon Bodner Michael Fenech

JRS USA CSIRO Human Nutrition,
Schoolcraft, Michigan, U.S.A. Food Science Australia
Adelaide, Australia
Douwina Bosscher
Orafti Active Food Ingredients E. Terry Finocchiaro
Tienen, Belgium National Starch Food Innovation
Bridgewater, New Jersey, U.S.A.
Sebastien Baray Jürgen Fischer

Colloïdes Naturels, Inc. Herbafood Ingredients
Bridgewater, New Jersey, U.S.A. Havel, Germany
Jonathan David Buckley Anne Franck

School of Health Sciences Orafti Active Food Ingredients
University of South Australia Tienen, Belgium
Adelaide, Australia
Fabienne Guillon
Susan Cho UR1268 Biopolymères Interactions
Nutrasource Assemblages
Clarksville, Maryland, U.S.A. INRA
Nantes Cedex 03, France
Peter Clifton Chieko Hashizume

CSIRO Human Nutrition, Matsutani Chemical Industry Co.,
Food Science Australia Ltd.
Adelaide, Australia Itami City, Hyogo, Japan
Hans Ulrich Endress Peter Howe

Pektin-Fabrik Neuenbuerg School of Health Sciences
Herbstreith & Fox KG University of South Australia
Neuenbuerg, Germany Adelaide, Australia
xi
xii Contributors
Lekh R. Juneja Kazuhiro Okuma

Interface Solution Division Matsutani Chemical Industry Co.,
Taiyo Kagaku Co. Ltd. Ltd.
Yokkaichi, Mie, Japan Itami City, Hyogo, Japan
Talwinder S. Kahlon Marie-Christine Ralet

Western Regional Research UR1268 Biopolymères Interactions
Center Assemblages
USDA, ARS INRA
Albany, California, U.S.A. Nantes Cedex 03, France
Mahendra P. Kapoor Catherine Renard

Interface Solution Division UR1268 Biopolymères Interactions
Taiyo Kagaku Co. Ltd. Assemblages
Yokkaichi, Mie, Japan INRA
Nantes Cedex 03, France
Catherine Lefranc-Millot
Nutrition Management Jean-Michel Roturier
Roquette Freres Nutrition Management
Lestrem, France Roquette Freres
Lestrem, France
Frank Mattes
Pektin-Fabrik Neuenbuerg Priscilla Samuel
Herbstreith & Fox KG Nutrition Department
Neuenbuerg, Germany The Solae Company
St. Louis, Missouri, U.S.A.
Manny Noakes
CSIRO Human Nutrition, Marie-Hélène Saniez-Degrave
Food Science Australia Nutrition Management
Adelaide, Australia Roquette Freres
Lestrem, France
Monika Okoniewska
National Starch Food Essi Sarkkinen
Innovation Foodfiles
Bridgewater, New Jersey, U.S.A. Kuopio, Finland
Contributors xiii
Julian D. Stowell David Topping

Danisco Sweeteners CSIRO Human Nutrition,
Redhill, Surrey, U.K. Food Science Australia
Adelaide, Australia
Toru Takahashi
Mimasaka University
Tsuyama City, Japan Daniel Wils
Nutrition Management
Roquette Freres
Niina Tapola Lestrem, France
Foodfiles
Kuopio, Finland
Seyed Ali Ziai
Jean-Francois Thibault Department of Pharmacology
UR1268 Biopolymères Interactions Faculty of Medicine
Assemblages Shaheed Beheshti University of
INRA Medical Sciences
Nantes Cedex 03, France 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 (Bing-
ham 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 con-
sume an amount equal to or greater than their age plus 5 grams per day (Wil-
liams 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 Asia-
Pacific 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 poly-
saccharides and lignin that are not hydrolyzed by human alimentary
enzymes (Burkitt et al. 1974; Burkitt and Trowell 1975). Recently, the Insti-
tute 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 meth-
odologies; 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 perspec-
tives. The survey results indicated that 65% of people supported the cur-
rent 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 (for-
merly 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 Nash-
ville, Tennessee, in October 1995 (Cho and Prosky 1999).
Functional and Dietary Fibers: Introduction 3
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 supple-
ment and risk of a disease. So far, the U.S. Food and Drug Administra-
tion (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 Low-fat diets rich in fiber-containing
products, fruits, and grain products, fruits, and
vegetables (101.76) vegetables may reduce the risk of
some types of cancer, a disease
associated with many factors.
CHD Diets rich in fruits, vegetables, Diets low in saturated fat and
and grain products that cholesterol and rich in fruits,
contain fiber, particularly vegetables, and grain products that
soluble fiber (101.77) 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 Soluble fiber from psyllium and
foods (oats and/or psyllium) foods such as [Product Name], as
(101.81) 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.
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 character-
ized 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 impor-
tant risk factors for type 2 diabetes, such as being overweight, being physi-
cally 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 evi-
dence on risk of reduction of diabetes as a secondary endpoint to support a
recommended intake level for total fiber that is primarily based on preven-
tion 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 over-
all 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 con-
sistency, 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 move-
ments 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, Dorron-
soro 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: Lan-
cet 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.
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; nutri-
tion 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
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62(1):11–55.
Lee SC, Prosky L (1992) Dietary fiber analysis for nutrition labeling. Cereal Foods
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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. Diabe-
tologia 49(5):912–20.
Lopez-Miranda J, Williams C, Lairon D (2007) Dietary, physiological, genetic and path-
ological influences on postprandial lipid metabolism. Br J Nutr 98(3):458–73.
Marlett JA, McBurney MI, Slavin JL (2002) Position of the American Dietetic Associa-
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intake, dietary glycemic index and load, and body mass index: a cross-sectional
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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-1,4-
glycosidic 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 pro-
duced 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 mol-
ecule 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 for-
mation of α-, β-, and γ-cyclodextrin, respectively [1].
More than 80 years ago it was discovered that α-CD is resistant to diges-
tion by the pancreatic juice of dogs [2]. This resistance to hydrolysis by pan-
creatic amylase was confirmed in subsequent studies, which also identified a
resistance to hydrolysis by salivary amylase [3–5]. This resistance to hydroly-
sis 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 sali-
vary amylase means that it remains almost undigested in the small intestine,
it is completely fermented in the large intestine [7, 8].
9
OH
OH
O
O HO O O
O O HO O OH
O O
O O HO O OH H H
HO H H HO
HO O
OH
O
O HO
O OH OH
O
OH HO O
HO
HO O HO
O
OH OH
OH H H O H
O O OH H O O
HO O OH OH H O O
O O O H
O O O O
O
HO HO
OH
α-CD β-CD
OH
HO
O O
O O O
H H HO O OH
O OH HO
O OH O
HO HO
O
OH
HO
O
OH
OH
O H
O
H O
OH O O
HO O OH
OH H
O
O
O 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 sol-
uble 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 solu-
bility, 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 com-
plexes 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 pho-
todegradation [13, 14]. It has also been proposed that, because α-CD is taste-
less 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 indigest-
ible 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-
160
Area under Plasma Glucose Curve

140
120
(m mol.l–1.min1) 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 addi-
tion 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 devel-
oping 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
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 concentra-
tions 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 associ-
ated 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 gas-
trointestinal complaints associated with the consumption of any non-digest-
ible, fermentable dietary fiber (e.g., bloating, nausea, flatulence, diarrhea).
A number of studies have been conducted to test the maternal and embry-
onic/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 gesta-
tion was well tolerated with no adverse effects on maternal reproductive per-
formance, and no embryotoxic, fetotoxic, or teratogenic effects were found.
Similar studies have been carried out in both rats and mice [15, 16, 47–49],
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 neces-
sarily give a positive Ames test, the potential for α-CD to damage DNA (and
therefore its carcinogenic potential) was also tested using in vivo micronu-
cleus 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 con-
sistently, 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 con-
version 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 manufac-
ture, 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-
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 con-
sumption of carbohydrate-containing foods. Reducing the glycemic response
to carbohydrate foods can potentially reduce the risk of developing cardio-
vascular 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, ferment-
able 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.
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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 his-
tory of human evolution. The human diet has changed from a plant-based
non-purified regimen to a few cereal-based purified diets. The first conse-
quence of this change is the decline of dietary fiber consumption. The asso-
ciation of health effects with dietary fiber was described as early as the 4th
19
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 com-
ponents 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 absorp-
tion [3].
On the contrary, non-viscous soluble fibers like oligosaccharides and resis-
tant 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 harm-

ful 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 out-

standing digestive tolerance that is in agreement with its health-promoting
effects. Particularly, as a carbohydrate with low content in mono- and disac-
charides, this fiber is very apt to meet the WHO’s recommendations con-
cerning 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% mois-
ture 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 tem-
perature 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 stan-
dard maltodextrins, and in dextrins.
Chromatography can be utilized to further increase the fiber content and
tailor the molecular weight distribution. Different kinds of resistant dex-
trins, 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 chromato-
graphic step.
Table 3.1
Results of Interlaboratory Study for the AOAC 2001.03 Method
70% 70% 60% 95 %
NUTRIOSE® Fiber Fiber Fiber NUTRIOSE® Fiber
FB06 Dextrin Dextrin Dextrin FM06 Dextrin
Mean g/100 g 84.7 72.3 72.8 59.9 84.4 97.3
D.S.a
Sr 0.61 1.42 0.46 0.89 1.06 1.43
RSDr % 0.71 1.96 0.67 1.48 1.25 1.47
rb 1.70 3.96 1.30 2.48 2.96 4.01
SR 2.80 2.76 1.46 1.52 2.57 2.80
RSDR % 3.29 3.82 2.00 4.26 3.05 2.88
Rc 7.85 7.73 4.08 2.54 7.21 7.83
Note: D.S.: dry substance.
a Average of values obtained from the interlaboratory study.
b 2.8 x Sr.
c 2.8 x SR.
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 consen-
sual 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 sup-
port from the scientific community. Oligosaccharides, which are resistant
short-chain polysaccharides with a degree of polymerization convention-
ally 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.
CH2OH CH2OH CH2OH

O O O
OH OH OH
O O O O
OH OH OH
CH2OH CH2OH CH2 CH2OH
O O O O
OH OH OH OH
O O O O O
OH OH OH OH
CH2OH CH2OH CH2OH CH2OH CH2 CH2OH CH2OH
O O O O O O O
OH OH OH OH OH OH OH
O O O O O O O OH
OH OH OH OH OH OH OH
1a: Starch
(a) Starch
CH2OH CH2OH
O O
OH OH
O O O
OH OH
CH2 CH2OH CH2OH
O O O
OH OH OH
O O O O
OH OH OH
CH2OH CH2OH CH2OH CH2 CH2 O
O O O O O
OH OH OH OH
O O O O O
O
OH OH O OH OH
CH2 CH2OH CH2OH CH2OH O
O O O O
OH OH OH OH
HO O O HO
OH OH OH OH
1b: NURIOSE 06 ®
(b) Nutriose® 06
Figure 3.1
Respective structural formulas of starch (a) and NUTRIOSE® 06 (b) one type of resistant dex-
trin 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
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 obtain-
ing 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).
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 NUTRI-
OSE® 06 is 85% per dry substance including 50% of fibers insoluble in etha-
nol [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 toler-
ance threshold is the highest ingested dose inducing no major gastrointes-
tinal 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 prebi-
otic benefits. The fermentation results in the production of gas (mainly CO2,
CH4, and H2) naturally excreted in both breath air and flatulence. With con-
sumption of high doses of fermentable carbohydrates, the quantity of pro-
duced gas can exceed the capacity of breath excretion; therefore tolerance
threshold knowledge is needed in order to confirm that the required physi-
ological 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 administra-
tion of increasing amounts of 10, 15, 30, 45, 60, and 80 grams indigestible dex-
trin 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,
26
110
Product n°1 Product n°2 Product n°3 Product n°4 Product n°5 Product n°6
105
100
95
90
85
80
75
70
65
60
55
50
45
40
Fiber Content % DS
35
30
25
20
15
10
5
0
Black bars: Low molecular weight fiber Gray bars: High molecular weight fiber (alcohol precipitated)
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 Ingredients: Food Applications and Health Benefits
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 vol-
unteers 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 polym-
erization 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.
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 carbohy-
drate 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 resis-
tant 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 adapta-
tion 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 tech-
nical 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
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 recommen-
dations [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].
10
8
®
NUTRIOSE FB 06
Glycaemia (mmol/L)
Dextrose
7
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
40
35
Insulinaemia (mUI/L)
30
25 Dextrose
®
NUTRIOSE FB 06
20
15
10
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).
Gut Well-Being
Soluble dietary fibers reach the colon almost unchanged where they can
induce “prebiotic effects” characterized by (a) an increase in “beneficial bac-
teria” 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 bac-
terial 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 Type of Flora Quantified Before After
NUTRIOSE® in the Human Feces
Administered;
Duration of the Diet
10 g/d – 14 days Bacteroides (Log CFU/g) 8.543 ± 0.51 8.958 ± 0.68
15 g/d – 14 days Clostridium perfringens 3.521 ± 1.65 2.360 ± 1.53
(Log CFU/g)
45 g/d – 35 days Lactobacilli (Log CFU/g) 7.2 ± 1.4 8.2 ± 1.2
70 (**): P < 0.01

***
60 (***): P < 0.005
**
50
SCFAs (mg/caecum)
40
30
20
10
0
2.5% 5% 10%
Control
® ®
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 indi-
gestible dextrin consumption. In study 1, fecal pH was 6.67 before the inter-
vention 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 differ-
ence 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 adminis-
tered 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 (Fig-
ure 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. Spe-
cifically, 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-
35 (*): p < 0.05

30
*
25
bglucosidase (U/min/g)
20
15
10
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 begin-
ning 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. Glucosi-
dases 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 desir-
able colonic bacteria. They contribute to maintaining a healthy colon.
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 fermenta-
tions, 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 pro-
duction 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-
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 utili-
zation 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 process-
ing, 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 table-
top 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 fin-
ished products. In products like reduced-sugar beverages or fruit fillings,
reduced-sugar or low-fat biscuits, bars, and toppings, they will allow balanc-
ing 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 produc-
tion lines, in warehouses, and for use in tropical countries.
As it does not provide cloudiness in solution, it is dedicated for applica-
tions 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 pharmaceuti-
cal areas.
Resistance to Various Industrial Processing

The resistant dextrin’s product range is stable in high-temperature process-
ing conditions, including sterilization, UHT treatment, or baking. It remains
stable in acidic conditions, such as fruit and vegetable juices. These prop-
erties have been validated through measurement of the change in molecu-
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 hard-
boiled 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 guaran-
tee 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 pro-
cessable 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 viscos-
ity 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
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 heat-
treated 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. There-
fore 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 food-
stuffs, 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.
References
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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 Jen-
kins, 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.
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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
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 for-
mulations, inulin improves the organoleptic characteristics, upgrading both
taste and mouthfeel in a wide range of applications. In particular, this taste-
free 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 ben-
efits 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 compro-
mising on taste and texture, while delivering nutritional benefits to the final
product. Inulin, therefore, represents a key ingredient offering new oppor-
tunities 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 oligo-
saccharides. 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
Inulin 43
HOCH2
O O OH
OH HO
HO HO CH2
HO OH
O O
HOCH2 HOCH2
O O
HO HO
HO CH2 HO CH2
n–1 m–2
HOCH2 O O
HOCH2
O O
HO HO
CH2OH CH2OH
HO HO
(GFn) (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 oligofruc-
tose 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 con-
tents 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.
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 glu-
cose originating from the starch or maltodextrins present.
Although the AOAC method 997.08 is very reliable, it is very labor inten-
sive and requires the use of chromatographic equipment. The AOAC method
999.03 [6], completely based on the use of enzymes as well for the hydroly-
sis as for the sugar determinations, requires only a spectrophotometer and
some other standard lab equipment. This method is reliable for the determi-
nation 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 (Helian-
thus tuberosus), and chicory (Cichorium intybus) could be considered good can-
didates 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 sec-
ond 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 enzy-
matic hydrolysis of inulin, oligofructose (Orafti® oligofructose) is obtained.
A purified endo-inulinase is used since the aim is to produce inulin oligom-
ers with the least possible formation of mono- and disaccharides. Oligof-
ructose 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 sweet-
ness [8]. It behaves like a bulk ingredient, contributes to body and mouthfeel,
provides a better-sustained flavor with reduced aftertaste (e.g., in combina-
tion 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
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 dry-
substance 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 long-
chain 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 incorpo-
rated 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 distri-
bution 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 fat-
Table 4.1
Physicochemical Properties of Chicory Inulin
Inulin Inulin HP
Chemistry GpyFn GpyFn
DP 3-60 DP 10-60
DPav 12 25
Inulin content (% dry matter) 92 99.5
Dry matter (%) 95 95
Sugars (% dry matter) 8 <0.5
pH (10% in H2O) 5-7 5-7
Ash (% dry matter) <0.2 <0.2
Heavy metals(% dry matter) <0.2 <0.2
Color White White
Taste Neutral Neutral
Sweetness vs. sucrose (%) 10% None
Water solubility (% at 25°C) 12 2.5
Water viscosity (5% at 10°C) 1.6 mPa 2.4 mPa
Source: Adapted from Franck, A., Technological functionality of inulin and oligofructose, Br.
J. Nutr., 87 (suppl. 2), S287–S291, 2002.
Inulin 47
replacing and stabilizing properties. They have a slower and more sustained
fermentation along the large intestine. The shorter chains show technologi-
cal 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 volun-
teers [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 com-
parison 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 fac-
tors together explain the reduced caloric value of inulin.
Based on 14C studies in humans, the caloric value of fructooligosaccha-
rides 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 sug-
gested 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
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 bac-
terial 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 triglyc-
erides 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 fat-
rich diet reduced postprandial serum triglyceride contents, as well as serum
cholesterol, by more than 50% compared with controls. Enhanced triglycer-
ide-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-fer-
mentable) 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 hyper-
lipemia are involved in the disease development. This has been demon-
strated 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 function-
ing 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 research-
ers observed a decreased transit time.
Modulation of Gut Microflora

The large intestine harbours over 400 different types of bacteria that repre-
sent over 50% of the dry solids content in the colon. This microbial ecosystem
in the large intestine is important for maintaining good health, and imbal-
ances are thought to be a basis for the ethiology of various diseases.
Inulin selectively promotes the growth and/or metabolic activity of a lim-
ited 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 long-
chain 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 prebiot-
ics. 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 Bifido-
bacteria. Objective observations support their potential as health-promoting
bacteria. As Bifidobacteria counts increase after ingestion of inulin, a concomi-
tant decrease in (potentially) pathogenic populations is often observed in
vitro, in animal and human studies (e.g., Clostridia, E. coli, Salmonella, Veil-
lonella, Shigella, and Listeria) [43, 44]. In experiments with gnotobiotic quails
inoculated with a flora from a baby with necrotizing enterocolitis (comprising
Clostridium butyricum) most of the quails died. However, quails that were
given Bifidobacteria made a complete recovery. This was one of the first stud-
ies demonstrating the health effects of Bifidobacteria in living beings [50].
Also, in vitro, the antagonistic (antibacterial) activity of lactic-acid-produc-
ing 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 addi-
tion, 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 vari-
ous animal models have shown that inulin and oligofructose accelerate the
recovery of beneficial bacteria, slow down pathogen growth, decrease patho-
gen 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 dis-
ease, or prone to critical illness, found that inulin and oligofructose restore
the balance when the gut microbial community is altered, inhibit the pro-
gression of disease, or prevent it from relapsing [55, 56]. In patients with
C. difficile-associated diarrhea, triggered by antibiotic therapy, the admin-
istration of oligofructose significantly increased the numbers of Bifidobacte-
ria and lowered relapse episodes of diarrhea compared to the controls [57].
Also in chronic gastrointestinal diseases such as inflammatory bowel dis-
eases (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 bifidobacte-
rial 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 clin-
ical 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] recom-
mended 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 appli-
cations 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 interac-
tion 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 appetite-
suppressing 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 lev-
els 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 sys-
temic effects of oligofructose (e.g., improved glucose tolerance, fasting blood
glucose, glucose-stimulated insulin secretion, insulin-sensitive hepatic glu-
cose 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-
tion study including 10 healthy volunteers (2*8 g/day of BeneoTM oligof-

ructose) 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 combi-
nation 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 sig-
nificant 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 trans-
planted in the thigh and peritoneum of mice [71].
The preventive effect of oligofructose-enriched inulin (Synergy1), espe-
cially 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 pla-
cebo-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 inflam-
mation 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 dem-
onstrate the protective effect of the synbiotic against colon cancer develop-
ment [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 ovariecto-
mized 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 inu-

lin or oligofructose taken alone [76, 77].
In a study with healthy adult volunteers who were given 40 g/day of inu-
lin, a significant increase in calcium absorption was observed using the bal-
ance 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 absorp-
tion already after eight weeks of supplementation and the higher absorp-
tion 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 pres-
ence 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 tol-
erate 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 inu-
lin are well tolerated by most people and that daily doses of 10 to 20 grams
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 orga-
noleptic 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 develop-
ment of low-fat foods without compromising on taste and texture. This is
particularly true in spreadable products. In table spreads, both fat and water-
continuous, 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 prod-
ucts, 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 mouth-
feel, 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 (par-
tially) 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 mouth-
feel, reduces syneresis, and offers a synergistic taste effect in combination
with high-potency sweeteners such as aspartame, acesulfame K, and sucral-
ose, 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-cheese-
based 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 ingredi-
ent 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 bacte-
rial ecosystem on the host’s health status will be better elucidated. Modula-
tion 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 pre-
vention of obesity. Given the high burden of these diseases in Western societ-
ies, 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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lescents, 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 inulin-
type 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 contin-
ued 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 ben-
efits of other essential nutrients. The beneficial effects of diets rich in dietary
fiber include decreased risk of coronary heart disease and improvement in
61
40
35
Adequate Intake
30
DF Intake (g/day)
25
20
15
10 Actual I for males

Actual Intake Actual I for females
5 Adequate I for males
Adequate I for females
0
3
0
13
+
1–
4–
–1
–3
–5
–7
71
9–
14
19
31
51
(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 Refer-
ence 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 (approxi-
mately 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 industrial-
ized 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 outstand-
ing 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 proper-

ties 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 charac-
teristic stage in the production process, Hydrolysis with amylases
both hydrolysis and transglucosidation of
starch occur (dextrinization process). The Removal of glucose by filtration
resulting dextrin solution is hydrolyzed Decolorization by active carbon
by enzymes, before being refined by fil-
tration through activated carbon and an Deionization by ion-exchange resin
ion-exchange resin. After concentration, Concentration and spray-drying
the non-digestible material is spray-dried.
The final product is stable to any further Weighing and packaging
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 polysaccha-
rides 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. Approxi-
mately 50% is fermented in the large intestine and the remaining approximate
CH2OH CH2OH
O O
OH OH
O O OCH2
OH
CH2OH OH CH2OH CH2OH CH2O
O O O O O
OH O OH OH OH
HO CH2 HO O O O
OH OH OH OH OH
CH2OH CH2OH CH2OH O
O O O O
OH OH OH OH
O O O O
OH OH OH
CH2OH CH2OH CH2OH O
O O O
OH OH OH
HO 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%
®
Fibersol -2 58.5% 27.0% 3.2% 11.3%
Figure 5.3
Structural characteristics of resistant maltodextrin: comparison with conventional maltodex-
trins 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.
Table 5.1
Improvement of Stool Conditions by Resistant Maltodextrin
Stool Stool Defecation
Wet Weight Dry Weight Moisture Frequencies
(g) (g) (%) (n)
Test Group 778.2 ± 93.2* 180.5 ± 12.9* 76.8 ± 1.8 5.92 ± 0.40a
(n = 8)
Control 571.5 ± 58.7 137.9 ± 5.6 76.2 ± 1.7 4.76 ± 0.36
(n = 8)
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 five-
day 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 malto-
dextrin (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
Table 5.2
Fermentability of the Resistant Maltodextrin by Various Intestinal
Bacteria
Strains Fermentability
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 –
Note: Acid production: +++, within 1 day; ++, 2 days; +, 3 days. ± ~ –: negative.
Source: Adapted from Ohkuma, K. et al., Pyrolysis of Starch and Its Digestibil-
ity by Enzymes, Denpun Kagaku, 37, 104–114, 1990.
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 49.4 ± 6.0 43.2 ± 2.5 49.8 ± 3.9
Bifidobacterium 10.5 ± 3.4 17.9 ± 2.7 13.7 ± 1.9
Others 40.1 ± 4.2 38.9 ± 2.5 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 per-
centages 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 reabsorp-
tion thus lowering blood cholesterol levels.
An in vitro experiment using human feces to ferment resistant maltodex-
trin 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 for-
mation of SCFA and changes in pH were observed over a 24-hour period.
Fructooligosaccharide is known to be completely fermented. The fermenta-
tion 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 pro-
duction 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-
7.0
FOS
Total SCFA (mmol/g) RMD
Time (hr) FOS MD GA GA
1.5 1.08 1.02 0.06 6.5
6 7.12 3.20 0.30
pH
11 7.26 4.08 1.42
24 7.66 6.01 8.08 6.0
FOS: Fructo Oligo Saccharide

MD: Fibersol-2 5.5
GA: Gum Arabic 0 6 12 18 24
Time (hr)
SCFA Production 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 maltodex-
trin observed at the start of the incubation indicates that the low-molecular-
weight 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 sys-
tem is administrated for a long period of time, the patient can suffer from
gastrointestinal malfunctions such as diarrhea, constipation, or abdomi-
nal 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% Fiber-
sol®-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 for-
mula 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
Control Enteral Formula Enteral Formula

(Stock Diet) (no fiber)
®
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 post-
prandial 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 monosaccha-
rides [6].
The effects of feeding a single meal with Fibersol®-2 are reported by Toku-
naga 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 consum-
ing 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 individu-
als caused no change in their postprandial blood glucose levels (Figure 5.6d),
250
a b c d
Blood Glucose Levels (mg/dl)
200
150
100
50
0 1 2 0 1 2 0 1 2 0 1 2
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 hypoglyce-

mia or hyperglycemia.
The attenuation of postprandial blood glucose achieved with the con-
sumption of resistant maltodextrin has been verified in other meal-loading
experiments [8–11]; as part of the evidential studies for approving the Japa-
nese Foods for Specified Health Use (FOSHU) products, more than 30 clini-
cal 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 demon-
strated decreases in total cholesterol and triglyceride levels [12–14].
In rat studies, these animals were fed diets high in sucrose without cho-
lesterol and their serum lipids were monitored. Total serum cholesterol and
triglyceride levels were found to be significantly decreased with the admin-
istration 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 experi-
ment, fasting blood glucose levels, total cholesterol levels, and triglyceride
levels were above normal ranges. However, after 12 weeks, significant reduc-
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) 0 2 4 8 12
FPG (mg/dl) 147 ± 17 112 ± 25 107 ± 7 147 ± 21 103 ± 7a
Cholesterol (mg/dl) 265 ± 10 211 ± 29 209 ± 22a 205 ± 10b 209 ± 9b
HDL-Cholesterol (mg/dl) 49 ± 2 45 ± 1 47 ± 3 49 ± 3 40 ± 3b
Triglyceride (mg/dl) 243 ± 34 163 ± 33 134 ± 24a 148 ± 11a 176 ± 42
Ca (meq/l) 4.5 ± 0.3 4.3 ± 0.3 4.5 ± 0.2 4.5 ± 0.2 4.5 ± 0.2
Mg (mg/dl) 2.0 ± 0.2 2.0 ± 0.2 2.0 ± 0.2 2.0 ± 0.2 2.0 ± 0.1
P (mg/dl) 3.0 ± 0.2 3.3 ± 0.4 3.3 ± 0.5 3.2 ± 0.4 3.4 ± 0.3
Fe (μg/dl) 96 ± 43 98 ± 29 99 ± 18 97 ± 16 88 ± 14
RBC (×104/mm3) 488 ± 31 — — — 488 ± 14
GOT (IU/l) 22 ± 10 — — — 19 ± 4
GPT (IU/l) 22 ± 5 — — — 19 ± 4
γ-GTP (IU/l) 69 ± 38 — — — 63 ± 54
LDH (IU/l) 293 ± 36 — — — 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 (with-
out resistant maltodextrin) three times a day for four weeks. Triglyceride
levels were significantly reduced (p<0.05) after consumption of the tea con-
taining 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 postpran-
dial 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
60
Test group
40
Placebo group
20
∆ Triglyceride (mg/dl)
0
*
–20
–40
** *p < 0.026 (t-test)
Administration **p < 0.003 (paired t-test)
–60 Period
–80
Before Before After After
Pre-administration Administration 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 resis-
tant 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 maltodex-
trin. It is assumed that resistant maltodextrin prevents the accumulation of
fat (obesity) by moderating the postprandial rise in blood glucose and insu-
lin 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
Physiological Examination
Before Intake (start) 3-Month Intake

Age (years old) 46.1 ± 3.0
Height (cm) 168.8 ± 1.3
Body Weight (kg) 73.7 ± 3.4 73.0 ± 3.3
BMI 25.8 ± 0.9 25.6 ± 0.9
Body Fat (%) 27.7 ± 0.9 25.9 ± 1.0*
Waist (cm) 90.8 ± 2.4 89.5 ± 2.3
Hip (cm) 98.8 ± 2.1 98.3 ± 2.1
W/H 0.91 ± 0.01 0.91 ± 0.01
V: Area for Visceral Fat (cm2) 108.0 ± 13.7 101.9 ± 11 .6
S: Area for Subcutaneous Fat (cm2) 175.2 ± 25.2 163.9 ± 19.9
V/S 0.70 ± 0.1 0.64 ± 0.07
“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 Insulin levels

250 100
Blood Glucose (mg/dl)
200 75
Insulin (µU/ml)
150 50
100 25
50 0
0 30 60 90 120 30 60 90 120
Time (min) Time (min)
Start 3-month Start 3-month

administration administration
“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 resis-
tant 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.)
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 func-
tional 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 prod-
uct contained 58% dietary fiber. Feeding these varied amounts of resistant
maltodextrin to these subjects did not cause any clinical or problematic gas-
trointestinal 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 con-
taining 58% total dietary fiber (63 grams for a 100% dietary fiber product)
[20]. Resistant maltodextrin would have less tendency to cause diarrhea com-
pared 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
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 neces-
sary to determine its actual dietary fiber content for the purpose of nutri-
tion 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 ana-
lytical 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 res-
ins. The deionized filtrate is analyzed by high-performance liquid chromatog-
raphy 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.
(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)
Residue Filtrate
Ash and Protein Correction Evaporation
IDF + HMWSDF 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 Interna-
tional, 2006.)
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 inges-
tion, J. Jpn. Clin. Nutr., 26(4), 281–286, 2005 (in Japanese).
10. Morita, H., et al., Effect of yogurt containing indigestible dextrin on blood glu-
cose 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 contain-
ing 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 glu-
cose 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).
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 adminis-
tration 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 malto-
dextrin: 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
79
Introduction
Dietary fiber is a vital component of a healthy diet. In recent years, the benefi-
cial 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 read-
ily dissolves in water. Soluble fibers may play a role in lowering blood choles-
terol 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 fermenta-
tion in the large intestine [2]. These fermentable fibers yield short-chain fatty
acids that affect blood glucose and lipid levels, improve the colonic environ-
ment, 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 intesti-
nal tract or gut.
Dietary fibers, especially soluble fibers, have several biological functions.
They help with slowing down the absorption of toxic materials in the intes-
tines, 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 long-
term 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, emulsifica-
tion, suspending water-soluble carbohydrates, stabilization, and mouthfeel.
Unlike gelatin products, gum products do not melt away at room tempera-
ture. 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
Partially Hydrolyzed Guar Gum Dietary Fiber 81
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 traga-
canth 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 carbo-
hydrate 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,
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 influ-
ence 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 lev-
els 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 avail-
able for colonic fermentation, with the production of short-chain fatty acids,
particularly propionate, which has been shown in animal and human stud-
ies 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
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 poly-
saccharide with a molecular weight in the range of 200 to 300 kilodaltons
(kDa). The recognized chemical name of galactomannan is d-galacto-d-
mannan, which is a straight backbone chain composed of (1,4)-linked-β-d-
mannopyranosyl residue with side-branching α-d-galactopyranosyl residue
linked through the O-6 position of approximately every second mannopyra-
nosyl 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 Gener-
ally 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 pro-
duces shorter chains having molecular weights between 1 and 100 kDa, with
OH OH
OH OH
H H
O O
H H
HO 1 H HO 1 H
H OH α H OH α
H H O H H O
H H 6 H H
4
4 OH OH
O H H 1 O H H 1
O HO β O HO β O
HO 1 4 HO 1 4
O O
H β O H β O
H H
OH OH
H H H H
H OH H OH
OHOH OH
OH
H H
O O
H H
HO 1 H HO 1 H
H OH α H OH α
H H O H H O
H H 6 H H
4
4 OH + OH
O H H 1 HO O H H 1
O HO β OH HO β O
HO 1 4 HO 1 4
O O
H β O H β O
H H
OH OH
H H H H
H OH H OH
Figure 6.2
Chemical structure of intact guar gum and partially hydrolyzed guar gum.
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-man-
nopyranosyl 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 man-
nan chain and results in shorter chain galactomannans (MWavg = 20 kDA).
The enzyme employed in the partial hydrolysis of guar gum was 1,4-β-d-
mannan 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 rela-
tively 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-d-
mannase is added and the concentration and reaction time are controlled to
provide the desired degree of hydrolysis. The temperature is raised to inac-
tivate the enzyme as well as halt the hydrolysis process. The solution is buff-
ered with sodium hydroxide or potassium hydroxide as needed and then
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
Intestinal Microflora Balance

and Prebiotic Effects
Partially Hydrolyzed Guar Gum Irritable Bowel Syndrome (IBS)
(PHGG)
Glycemic Index
Weight Control and Satiety
Immunological Effects
Mineral Absorption
Effective Beauty Supplementation
Figure 6.3
Potential metabolic benefits of PHGG.
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 formu-
las 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 compari-
son to intact guar gum and the resulting product is suitable for oral supple-
mentation 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 postpran-
dial (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 con-
sume 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 post-
prandial 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 inges-
tion. When 5 grams of PHGG was ingested simultaneously with 30 grams
sucrose, the blood glucose level after 60 minutes of ingestion was signifi-
cantly 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
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 min-
utes 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 postpran-
dial 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 dif-
ferences in plasma concentrations of glucose and insulin. Similarly, Yama-
toya 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 stud-
ies to the significant success of PHGG in improvement of acute postprandial
plasma glucose and insulin response. However, it may be attributed to typi-
cal problems associated with the protocol design and evaluation of the statis-
tical data with flawed or incomplete experimentations.
Therefore, it can be proposed that PHGG lowers postprandial serum glu-
cose level at least by three mechanisms. First, PHGG increases the viscos-
ity 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 capsul-
ing 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].
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-low-
ering 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 hydro-
lyzed 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 par-
tially 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 triacyl-
glycerides 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 choles-
terol concentrations.
In a study with rats, Suzuki and Hara [45] studied hypertriglyceridemia
associated with fructose feeding to obtain a dietary model of insulin resis-
tance, which was ameliorated by supplementation with a guar gum hydro-
lysate. 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 tria-
cylglyceride-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
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 triacylg-
lycerides was evaluated in a 12-week double-blind, placebo-controlled clini-
cal 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, par-
ticularly in LDL. There were no significant differences in HDL or in triacylg-
lyceride 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 placebo-
controlled 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
triacylglycerides and remnant-like lipoprotein particle cholesterol (RLP-C).

The authors suggested that PHGG might have affected the rate of fat absorp-
tion. 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, anti-
biotic 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 bacte-
rial flora, in which short-chain fatty acids (SCFA) are produced. The SCFAs
are absorbed by the colon, stimulating sodium transport in several spe-
cies, 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 chemi-
cal 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 lim-
ited 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,
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 fre-
quency 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, colono-
cyte proliferation, metabolic energy production, colonic blood flow, stimula-
tion 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 contain-
ing 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 mini-
mal. 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.
130.8
150
114.5
120
Weight
90 104.4 Moisture weight
87.3
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 consti-

pated 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 fre-
quency 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 dur-
ing 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
four ounces of juice or water [65]. A three-week observational baseline and

a five-week PHGG-supplementation phase were implemented. Sixteen resi-
dents 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 occur-
rence 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 gastroin-
testinal side effects was monitored. In another study, Rushdi et al. [68] per-
formed 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. Sup-
plementation 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 reli-
ant 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 Rehydra-
tion Solution (ORS) or ORS supplemented with 20 g/L of PHGG until recovery.
The average consumption of ORS was 429 mg/kg, providing approximately
8.6 mg/kg of PHGG. No side effects were reported while significant reduc-
tion 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 con-
trolled 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 with-
out 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 improve-
ments in the participants’ laxation parameters as a result of PHGG supple-
mentation. 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 improv-
ing 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 condi-
tions 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 environ-
ment 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 administra-
tion 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, poly-
dextrose, 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
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 per-
formed 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 fructooligosac-
charide 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 Bifidobacte-
ria values at the beginning of the trial and the degree of increase after inges-
tion 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 lev-
els 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
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 car-
bohydrates that provide a substrate upon which these bacteria can grow.
Several in vitro studies have explored the ability of PHGG to encourage pro-
liferation 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 discus-
sion 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 reduc-
tion of constipation, diarrhea, and pain. Fiber supplementation [84] is gener-
ally 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. Sol-
uble fiber is widely metabolized in the large bowel, producing short-chain
fatty acids and selective stimulation of microbial growth, eventually increas-
ing 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 nor-
mal 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
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 per-
mitted 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 subjec-
tive 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 signifi-
cantly 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 treat-
ment. Forty patients suffering from constipation-predominant IBS and non-
complicated 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 evacua-
tions per week increased significantly. Both groups significantly improved
in symptoms such as meteorism, abdominal pain, and incomplete evacua-
tion, but the PHGG group had greater reduction in bloating. The diet supple-
mentation 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 metabo-
lized (digested) into glucose and how much it causes the blood glucose (sugar)
to rise. The glycemic index describes this difference by ranking carbohy-
drates 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.
The World Health Organization (WHO) claims the glycemic index is con-
sidered 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 lev-
els 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 rat-
ing 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 choles-
terol 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 postpran-
dial 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 indi-
viduals 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 con-
tained mostly carbohydrates (53.5%) and dietary fiber content was estimated
at nearly 2.3%. Rice used in the study contained 80.3% carbohydrates with-
120
a a
100
b b
Glycemic Index
80 b b
b b
c c
60
40
20
0
White Bread WB+3g WB+5g WB+10g WB+15g
Diabetic subjects Control subjects

n=9 n = 11
Figure 6.6
Glycemic index of normal and diabetic individuals consuming white bread (WB) doped with var-
ied 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 absorp-
tion 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 nor-
mal 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.
PHGG has significant water-holding ability, but produces very low viscos-
ity, contributing to a low glycemic index. In contrast, Citracel, hydroxycel-
lulose, 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 consump-
tion 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 addi-
tion, 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 consider-
able 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
average body mass index about 35 on a controlled weight-loss diet for two suc-
cessive 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 measure-
ments 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. How-
ever, 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-insol-
uble cellulose or a water-soluble fiber: intact guar gum, PHGG, glucoman-
nan, or highly methoxylated pectin to study the effects on serum lipids and
immunoglobulin (Ig) production [43]. All soluble fibers reduced total cho-
lesterol 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 eight-
month-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 cor-
roborating 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 disrup-
tion of mucosal cells, as well as reduced tissue-associated myeloperoxidase
activity. These findings were interpreted as inhibition of mucosal inflam-
matory response due to the presence of PHGG. In conclusion, the hypoth-
esis of a beneficial immunological impact of PHGG is not well supported by
the available data.
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 min-
erals. 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 persis-
tent 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 cal-
cium absorption was attributed to the cecum and large intestine, wherein it
was suggested that nephrectomy does not influence the absorption of cal-
cium in the large intestine induced by PHGG feeding, and the increase in
ceco-colonic adsorption compensates the decreasing proximal intestinal cal-
cium 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 cal-
cium 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 bacte-
rial translocation compared to enteral supplemented formula without PHGG
addition. Gulliford et al. [111] revealed that guar delays intestinal calcium
absorption in humans.
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 ab
20% ID + PHGG (5%) 36.7 b
50% ID + PHGG (5%) 39.9 b
0 10 20 30 40 50
Iron Absorption Ratio (%)
(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 Cas-
sia 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 consecu-
tive weeks and noticeable effects on skin conditions were monitored such as
reduced acne, seborrhea and xeroderma (Figure 6.8).
70 After 4 weeks
60
Improvement, %
50 58.3
50.0
40
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 signifi-
cantly 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 physi-
ological 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 dos-
age 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-
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 typh-
imurium 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 hyperinsu-
linemia on Day 28. Additionally, fructose lowered the glycogen concentra-
tion 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] summa-
rized 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 hema-
tologic, 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 dif-
ferent 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 two-
hour 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 evi-
dence, PHGG is considered safe and appropriate to use as an ingredient in
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 gav-
age 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 compound-
related dose-dependent effects on body weight gain, feed consumption, gen-
eral 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 phe-
nobarbital 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 typh-
imurium strains TA98 and TA100, with and without S9 activation. No indica-
tions 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 WP2-
uvrA, 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.
Similarly, the chronic oral toxicity, carcinogenicity bioassay, developmen-

tal 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 nutri-
ent 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 fiber-
enriched 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 gastrointesti-
nal 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 bioavail-
ability, 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 pro-
duced 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
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 transloca-
tion 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 anasto-
motic 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 publish-
ing 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]. There-
fore, 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 liq-
uid foods in 1996. During this period, the Spanish Ministry of Health also
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 interac-
tion with common food ingredients and it does not destabilize emulsions,
change the viscosity of protein solutions, affect the flavor or color of prod-
ucts, 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 bever-
ages. 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 firm-
ing 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 bever-
ages. PHGG (3%) was mixed with milk and starter yogurt (20%) and incu-
bated 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 mon-
itored by counting the lactic acid bacteria per mL of the substance after fer-
mentation (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 sig-
nificant 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
Food Stabilizer
(whipped cream)
Bulking Agent Alternative of

(yogurt, ice cream) Wheat Flour
(cookies)
PHGG
as a Food Additive
Sugar Substitute Inhibitor of Starch

(whipped cream, Dispersion
steamed bread) (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 moisten-
ing 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, prevent-
ing 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 applica-
tions 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,
1 1
100
80 2
Dietary Fiber (%)
4
60 3 2 4
40 3
20
0
After fermentation After 1 week (4°C)
(a)
8.5 2
Lactic Acid Bacteria (count/mL)
4 4 Resistant Dextrin
8.4
3 Polydextrose
3
1 2 Inulin
8.3
0 1 PHGG
0 No fiber
8.2
8.1
Mean (Log10)
8
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 molec-
ular 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 some-
what 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 par-
ticular illness, severely ill patients, and infants. There is strong evidence sup-
porting 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
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 rea-
sonably low viscosity, is tasteless and odorless, and thus produces clear solu-
tions 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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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 appli-
cations 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
Figure 7.1
Schematic representation of acacia gum molecule (Fincher et al., 1983).
polyphenols (catechins, epicatechins, etc.), and minerals (magnesium, potas-

sium, 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 addi-
tive 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).
Acacia Gum 123
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 sol-
uble 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 tol-
erated 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 aca-
cia gum.
Flatus Bloating 100 Borborygmi 100 Cramps

% 100 100
75 75 75 75
50 50 50 50
25 25 25 25
0 0 0 0
0 20 40 60 80 0 20 40 60 80 0 20 40 60 80 0 20 40 60 80
Dose (g/d) Dose (g/d) Dose (g/d) Dose (g/d)
Sucrose Fibregum FOS
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 sys-
tem, 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 con-
suming either Fibregum™ or sucrose as control at the dose of 10 g/d during
10 days, concentrations of Bifidobacteria, Lactobacilli, and total lactic acid bac-
teria 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 vol-
unteers [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-
Acacia Gum 125
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 ferment-
able 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 gas-
trointestinal tract, the possible linkage might be exerted via a purely physi-
cal 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].
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 diar-
rhea 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 pro-
gressive 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 stud-
ies, in rat models of acute renal failure, suggest that acacia gum may also
improve renal function independently of its action on fecal bacterial ammo-
nia 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 intes-
tine, 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 aca-
cia gum may have a potential beneficial effect in renal disease, by increas-
ing 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-cal-
orie 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 vascu-
lar access [45].
These effects enable lowering of the kidneys’ workload with the objec-
tive of decreasing adverse clinical symptoms such as nausea, anorexia, and
fatigue associated with renal failure. Acacia gum could also be used to pre-
vent 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 gentamicin-
induced nephrotoxicity in rats [47]. Its administration lessened the negative
effects of this nephrotoxicity possibly by inhibiting a free-radical-mediated
Acacia Gum 127
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 low-
ering 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 proper-
ties [56]. The production of SCFAs (especially propionate) and also possible
binding with cholesterol and bile acids in the small intestine may be respon-
sible 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 addi-
tion 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 examina-
tion, and at intervals of 30 minutes during 150 minutes after supplementa-
tion. 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 sig-
nificantly 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
supplementation was significantly decreased in test groups compared to pla-

cebo 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 con-
sumed 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]: Gly-
cemic 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 acti-
vation, 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 alter-
ing 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.
5000
4000
Viscosity (cP)
3000
2000
1000
0
0 10 20 30 40 50
Concentration (%)
Figure 7.3
Influence of concentration on viscosity of acacia gum (at 75°F).
Acacia Gum 129
No Heat Treatment
120
100
% Remaining Fibre
80
60
40
Fibregum
20
FOS
0
0 15 30 45 60
Time (days)
Heat Treatment 5 min at 85°C/185°F

120
100
% Remaining Fibre
80
60
40
Fibregum + T°C
20 FOS + T°C
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 sta-
ble 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, cere-
als, 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 tex-
ture brought by sucrose or fruit juice. Studies on rats clearly showed that
water, glucose, and mineral absorption were significantly enhanced when aca-
cia gum was added into oral rehydration solutions or sports drinks [24–27].
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.
Acacia Gum 131
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 cook-
ing 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 compres-
sion, purified and agglomerated acacia gum is mixed with the other powders
(having the same mesh size) before filling the die. In the wet granulation, aca-
cia 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.
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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
135
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 tech-
nological 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 lin-
ear 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-Galac-
Carboxyl-group Amid-group Methylester-group
O O O O
C OH C NH2 C OCH3 C OCH3
O O O O
OH O OH O OH O OH O
O
OH OH O O
C=O C=OH
CH3 CH
Acetyl-group CH
MeO
HO
Ferolyl-group
Figure 8.1
Chemical structure.
Pectin 137
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 pectinest-
erases de-esterify pectin block-wise during maturation. Pectin, which is
de-esterified during the extraction process, has randomly distributed methy-
lester 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 consist-
ing 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 ara-
binofuranosyl 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 heteropolysaccha-
ride side chains containing L-arabinose and L-galactose can be found and
are commonly named arabinogalactans. Two structurally different arabi-
nogalactans 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-arabino-
furanosyl 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 rham-
nose 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
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 pec-
tin. 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 exam-
ple, 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 galac-
turonic acid units. β-elimination is a process driven by hydroxide ions lead-
ing 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 carboxy-
lic acid groups are used.
The most important commercial application of pectin is gelation. Under
certain conditions pectin forms a three-dimensional network, which is sta-
bilized by interactions between pectin molecules. For initiating the gela-
tion process a minimum concentration of the pectin is necessary. Important
Pectin 139
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 sta-
tus. 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 high-
methylester 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 sur-
rounding pectin molecules. Acidic conditions are required to reduce the dis-
sociation 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 repel-
ling 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 con-
ditions, low-methylester pectin is able to form gels relatively independent
from the content of total soluble solids content and pH value by forming junc-
tion zones under the influence of divalent metal ions. Low-methylester pec-
tins 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 pec-
tin molecules forms. As a result two galacturonic acid units form a hollow
body. Into the hollow body a positively charged calcium ion can be imbed-
ded, 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 affin-
ity 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
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 so-
called 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 dif-
ferent 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 tempera-
ture as well as increasing total soluble solids, and, in the case of low-meth-
ylester 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-gela-
tion 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 occur-
rence of pectin in nature only a few materials are used as sources for man-
ufacturing 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 store-
able 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.
Pectin 141
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 ammo-
nia is used to introduce amide groups. Pectin types obtained in such a pro-
cess are also called low-methylester-amidated pectins.
Pectin extracted from apple pomace or citrus peel typically has high molec-
ular 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 enzy-
matic 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. How-
ever certain bacteria of the gut flora are able to use pectin as substrate. With-
out 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 pro-
cess 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
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 bac-
terium located in the large intestine [26]. Studies with rats showed that pec-
tin degradation is reduced in the digestive system of rats and degradation is
influenced by degree of esterification and adaptation time of the pectin-con-
taining 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 short-
chain 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 pro-
portion 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. Homo-
genates 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 dif-
ferent 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-galac-
turonic 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 fer-
mentation process a time lag in degrading of the substrate is seen. The fer-
Pectin 143
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 di-
and tri-galacturonic acid was found. In all pectin-fed groups the concen-
tration 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 esterifi-
cation 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 oligo-
galacturonic acids were formed and pectin with lower degree of esterifica-
tion 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 endopo-
lygalacturonase. 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 organ-
isms, for example Treponema saccharophilum [47], Butyrivibrio fibrisolvens, Pre-
votella ruminicola [48], and Lachnospira multiparus [49], while no KDPG activity
was seen in cell extracts obtained from Bifidobacterium species or Streptococ-
cus 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 pec-
tin 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 signifi-
cantly 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 nutri-
tion 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 pec-
tin’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
Pectin 145
• 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 stabil-
ity 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 stud-
ies 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 avail-
ability 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
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 nega-
tively 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 fac-
tor 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 short-
term 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 signifi-
cantly 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 pec-
tin 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 sub-
stances 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 inves-
tigated, showed that binding affinity increased with increasing degree of
polymerization [104]. Ca, Sr, and Zn were bound very weakly by electro-
static interactions, while strong complexes were formed with Cd, Cu, and
Pb. The strongest complex was formed by lead with galacturonic acid oli-
Pectin 147
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 oligogalactur-
onates and by 600% with a mixture of mainly unsaturated di-, less unsatu-
rated 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 measure-
ments 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].
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 mal-
absorption. Pectin improves small and large bowel mucosal structure, pro-
longs 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 mes-
enteric 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 inves-
tigated 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, ben-
tonite, alkyl polyalcohols, aluminium phosphate, activated charcoal, sweet
whey, and nickel-pectinate [121].
Clinical studies showed that pectin has the potential to reduce acute intes-
tinal 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
Pectin 149
the study was commercially available as Diarrhoesan. A study with a pectin-

supplemented 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 sig-
nificantly 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 dis-
ease 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 develop-
ment of coronary heart disease. The risk is increased with high serum cho-
lesterol levels. Coronary heart disease and stroke caused by atherosclerosis
and its related problems of hyperinsulinemia, hyperlipidemia, and hyper-
tension 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 fibrin-
ogen 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 thick-
ness (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 cho-
lesterol 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, espe-
cially pectin, appears to protect against IMT progression. Serum lipids may
act as a mediator between dietary fiber intake and IMT progression.
Frequent and long-lasting high insulin concentrations promote vascular

lesions, the primary stadium of atherosclerosis. Suppression of postpran-
dial insulin levels by pectins may therefore have an anti-atherogenetic effect
[129]. Dietary fibers like pectin may also increase peripheral insulin sensitiv-
ity 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 pec-
tin 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 interac-
tion 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 posi-
tive 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 health-
ier LDL:HDL ratio. In discussion is the influence of degree of esterification of
pectin on the potential of pectin to reduce cholesterol. Studies [150] indicat-
ing 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-
Pectin 151
Table 8.1
Influence of Pectins on Lipid Metabolism
Cholesterol
Pectin g/d
Subjects Time + a, b, c Total LDL HDL TG Reference
30 c 3 wk 2020 –17 –21 +4 n.d. Schuderer
15 s 3 wk –12 –14 +12 n.d. (151)
27 ? 4 wk 15 –15 n.d. n.d. n.d. Cerda et al.
(152)
54 90 d 15 + a –34,4 n.d. +24,6 –24,6 Grudeva
55 –34,5 n.d. +34,0 º 26,2 (153)
47 90 d 15 + b –36 –23,5 +36,3 –18,8 Grudeva et al.
(154)
10 4 wk 15 –11,6 –11,5 +21,3 n.d. Veldman et al.
(155, 156)
40 4 wk 10 + c –44 –45,5 +14 –55 Bartz et al.
(157)
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 meta-
analysis 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 choles-
terol 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 proper-
ties 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 choles-
terol 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 fac-
tor 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. Com-
paring different pectin substances at different conditions resulted in the find-
ing 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
Table 8.2
Change of Lipid Parameters under Consumption of Soluble Dietary Fibers
(Meta-analysis) [160]
Soluble Number Change per g Fiber
Dietary Fibers of Studies Participants [mg/dL]
Cholesterol
Oat products 26 1600 – 1,43
Psyllium 17 757 – 1,08
Pectin 7 277 – 2,71
Guar 17 341 – 1,00
LDL cholesterol
Psyllium 17 757 – 1,12
Pectin 4 117 – 2,13
Guar 12 218 – 1,28
HDL cholesterol
Psyllium 17 757 – 0,07
Pectin 7 277 – 0,14
Guar 15 302 – 0,11
Triglycerides
Oat products 20 1374 + 0,7
Psyllium 16 720 + 0,3
Pectin 6 247 – 1,8
Guar 17 338 – 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 mol-
ecules, 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 com-
plexes [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 chy-
mus viscosity pectin delays the absorption of glucose and other monosac-
charides, as well as reduction of degradation of complex carbohydrates.
Pectin 153
Table 8.3
Influence of Pectins on Serum Glucose and Serum Insulin
Time Interval (min.) of Significant
Amount Decrease of
Pectin Serum
Subjects Added in g Serum Glucose Insulin Reference
8 d3 i 1010 30–90 30–120 Jenkins et al. (168)
30–120 —
13 n 10 at 15 min. 15–45 Jenkins et al. (169)
n.s.
30–90
5 g dumping 10,5 at 30 min improved — Leeds et al. (170)
syndrome retention of load
in stomach
6d 14,5 n.s. n.s. Jenkins et al. (171)
6d 9/sqma 30–60 n.s. Monnier et al. (172)
6n 14,5 30–45 — Holt et al. (173)
23 g 10–20 at 30 min — Labayle et al. (174)
3h 5 Hypoglycemia — Labayle et al. (174)
Overted
8i 15 15–90 — Vaaler et al. (175)
7i 7 60–90 >180 min. Poynard et al. (176)
6n 10 n.s. n.s. Gold et al. (177)
6n 10 60–90 n.s. Gold et al. (177)
13 d 10 at 60 min. n.s. Williams et al. (178)
5n, 6o, 5d 10 + guar Significant decrease Kanter et al. (179)
in all but greatest
change in obese
and diabetic
subjects
7n 20 n.s. — Schwartz et al. (180)
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 pec-
tin lowers blood glucose and insulin levels after consuming carbohydrate-
rich 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
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 excre-
tion 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 ben-
efits of pectin.
A project in which the effect of several pectin types on azoxymethane-
induced colon carcinogenesis in rats was investigated showed decreased mul-
tiplicity 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 tryp-
tophanase levels, with a significant decrease in the activity of glucuronidase
during the initiation stage [189, 190]. Diet supplementing by 20% apple pec-
tin 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 car-
cinogenic activation of 1,2-dimethylhydrazine in the colonic lumen. The abil-
ity 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 supple-
mented with apple pectin. Supplementing the diet with apple pectin reduced
the amount of colorectal tumors induced by 1,2-dimethylhydrazine signifi-
cantly 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 sig-
nificantly 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-oligo-
saccharides were obtained after three days incubation. Increased apoptosis
Pectin 155
frequency after incubation with 1% (w/v) pectin and/or pectic oligosaccha-

rides was seen by caspase activity and DNA laddering on agarose gel elec-
trophoresis [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-dimethyl-
hydrazine (DMH). The average number and volume of tumors per rat were
lower in rats fed with pectin. In general, pectin enhanced caspase-3 activ-
ity 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 com-
pared 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 sub-
stances 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. Cel-
lular 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 con-
sumption of modified citrus pectin (MCP) interfered with cell-to-cell inter-
actions 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 endothe-
lial cells (HUVECs). The effect depended on the dosage, but with a concen-
tration 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
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 sub-
stances are carbohydrates, which have a terminal ∆-4,5-unsaturated galac-
turonic 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 con-
tent 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 mate-
rial [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 pec-
tins 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 gell-
ing 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 molecu-
lar 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 lim-
its 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.
Pectin 157
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 gell-
ing 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 prop-
erties 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 prepa-
rations 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 solu-
ble solids in the fruit preparation. Molecular-weight-reduced pectin can be
added to fruit preparations to increase the respective product with soluble
dietary fiber.
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 pre-
vent pre-gelling. In order to standardize the production of confectionery
products buffer salts that have retarding properties, for example sodium cit-
rate, 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 stabi-
lize 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 pro-
viding a source of soluble fiber. More suitable would be molecular-weight-
reduced 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 methy-
lester 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
Pectin 159
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 condi-
tions 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 con-
trols 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 condi-
ments, 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-molecular-
weight 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 proper-
ties, pectin can play a distinctive role obtaining the desired dough rheol-
ogy. 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 com-
pressed to tablets or sold as dry powder for beverages or other products.
Manufacturing pectin tablets or capsules is a way to offer consumers the pos-
sibility 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 bever-
ages that are prepared by the consumer.
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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
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 ingre-
dient that could be used in conjunction with intense sweeteners when replac-
ing 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 ben-
efits of polydextrose were recognized early on and the product has been used
extensively there to enhance the dietary fiber content of foods since the mid-
1980s.
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 non-

cariogenic
• 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.
Polydextrose 175
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. Fur-
ther purification steps are then involved to generate a range of products with
improved organoleptic properties. Pfizer has patented a partially hydroge-
nated 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. Auer-
bach 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 molecu-
lar weight of ~2,000 Daltons, with a range of 162 to ~20,000). Stumm and Bal-
tes [4) also determined that polydextrose is a highly branched material.
Recent efforts by Danisco Sweeteners have been aimed at further elucidat-
ing 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 chromatogra-
CH2OH CH2OH
O O
OH O CH2 OH O
CH2OH
O HO CH2 O
HO
OH O CH2 OH O O CH2
CH2OH O OH O CH2
HO O
HO
O OH OH O O OH OH OR
OH O OH OH O
HO HO
HO OH OH
HO
OH CH2OH
R = H, sorbitol or
CH2OH O more polydextrose
O OH O
OH O
OH
HO
OH
Figure 9.1
Representative structure for polydextrose. R = H, sorbitol, sorbitol bridge, or more polydextrose.
Branching, Furanoses, Branch/Terminal Ratio and Linkage Positions

45
40
35
30
25
Area %
20
15
10
0
al
ed
e b ch
So ch
ra s
s
Br l te nts
/te nal
al
al
ed
ed
ed
ed
Fu itol
se
ip anc
in
in
in
ch
nk
nk
nk
nk
an
an
no
i
ta oi
rm
rm
rm
rm
rb
an
br
r
br
Li
Li
Li
Li
To h p
Te
Te
6-
4-
3-
2-
br
le
le
nc
bl
ng
ch
on
ou
ra
Tr
Si
an
N
lb
D
ta
To
Type of Linkage or Branching
Figure 9.2
Linkage analysis of polydextrose.
phy-mass spectrometry (GC-MS). Prereduction was carried out on the poly-

dextrose 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 trifluoroa-
cetic acid (2 hr in sealed tube at 121°C), reduced with NaBD4, and acetylated
using acetic anhydride/trifluoroacetic acid. The resulting PMAAs were ana-
lyzed on a Hewlett-Packard 5890 GC interfaced to a 5970 MSD (mass selec-
tive 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 spec-
trometer operated in the positive ion mode. The spectrometer was calibrated
Polydextrose 177
DP Distribution of Polydextrose by MALDI-TOF Spectroscopy

9.00
8.00
7.00
6.00
Peak Height
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 des-
orbed 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 con-
fusion 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
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. Insti-
tute of Medicine as laxation or regularization of bowel function, normaliza-
tion 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 conjunc-
tion with polydextrose supplementation.
Two human studies have reported increased stool frequency on consump-
tion 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 poly-
dextrose consumption while two human studies showed no effect [12, 13].
Decreased colonic pH, associated with the increased production of short-
chain 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 choles-
terol in animals and humans [11, 21–23], although the body of data is equivo-
cal. 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, trig-
lycerides, 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 pro-
duced 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 choles-
terol into bacterial biomass, thus reducing reabsorption in the colon.
Polydextrose 179
More recently Pronczuk and Hayes [24] studied the effectiveness of poly-
dextrose in lowering plasma and liver cholesterol in gerbils, a diet-sensitive
model for the manipulation of plasma lipids [25, 26]. In one experiment, ger-
bils 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 demon-
strated 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 placebo-
controlled, 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. Dur-
ing the polydextrose intervention the concentrations of high-density lipo-
protein 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 acknowl-
edged 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 Inter-
national Table of Glycemic Index and Glycemic Load Values [29] lists Litesse
(Danisco’s branded polydextrose) as follows:
Glycemic Index Glycemic Load

(versus glucose) (per serving)
591 Litesse II 7±2 1
Litesse III Ultra 4±2 0
300 80
Plasma glc. conc. (mg%)
Plasma Insulin conc.

250 60
(uU/ml)
200 40
150 20
100 0
0 1 2 3 4 5 0 1 2 3 4 5
Time (h) Time (h)
GLC PDX GLC PDX
Figure 9.4
A comparison of postprandial plasma glucose and insulin response to either glucose or poly-
dextrose 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.
Polydextrose 181
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 gas-

trointestinal absorption
2. To be fermented by the gastrointestinal microflora
3. To stimulate selectively the growth and/or activity of intestinal bac-
teria 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 interven-
tion 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 consider-
ably reduced the formation of aberrant crypt foci (ACF) in the presence of a
carcinogen. The effect was most pronounced in the rectum where the reduc-
tion was up to 65%. The authors concluded that ingestion of polydextrose
may prevent colorectal carcinogenesis.
80
70
PDX mg/g Dry Matter
60
50
40
30
20
10
0
Distal small Caeeum Proximal colon Middle colon Distal colon
intestine
Figure 9.5
Progressive fermentation of polydextrose in the pig colon.
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 Bifido-
bacteria 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 enhance-
ment 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 inflamma-
tory diseases in the intestine. Mäkivuokko et al. [20] combined two differ-
ent 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 expres-
sion associated with the colonic fermentation of polydextrose further sug-
gests 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.
Polydextrose 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 con-
fectionery with “tooth-friendly” properties [40]. Of course products as con-
sumed 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 deter-
mine 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 pur-
poses 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 question-
able 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 indepen-
dent 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 spe-
cialty 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
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 gastrointes-
tinal 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 laxa-
tive 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. Compre-
hensive 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,” mean-
ing 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 treat-
ment, and subsequent HPLC measurement [47]. A collaborative study con-
firmed 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).
Polydextrose 185
1.2
0.8
0.6
0.4
0.2
0
e
ol
ol
se
in
ito
ito
to
ito
al
os
lit
tit
ul
ro
om
ni
cr
hr
rb
ct
In
Xy
al
xt
an
La
Su
So
yt
Is
M
de
M
Er
ly
Po
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 car-
bohydrates 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 exam-
ple, 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].
18
16
“score” Compared to Control

14
Increase in Sweetness
12
3% w/v
10 Polydextrose
8 6% w/v
Polydextrose
6
4
2
0
4% w/v 4% w/v
Sucrose 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 devel-
opment 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 compos-
ite 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 tran-
sition 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 materi-
als. 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/
Polydextrose 187
125
100
75
50
Tg (°C)
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 (typi-
cally –18ºC for a home freezer) is minimized.
The concepts of water as a plasticizer of foods and how this affects the sta-
bility 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 sys-
tem. 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 immo-
bile 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].
Water Activity versus Concentration in Solution

1,0
0,8
Water Activity
0,6
Sucrose
0,4
Polydextrose
0,2
0,0
0 20 40 60 80 100
Concentration w/w%
Figure 9.9
Water activity (Aw) at various concentrations of sucrose and polydextrose.
Sorption
40 Desorption
Water Content % wb
30
20
10
0
0 20 40 60 80 100
RH %
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
Polydextrose 189
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 appli-
cations, 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 reduced-
fat/reduced-sugar shortcrust pastry. How this is achieved is not fully under-
stood. 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 aque-
ous 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
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, indi-
cating 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 con-
tinuous development of gluten structure producing a “short” texture. When
polydextrose is used in reduced-fat pastry, it hydrates, and this rapid absorp-
tion of water reduces the amount of water available for gluten development,
producing the same “short” texture as the full fat product. On baking and
Polydextrose 191
Figure 9.14
CryoSEM – polydextrose sample (more icy matrix, less hydration of the gluten).
TGA Vigo 011-30

100
80
60
Weight %
40
20
0
20 60 100 140 180 220 260 300 340 380 420 460
Temperature (°C)
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
100
80
60
Weight %
40
20
0
20 60 100 140 180 220 260 300 340 380 420 460
Temperature (°C)
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 Time in Hours

Monomers 0 1 5
Polydextrose (Litesse ® 0.02 0.02 2.28
Two)
Polydextrose (Litesse® 0.08 0.3 2.38
Ultra)
Fructo-oligosaccharide 0.2 45.42 100
(Av DP 10)
approximately 300ºC when it begins to melt and decompose. These tempera-

ture 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
Polydextrose 193
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 impor-
tant 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 reduc-
tion, reduced glycemic load as well as sugar and fat reduction. The techno-
logical 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 poly-
dextrose 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 con-
trol 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 confec-
tionery [65].
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 tex-
ture 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 applica-
tions. 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.
Polydextrose 195
Beverages and Dairy Drinks

Polydextrose is used in dairy drinks; neutral or flavored, or low pH, pasteur-
ized, 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 pre-
vent migration of moisture from fruit fillings into dough and pastry, increas-
ing 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 with-
out 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 polydex-
trose 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 polydex-
trose as well as some process improvement benefits to the mechanical prop-
erties 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].
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 compress-
ible tableting excipients [73].
It also acts as a bulking agent in the formulation of sugar-free confection-
ery 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 applica-
tions 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 pre-
cluded 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
Polydextrose 197
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 Mitch-
ell, 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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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
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 High-
Moisture 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
References............................................................................................................. 240
205
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 amylopec-
tin. Starch is largely a digestible polymer; however, some starch, called resis-
tant 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 pro-
cess known as gelatinization. Thus gelatinization is a function of tempera-
ture, 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 cook-
ing 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
Resistant Starch (RS) 207
Table 10.1
Classes of RS (Brown et al. 1995; Sajilata et al. 2006)
RS Starch
Type Characteristic Properties Foods Other
RS1 Trapped in food Not completely Whole or Affected by
matrix swollen, gelatinized, partially milled milling,
or dispersed. Matrix grain, sweet pureeing,
is not easily corn, parboiled chewing, and
penetrated by rice, legumes gelatinization
digestive enzymes.
May or may not test
as dietary fiber
RS2 Granular, with Granular. May or may Raw potato, RS content
highly not test as dietary green banana, reduced if
crystalline fiber high amylose starch is
regions corn gelatinized
RS3 Retrograded Non-granular. May or Cooked and Increased with
amylose and may not test as cooled starches certain
amylopectin dietary fiber in potatoes, processing
rice, tortillas, techniques.
bread crumbs Occurs more
readily at
32°F–40°F
RS4 Chemically May or may not test Does not occur More evidence
modified as dietary fiber. in nature or in of
starches Could be soluble or naturally physiological
insoluble occurring effects is
foods required
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 chem-
ically converted with existing techniques). Resistant dextrins are starch-
based 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.

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 natu-
ral RS (Annison and Topping 1994).

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. Conse-
quently, commercial RS3 ingredients are generally based on this process,
sometimes in combination with amylase treatment to increase starch crys-
tallinity 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).

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 tra-
ditional (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. Lim-
ited 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
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 pro-
cessing, 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 unpro-
cessed 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 fac-
tors 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 com-
mercial 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 gen-
eration 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 com-
mercialization of Crystalean® by Opta Food Ingredients (Iyengar et al. 1991).
Both ingredients are prepared from high amylose corn starch, with approxi-
mately 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 cool-
ing 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
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 consid-
ered 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 prod-
ucts 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. Manu-
facturing is a relatively simple process, whereby high-amylose corn is dry
milled into flours or meals, then further processed with a proprietary treat-
ment. 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, gran-
ular 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).
Table 10.2
Physical Comparisons of Commercial Natural RS
Protein
Commercial Fat Content Content
Form (product RS Particle Size (weight (weight Label
Resistant Starch (RS)
example) Classification Source (μm) percent)d percent)d Declaration Key Suppliers

Starch RS1 & RS2 High amylose 5–25 0.8 0.8 Corn starch or National
(Hi-maize® 260) corn resistant corn Starch &
starch Chemical Co.
Flours RS1 & RS2 High amylose 100–300c 5 9 Yellow corn National
(Hi-maize® corn corn flour Starch &
flour) Chemical Co.
Meals RS1 & RS2 High amylose 200–600a 3 9 Yellow corn National
(Hi-maize® corn corn meal Starch &
meal) Chemical Co.
Maltodextrinb RS3 High amylose 30–40 0.8 0.8 Maltodextrin National
(NOVELOSE® corn, tapioca Starch &
330 starch) Chemical Co.
Whole grains RS1 & RS2 Varies Varies Varies Varies By source Multiple
a 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.
b Although RS3 is naturally occurring, National Starch does not promote NOVELOSE® 330 starch as natural.
c 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.
d Typical values for specific National Starch products listed above, information is not necessarily applicable to the entire category.
211
212
Table 10.3
Commercial Sources and Forms of Traditional (Natural) RS1, RS2, and RS3
Classification RSa TDFb
(grain source) Commercial Name Supplier (% db) (% db) Top Benefits Key Applications
RS1 (high amylose Hi-maize® Flour National Starch & 59 27 c High fiber content Baked & fried snacks,
corn grain) 120 Chem. Co., Increased bowl life in battered & breaded
Bridgewater, NJ ready-to-eat (RTE) cereals foods, cereals,
Superior adhesion in specialty bakery
breaded food goods (English
“Natural” ingredient muffins, corn tortillas,
declaration and waffles, handheld
Exhibits good process bakery goods, and
tolerance pizza crust)
RS1 (high amylose Hi-maize® Meal National Starch & 75 39 c High fiber content Baked & fried snacks,
corn grain) 130 Chem. Co., Increased bowl life of RTE battered & breaded
Bridgewater, NJ cereals foods, cereals, specialty
Superior adhesion in bakery goods (English
breaded foods muffins, corn tortillas,
Crisp texture and waffles, handheld
“Natural” ingredient bakery goods, and
declaration pizza crust)
Good process tolerance
RS1 & RS2 (high Hi-maize® Flour National Starch & 59 50 c High fiber content Baked & fried snacks,
amylose corn 150 Chem. Co., Increased bowl life of RTE battered & breaded
grain) Bridgewater, NJ cereals foods, cereals, specialty

RS1 & RS2 (high Hi-maize® Meal National Starch & 77 60 c High fiber content Baked & fried snacks,
amylose corn 150 Chem. Co., Increased bowl life of RTE battered & breaded
grain) Bridgewater, NJ cereals foods, cereals, specialty

RS1 (high amylose Hi-maize® Whole National Starch & 60 36 c Provides increased TDF and Baked & fried snacks,
corn grain) Grain Corn Flour Chem. Co., RS while delivering whole battered & breaded
Bridgewater, NJ grain benefits foods, cereals, specialty
Provides textural benefits bakery goods (English
Good process tolerance muffins, corn tortillas,
and waffles, handheld
bakery goods, and
pizza crust)
RS1 (high amylose Barleyplus™ Flour Ascentia Pty Ltd 59 30 c Provides health benefits to Extruded snacks,
barley flour) (CSIRO), consumers: low glycemic extruded breakfast
Canberra, index, high in β-glucan cereal, rolled cereal,
Australia breads, and muffins
RS2 granular starch Hi-maize® 220 National Starch & 80 20 c High fiber content RTE cereals, snacks,
(unmodified high starch Chem. Co., Enables labeling of health pasta/noodles, baked
amylose corn Bridgewater, NJ benefits substantiated by goods, and fried foods
starch) Hi-maize® starch clinical
data
Imparts excellent textures
without compromising
eating quality
Low water holding capacity
(WHC)
Small particle size
213
Clean flavor
(continued)
Table 10.3 (Continued)
214
Commercial Sources and Forms of Traditional (Natural) RS1, RS2, and RS3
Classification RSa TDFb
(grain source) Commercial Name Supplier (% db) (% db) Top Benefits Key Applications
RS2 granular Hi-maize® 260 National Starch & 53 60 c All natural Bakery products, other
starch (high starch Chem. Co., Fewer calories than flour low-moisture baked
amylose corn Bridgewater, NJ Proven health benefits goods, cookies/
starch) Prebiotic fiber biscuits, pasta &
Improves digestive health noodles, RTE cereals,
Enhances mineral absorption snack foods (cheese
Reduces glycemic response curls and pretzels),
of foods soups, cereal drinks,
Increases insulin sensitivity yogurt, and selected
Provides sustained energy dairy products
release
RS3 (high amylose NOVELOSE® 330 National Starch & 57 33 c Promotes digestive health Extruded foods (RTE
corn starch) starch Chem. Co., Good expansion aid in cereals & snacks),
retrograded Bridgewater, NJ extrusion; offers uniform pasta & noodles, some
crystalline cell size, excellent baked goods, and
amylose-non- expansion, improved fried foods
granular processing, improved
overall good eating quality
Low WHC, small particle
size and clean flavor
RS3 (high amylose Crystalean® SunOpta Inc., 57 33 c Provides concentrated Baked products
corn starch); Bedford, MA source of RS (improved mouthfeel
Crystalline Adds fiber, bulking agent, and volume), RTE
amylose and enhances texture, low cereal, extruded snacks,
WHC nutrition bars,
Thermally stable low-glycemic &
Increases strength & diabetic foods
crispness of cereals
Improves cell structure and
expansion in extruded
products
RS3 (tapioca- Actistar™ RM Cargill Texturizing 50 2 c All-natural Baked goods, breakfast
based) non- Solutions, (AOAC Promotes digestive health cereals, cereal bars,
granular resistant Minneapolis, MN 2002.02) Stable under high-heat & tortillas, snack foods,
maltodextrin high-acid conditions instant soups,
Low glycemic and powdered drinks &
insulinemic response mixes, smoothies,
Good dispersibility yogurt, UHT milk
Relatively low viscosity and drinks
water binding capacity

RS3 (tapioca, short C* Actistar Cargill, Min. 53% Does not Reduces intestinal pH Beverages, low-fat
chain amylose) Minneapolis, MN; (Goni analyze as Increases calcium and fermented milks, UHT
Cerestar, Cedar Method) fiber magnesium absorption flavored milk drinks
Rapids, IA
a Modified Englyst Assay: H. N. Englyst, S.M. Kingman, and J. H. Cummings: Classification and Measurement of Nutritionally Important Starch Frac-
tions. Eur. J. Clin. Nutr. Suppl. 2, 46 (1992) 33–50.
b TDF Assay Utilized
c AOAC Method 991.43 Total, Soluble, and Insoluble Dietary Fiber in Foods (Enzymatic-Gravimetric Method, MES-TRIS Buffer)
d AOAC Method 2001.03 Total Dietary Fiber in Foods Containing Resistant Maltodextrin
215
Resistant dextrins, which are soluble starches derived via pyrodextrini-

zation, 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 gran-
ules 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) bever-
ages 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; how-
ever, there is comparatively little nutritional research on their physiologi-
cal 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 per-
formance, including shelf stability. The potential for using such starches at
macronutrient levels in foods is fairly new and warrants careful consider-
ation 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 manu-
facturers 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 con-
sumed (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:
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 pel-
let 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 Ter-
mamyl (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 rap-
idly 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 ana-
lytical tool for RS research.
218
Table 10.4
Commercial Sources and Forms of Non-Traditional RS4
Classification Commercial RSa TDFb
(Grain Source) Name Supplier (% db) (% db) Key Benefits Key Applications
RS4 (pre- FiberRite™ RW MGP Ingredients, 16 72 Fat replacement properties High moisture foods, bakery
gelatinized wheat Atchison, KS (high WHC) mixes and sweet goods, icings
starch) Caloric reduction and crème fillings, sauces,
Smooth texture, white color, yogurt and sour cream,
neutral flavor confectionary products, salad
Excellent freeze-thaw dressings
stability
RS4 (wheat starch) Fibersym® 70 MGP Ingredients, 82 76 Low WHC Bakery products, pasta, snack
Atchison, KS Smooth texture foods, batters & breadings,
Neutral flavor & white color RTE breakfast cereals
RS4 (potato) Fibersym® 80ST MGP Ingredients, 97 82 Low WHC Bakery products, pasta, snack
Atchison, KS Smooth texture foods, batters & breadings,
Neutral flavor, white color RTE breakfast cereals
RS4 (tapioca) Actistar™ RT Cargill, 54 82 Low WHC Baked goods, breakfast cereals,
Minneapolis, MN Small particle size cereal bars, snack foods,
Bland flavor profile yogurt, powdered & drink
Replacement for flours in mixes, instant soups,
baked goods smoothies, low-fat fermented
milks
Resistant Nutriose® FM06 National Starch, ~ 90 85 b Water soluble RTD beverages, sweet baked
maltodextrin Bridgewater, NJ & Easily dispersed in water goods, frozen dairy/desserts,
(maize-based) Roquette Extended energy release sauces/gravies, pasta, meats,
America, Inc., Acid and heat stable savory dips, cereals, snacks
Keokuk, IA Low viscosity (sheeted/extruded, fried/
Clean flavor baked)
Resistant Nutriose® FM10 National Starch, ~ 90 70 b Water soluble Ready meals, soups, side
maltodextrin Bridgewater, NJ & Easily dispersed in water dishes, dairy beverages,
(maize-based) Roquette Acid and heat stable yogurts, yogurt beverages

America, Inc., Low viscosity
Keokuk, IA Clean flavor
Resistant Nutriose® FB06 National Starch, ~ 90 85 b Water soluble Ideal for high moisture
maltodextrin Bridgewater, NJ & Easily dispersed in water applications: beverages, dairy,
(wheat-based) Roquette Acid and heat stable fruit fillings (breakfast bars)
Resistant Nutriose® FB10 National Starch, ~ 90 70 b Water soluble Ideal for high moisture
maltodextrin Bridgewater, NJ & Easily dispersed in water applications: beverages, dairy,
(wheat-based) Roquette Acid and heat stable fruit fillings (breakfast bars)
Resistant Fibersol-2 Matsutani 90 Min. 90 b Water soluble Beverages, nutritional &
maltodextrin America, Inc., Easily dispersed in water functional foods, bars, cereal,
(corn starch) Decatur, IL No off flavors dairy foods, dry mixes,
Very low viscosity cultured dairy products,
Acid and heat retort stable frozen dairy desserts
a Modified Englyst Assay: H. N. Englyst, S.M. Kingman, and J. H. Cummings: Classification and Measurement of Nutritionally Important Starch Frac-
tions. Eur. J. Clin. Nutr. Suppl. 2 46 (1992) 33-50.
b 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
219
Table 10.5
220
Key Methods employed in the Detection of RS

Sample Validation in
Method Pre-treatment Digestion Recovery Detection Vivo Advantages/Disadvantages
RS Methods
Berry [1986] Grinding 42°C Alcohol Glucose Oxidase No Underestimation of RS2 and
Pancreatic precipitation Assay possibly RS3
α-amylase RS dispersion in May overestimate RS1 in
Pullulanase KOH & absence of proteolytic
amyloglucosidase digestion step
No mechanism to detect RS4
Underestimation of RS1 if
grinding is too fine
Bjôrck et al. Grinding 100°C, 37°C Alcohol Glucose Oxidase Rats Underestimation of RS1, RS2,
[1986] Pepsin precipitation Assay and possibly RS3
Heat stable RS dispersion: KOH No mechanism to detect RS4
α-amylase & Underestimation of RS1 if
Pancreatin amyloglucosidase grinding is too fine
Englyst et al. Mincing 37°C Alcohol Glucose Oxidase Humans Analyzes all RS types
[1992, 1996] Pepsin precipitation Assay or Detection of various digestion
Pancreatin Supernatant is used chromatography products only if HPLC is
Amyloglucosidase for further assays used
Invertase Complicated and laborious
Widely used in research labs
Muir & O’Dea Chewing 37°C Centrifugation Glucose Oxidase Humans Used primarily by the authors
[1992] Pepsin RS dispersion in Assay No means to detect RS4 or
Pancreatin DMSO followed by small MW indigestible
Amyloglucosidase heat stable components
α-amylase
Goni et al. [1996] Milling and 40°C, 37°C Centrifugation Glucose Oxidase Based on No means to detect RS4 or
sieving Pepsin RS dispersion in Assay comparison to small MW indigestible
Pancreatic KOH followed by EURESTA components
α-amylase amyloglucosidase 1994 Underestimation of RS1 if
milling is too fine
Use not recently reported
Champ et al. Grinding 37°C Alcohol Glucose Oxidase Humans No means to detect RS4 or
[1999] Pancreatic precipitation Assay small MW indigestible
α-amylase RS dispersion: KOH components

Amyloglucosidase &
amyloglucosidase
McCleary & Grinding 37°C Alcohol Glucose Oxidase Humans No means to detect RS4 or
Monaghan Pancreatic precipitation Assay resistant maltodextrin
[2002] α-amylase RS dispersion: KOH Underestimation of RS1 if
Amyloglucosidase & grinding is too fine
amyloglucosidase Robust
The only AOAC method for
detection of RS
Dietary Fiber Methods

AOAC 991.43 Grinding 100°C, 60°C Alcohol Gravimetric No Underestimation of RS2 and
Heat stable precipitation RS3
α-amylase No detection of resistant
Protease maltodextrin or other small
(Subtilisin) MW fragments
Amyloglucosidase
AOAC 2001.03 As AOAC As AOAC 991.43 As AOAC 991.43 Gravimetric & Yes Underestimation of RS2 and
991.43 Chromatographic RS3
221
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; how-
ever, 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 speci-
ficity compared with human digestive enzymes. As research and develop-
ment tools, however, such methodology can be quite useful. For example,
National Starch has adopted two methods to support internal product devel-
opment: 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 diges-
tion for 2 hr at 37oC. The AOAC (McCleary) method 2002.02 does not simu-
late 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 meth-
odologies was prepared by DeVries (2004). The fiber methods most com-
In Vitro Measurement of Resistant Starch

AOAC 2002.02
Enzymatic Digestion
Pancreatic
Incubation at 37°C 16 hr 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 gravi-
metric and employ an enzymatic digestion step at 100oC, which was origi-
nally 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 compo-
nents from a supernatant that is normally discarded in AOAC 985.29 (Fig-
ure 10.4). The final dietary fiber value in AOAC 2001.03 includes insoluble
fiber and two fractions of soluble fiber; the high molecular weight compo-
nent that can be precipitated by alcohol and the small molecular weight
component detected by HPLC.
Additional analytical complexity is introduced when AOAC fiber meth-
ods 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 esti-
mation 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.
Table 10.6
Dietary fiber and RS contents of commercial products by different methods
TDF (% db) RS (% db)

AOAC AOAC
RS Type Product 991.43 Englyst a 2002.02
RS1 Hi-maize Flour 120
® 25 67 31
Hi-maize® Flour 150 58 66 37
Hi-maize® Meal 130 38 68 37
Hi-maize® Meal 150 62 75 45
Hi-maize® Whole Grain Corn Flour 36 60 22
Barleyplus™ Flour 30 59 3
RS2 Hi-maize® 220 starch 17 76 48
Hi-maize® 260 starch 60 51 46
RS3 NOVELOSE® 330 starch 37 56 48
CrystaLean® 33 57 48
Actistar™ RM 2 65 50
C* Actistar 0 65 56
RS4 Nutriose® FM10 75 b 79 0
Nutriose® FM06 92 b 81 0
Fibersol-2® 98 b 92 0
Fibersym® 70 80 82 0
Fibersym® 80 97 97 3
FiberRite™ RW 72 16 0
Actistar™ RT 82 54 1
a RS values based on carbohydrate content which is 80–90% for evaluated flours and meals
[Englyst et al. 1996]
b 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 reten-
tion, nutritional impact, shelf stability, and clinical validation. Table 10.7 sum-
marizes 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.
Total Dietary Fiber Methods

AOAC 985.29 & 991.43
Enzymatic Digestion
Amylase
Incubation at 95°C
Protease
Filtration Amyloglucosidase
Filtrate Insoluble DF
+
Alcohol Precipitation
Soluble DF
Supernatant
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 2001.03
DF
Insoluble
Soluble
TDF & RMD

Supernatant Chromatography
Products
Small MW Non Digestible Fraction Fibersol
Nutriose
Godon & Okuma, J. AOAC Int., 2002, 85 (2): 435
Figure 10.4
Total dietray fiber methods AOAC 2001.03.
Table 10.7
Key Product Attributes of Commercial RSs
Particle Size of
Resistant
Key Physical Material RSa TDFb
Classification Form Solubility (microns) (% db) (% db)
RS1 Physically Insoluble Flours 150–250 55–80 25–60 b
inaccessible WGCF 175–420
starch (granular Meals 300–850
starch as starch,
flour, or meal)
RS2 Raw granular Insoluble 75–150 50–80 20–60 b
starch
RS3 Retrograded Insoluble 40–150 50–60 0–35 b
amylose
RS4 Chemically Insoluble 50–100 15–100 60–90 b
modified starch
Resistant Low molecular Soluble 40–500 ~ 90 70–90 b
Maltodextrin weight starch
fractions
a 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.
b TDF Assay Utilized:
AOAC Method 991.43 Total, Soluble, and Insoluble Dietary Fiber in Foods (Enzy-
matic-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 ileostom-
ates, 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 impor-
tance of reduced digestibility and increased fermentability, as researchers
learn about the relationship between the large intestine and integrated sys-
temic 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
most studies have used high-RS ingredients. In particular RS2 from high-
amylose 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 catego-
ries: digestive health (including prebiotic effects), glycemic management,
and weight management.
Human studies tend to indicate that RS is well tolerated, which is an impor-
tant 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 fer-
mentation 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 ferment-
able 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 pro-
duced 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, contribut-
ing to increased fecal weight and cecal content weight; laxation is enhanced;
and changes in bacterial activity occur, resulting in lower production with
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 General Physiological Effect Detailed Physiological Effect
Glycemic Improved glucose response Lower postprandial glucose response.
Management
Improved insulin response Lower postprandial insulin response;
Increased insulin sensitivity;
Delayed onset of insulin resistance.
Weight Reduced energy Non-digested;
Management Fewer available calories;
Increased excreted energy.
Increased satiety hormone Increased GLP-1 and PYY.
production
Modified body composition Decreased total body fat and regional
profile fat;
Decreased adipose lipogenesis.
Modified energy partitioning Increased lipid oxidation.
Digestive Health Modified intestinal Fermentable substrate;
environment 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.
Improved intestinal health Increased apoptotic index;
Decreased DNA damage.
Improved intestinal function Increased mineral absorption (calcium,
magnesium);
Reduced symptoms of diarrhea;
Increased fecal frequency;
Increased mucosal barrier strength;
Improved immune response.
Prebiotic 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.
Culture protagonist Improves yield of probiotic cultures
during growth;
Improves survival of probiotic cultures
during processing, in foods, in vivo.
Tolerance Well tolerated at high levels.
Table 10.9
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.
Subject Type & Amount of RS
Fecal
Weight
Fecal
Frequency
Fecal
SCFA
Fecal
Butyrate
Fecal pH
Fecal
Ammonia
Fecal
Phenols
Fecal
Secondary
Bile Acids
Duration Fed Reference

Healthy & hyper- 29 g RS O Behall et al. 2002
insulinemic; 14 wk
Healthy; 3 wk 39 g RS ↓ ↓ Birkett et al. 1996
Healthy; 4 wk 55 g RS ↑ O O O Hylla et al. 1998
Healthy; 3 wk 22 g RS ↑ ↑ ↑ ↓ ↓ ↓ Muir et al. 2004
Metabolic syndrome 20 g RS ingredient O ↑ ↑ ↓ Noakes et al. 1996
predisposed; 4 wk
Healthy; 3 wk 39 g RS ↑ ↑ ↑ ↓ Phillips et al. 1995
Healthy; 19 d 37 g RS ↑ ↓ O Silvester et al. 1997
Healthy; 2 wk 45 g RS ingredient ↑ O ↑ ↑ O ↓ van Munster et al.
1994
Healthy; 4 wk 51-60 g RS ↑ Wacker et al. 2002
Note: (↓ = decreased; ↑ = increased; O = no effect)

229
lower concentrations of potentially toxic substances such as ammonia, phe-

nols, 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 obser-
vations 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 utiliza-
tion 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-prod-
uct. Butyrate is important for colonic health because it is the preferred meta-
bolic 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 Bifidobacte-
ria 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 charac-
teristic could be usefully employed to reduce probiotic inclusion levels in
food formulations which would be necessary to achieve desired viable bacte-

rial 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 harm-
ful 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 apopto-
sis 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-depen-
dent 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 func-
tion 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-
amylose corn starch enhanced water salvage for children and adults suffer-
ing chronic diarrhea, with decreased time to first stool (Ramakrishna et al.
2000; Raghupathy et al. 2006). This is SCFA-mediated, similar to the mecha-
nism proposed for the increase in calcium, magnesium, zinc, iron, and cop-
per 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, cat-
egorized 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-di-
gested carbohydrates, combining RS with the nutrient improved the diges-
tive 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 appeal-
ing 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 diges-
tive health as part of multi-component diets.
Glycemic Management
Glucose management is of topical interest because prolonged extreme glu-
cose 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-
Table 10.10
Additive Effect of Nutrient Combinations with RS2 High Amylose Corn Ingredients on GI tract Related Events, Relative to the
Non-RS Ingredient Alone
Fecal Weight,
Cecal Contents
Tissue Weight
pH
SCFA
Butyrate
Ammonia
Phenols
Bifidobacteria
Apoptosis
Neoplasm
DNA Damage
Mucus Thick-
ness
Co-Nutrients Model Reference
Carbohydrates
RS + wheat bran Healthy ↑ ↓ ↑ ↑ ↓ ↓ Muir et al. 2004
Humans
(22 g RS fed)
RS + wheat bran Rat ↑ ↑ ↓ ↑ ↑ O Le Leu et al. 2002
RS + wheat bran Rat O ↑ O Henningsson et al. 2002
RS + wheat bran Pig ↑ ↑ ↓ ↑ ↑ ↓ Govers et al. 1999
RS + cellulose Rat ↑ ↑ ↓ ↑ ↑ O Le Leu et al. 2002
RS + psyllium Rat ↑ ↑ ↓ ↑ ↑ Morita et al. 1999
RS + FOS Pig ↑ Brown et al. 1998
Non-Carbohydrates
RS + probiotic Rat ↓ ↑ ↑ ↑ ↑ Le Leu et al. 2005
RS + resistant Rat ↑ ↑ ↑ ↓ ↓ Le Leu et al. 2006
potato protein
RS + whey Rat ↑ ↑ ↓ ↑ Toden et al. 2005A
RS + casein Rat ↑ ↑ ↓ ↓ ↑ Toden et al. 2005B
RS + red meat Rat ↑ ↑ ↓ ↑ ↑ ↓ ↑ Toden et al. 2006
233
Notes: (↓ = decreased; ↑ = increased; O = no effect)

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 glyce-
mic 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 serv-
ing, 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 compari-
son. 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 depen-
dent 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 replace-
ment (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 digest-
ible 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 insu-
lin sensitivity, and higher glucose clearance was observed in both adipose
and muscle tissue (Robertson et al. 2003; 2005). RS fermentation has been
Table 10.11
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.
Glucose
Response
(AUC)
(Timepoint)
Glucose
Response
Insulin
Response
(AUC)
Insulin
Response
(Timepoint)
Subject Type Food Amount of RS Fed Reference
Acute Studies
Healthy Bread 13 or 22 g RS ↓ ↓ ↓ ↓ Behall et al. 2002
Healthy Muffins 6.5 g RS O ↓ ↓ ↓ Behall et al. 2006
Healthy Cracker 1 g RS ingredient/kg bw O ↓ ↓ ↓ Behall et al. 1988
Healthy Sponge cake 60 g RS ingredient ↓ ↓ Brighenti et al. 2006
Healthy Bread 5%, 10%, 20% ↓ Brown et al. 1995
Healthy Arepas 45 g RS ingredient ↓ ↓ ↓ ↓ Granfeldt et al. 1995
Healthy Bread 16.5 g RS ↓ ↓ ↓ ↓ Hoebler et al. 1999
Healthy Pasta 20% flour replacement ↓ ↓ ↓ ↓ Hospers et al. 1994
Healthy Hot mixed meal of 41 g RS ingredient ↓ ↓ ↓ van Amelsvoort et al.
meat, veg., rice 1992
Healthy Bread 10 g RS O Weickert et al. 2005
Type 2 diabetics Cheesecake 16 g RS ingredient ↓ ↓ O Giacco et al. 1998
Type 2 diabetics Muffin 50 g RS ingredient ↓ ↓ O O Krezowski et al. 1987
Chronic Studies
Healthy and hyperinsulinemic Bread O ↓ ↓ Behall et al. 1995
Healthy Cracker 1g RS ingredient / kg bw O ↓ ↓ ↓ Behall et al. 1989
Healthy and hyperinsulinemic Bread ↓ ↓ ↓ ↓ Howe et al. 1996
Metabolic syndrome Muffin 20g RS ingredient O ↓ ↓ ↓ Noakes et al. 1996
predisposed
Notes: (↓ = decreased; O = no effect).
235
Control bread
7
High amylose
6.5 corn starch bread
6
Glucose (mmol/L)
5.5
4.5
3.5
0 20 40 60 80 100 120
Time (min)
400
350
300
Insulin (pmol/L)
250
200
150
100
50
0
0 20 40 60 80 100 120
Time (min)
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 adi-

pose 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 stud-
ies. Byrnes et al. (1995) fed rats diets containing digestible starch or RS2 and
observed that the rats fed the digestible starch diets developed insulin resis-
tance 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.
320
r = 0.91
Insulin Peak (∆ from baseline)

300
280
260
240
220
200
180
160
1.2 1.4 1.6 1.8 2 2.2
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 contribu-
tion 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 (excre-
tion). 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).
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 hor-
mones peptide YY (PYY) and glucagon-like peptide-1 (GLP-1). These hor-
mones 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 high-
RS-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 impor-
tant 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 macro-
nutrients and total fiber content controlled. Lipid oxidation was measured
by respiratory quotient (RQ), which represents the balance between carbohy-
drate 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
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 diges-
tion 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 advance-
ments have enabled food manufacturers to enrich and stabilize the RS con-
tent of many processed foods. RS is generally classified into four distinct
categories: RS1, RS2, RS3, and RS4. First generations of commercial RS ingre-
dients were based largely on crystalline amylose (RS3) with inherent orga-
noleptic 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 chemi-
cally modified materials including the soluble resistant dextrin types, more
clinical research is needed to fully understand the differences and similari-
ties 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 cat-
egory 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 world-
wide 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 physi-
ological 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.
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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Section III
Conventional Fibers
11
Oat Fiber from Oat Hull
J. Bodner and Susan S. Cho
Contents
Introduction.......................................................................................................... 249
Production of Oat Fiber....................................................................................... 250
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 (Dough-
erty 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 super-
ficially, reducing the particles’ swelling in the dough matrix (Gould et al.
1989). These physical properties of oat fiber have been improved by physico-
249
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) sug-
gests 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 large-
scale 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 tex-
tural 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 solu-
tion 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 por-
tion of the lignin, originally present in the lignocellulosic matrix. Thus pro-
cessed 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 impu-
rities 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
Oat Fiber from Oat Hull 251
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 generat-
ing 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, pro-
tein, 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.
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 rein-
forcing 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. For-
tification of various foods with oat fiber can help improve the fiber intake
status of the population. Manufacturers of low-carbohydrate bakery prod-
ucts 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 water-
binding capacity would be desirable for manufacturing of crackers, cook-
ies, and ice cream cones. In these products, too much water binding could
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 hydro-
gen 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 proper-
ties. 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 sus-
ceptibility 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, Fat-

Free 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 non-
meat 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 water-
holding capacity (Zarling 1994), thus it can be successfully used in the formu-
lations 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-
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 pro-
cessing 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 lactose-
hydrolyzed 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 tex-
ture 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, fol-
lowed 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
glucose dependent insulinotropic polypeptide (GIP )response after oat fiber.

A reduced postprandial glucose response occurred on the following day sub-
sequent 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 perfor-
mance 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), addi-
tion of 5% to 15% oat hulls (processed oat hulls, bleached oat hulls, and pro-
cessed 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 polysac-
charide per day. In a crossover study (10 days for each period with a 10-day
Table 11.1
Oat Fiber and Intestinal Regularity
Positive effects No effect
Broiler chickens (Hetland and Svihus. 2001) Broiler breeders (Hocking et al. 2004)
Rats (Lopez-Guisa et al. 1988) Human (Kapadia et al. 1995)
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)
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).
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 (Lopez-
Guisa 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-meth-
oxycinnamic acid), which is known to have inhibitory effects on oat hull bio-
degradability 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 triacylg-
lycerols, 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 broil-
ers. 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).
Fermentability
It is known that the physicochemical characteristics of fiber modify their fer-
mentation characteristics in the colon. Various studies (Titgemeyer et al. 1991;
Bourquin et al. 1993; Roland et al. 1995) indicated that oat fiber does not read-
ily 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 ferment-
ability 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 propor-
tions. 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 disap-
pearance 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 diges-
tive 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 concen-
trations 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, respec-
tively. A rat study of Younes et al. (1995) also indicated that as a percent-
age of total excreted nitrogen, fecal nitrogen was 20% in the oat fiber group,
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 car-
bohydrates 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 unin-
fected 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
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abolic effects of insoluble oat fiber on lean men with type II diabetes. Cereal
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Berry BW. 1997. Effects of formulation and cooking method on properties of low-fat
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Cherney DJ, Siciliano-Jones J, Pell AN. 1993. Technical note: forage in vitro dry mat-
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Fernandez-Garcia E, McGregor JU, Traylor S. 1988. The addition of oat fiber and natu-
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655–663.
Galdeano MC, Grossmann MVE. 2005. Effect of treatment with alkaline hydrogen
peroxide associated with extrusion on color and hydration properties of oat
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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 cotton-
seed 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 peroxide-
treated 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.
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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
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12
Cellulose
Toru Takahashi
Contents
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 cellu-
lose can be divided into two groups: crystalline and amorphous. The over-
all structure of natural cellulose is crystallized. Cellulose is one of the most
common biopolymers on earth because it forms the primary structural com-
ponent of all green plants, including vegetables.1 Accordingly, cellulose is a
common component of our diet.
263
Modified celluloses and cellulose derivatives are also used as food ingre-
dients. Cellulose and its derivatives include physically modified celluloses
such as powdered and microcrystalline cellulose and chemically modified
cellulose derivatives such as hydroxypropylmethyl, methyl, and carboxy-
methyl 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 crystalliza-
tion, 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 cel-
lulose 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 proper-
ties of microcrystalline cellulose in the gastrointestinal tract.

Functionality
Effects of Cellulose on Stool Output and Constipation
Epidemiologically, a lack of fiber (cellulose and pentose) may play an impor-
tant role in the etiology of chronic idiopathic constipation in children.8 Cellu-
lose 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 out-
put 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 Con-
sequently, 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.
Cellulose 265
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 capac-
ity 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 cellu-
lose might be important to feces quality by improving the physical proper-
ties 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 relation-
ship between the alteration of the physical properties of the intestinal con-
tents 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 effec-
tive 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 pow-
dered 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.
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 microcrystal-
line 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, cellu-
lose 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 intes-
tinal 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 subcu-
taneously 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 injec-
tion 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 microcrystal-
line cellulose may occur. However, numerous epidemiological studies assess-
ing 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 unpub-
lished 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 hard-
ened 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 proxi-
mal 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 stimu-
late hyperplasia of the mucosa in the distal colon.
Cellulose 267
Effects on Fats
Epidemiologically, there is no relationship between cellulose intake and
serum lipid levels in diabetic subjects.44 The administration of 10% micro-
crystalline 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 reduc-
ing 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 micro-
crystalline 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% methylcel-
lulose 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 superna-
tant 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) adminis-
tration of microcrystalline cellulose decreased postprandial blood glucose
and insulin levels changed in some cases (Table 12.1), whereas in other stud-
ies, postprandial blood glucose and insulin levels did not change signifi-
cantly.14,52,55,57–59 The time to gastric emptying, which is an important factor
influencing postprandial blood glucose levels, was delayed with the admin-
istration of microcrystalline cellulose in some studies and did not change
in others (Table 12.1). However, there are no reports indicating that cellu-
lose 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
Table 12.1
Effects of Cellulose on Gastric Emptying Blood Glucose, and Insulin.
Duration
Cellulose Type of Dose Effects Species Reference
Cellulose Single dose No effect on blood Rat Schwartz &
glucose Levine 1980
5 weeks Decreased blood
glucose
Cellulose 8 months Decreased blood Dog with DM Nelson et al.
glucose 1998
No effect on insulin
Purified cellulose 1 week No effect on blood Pig Nunes &
(15%) glucose, insulin, GIP Malmlof 1992
and glucagons
Cellulose 4 weeks Decreased blood Cat with DM Nelson et al.
glucose 2000
Cellulose 4 weeks No effect on blood Healthy Schwartz et al.
glucose, insulin, and volunteers 1982
gastric empty
Microcrystalline One shot in Decreased blood Pig Low et al. 1987
cellulose the SI glucose
Microcrystalline One shot in Decreased blood Rat Takahashi et al.
cellulose the SI glucose 2005
Crystalline Single dose Decreased blood Healthy Takahashi et al.
cellulose glucose volunteers unpublished
data
Wood cellulose Single dose Delayed gastric Pig Johansen &
empty Knudsen 1994
Microcrystalline Single dose No effect on gastric Healthy Bianchi &
cellulose empty volunteers Capurso 2002
Cellulose Single dose Cellulose phosphate Patients with Monnier et al.
phospate and (OGTT) decreased blood DM 1978
crystalline glucose;
cellulose No effect on blood
insulin
Carboxymethyl- 10 days Both delayed gastric Rat Begin et al. 1989
cellulose and empty.
crystalline Only CMC decreased
cellulose blood glucose
Solubilized Single dose No effect on blood Hyperchole- Daniela Geleva
cellulose glucose; Decreasde sterolemic et al. 2003
blood CCK volunteers
Carboxymethyl- 2 weeks Decreased blood Rat Vachon et al.
cellulose glucose 1988
Methylcellulose Single dose Decreased blood Healthy Jenkins et al.
glucose and insulin volunteers 1978
Notes: SI: Small intestine; DM: Diabetes mellitus; GIP: Gastric inhibitory polypeptide; OGTT:
Oral glucose tolerance test.
Cellulose 269
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 preven-
tion 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 micro-
crystalline cellulose in vitro.48 Microcrystalline cellulose in the small intestine
injected via a catheter diminishes plasma glucose increases.48 Microcrystal-
line 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 cellu-
lose 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 intes-
tine 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 short-
chain fatty acids does not significantly alter the blood glucose or insulin con-
centrations 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 poten-
tial.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 devel-
oped from the Hagen-Poiseuille law.6 Consequently, the water potential in
the small intestinal lumen with microcrystalline cellulose should increase,
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 absorp-
tion 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 contrac-
tions, which is consistent with the higher pressure and water potential with
microcrystalline cellulose ingestion.
The addition of powdered cellulose to the diet increases water absorp-
tion in the jejunum of pigs with two re-entrant cannulas.56 The addition
of powdered and microcrystalline cellulose, which increases digesta vis-
cosity, 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 pro-
duced from cellulose. Health benefits of HPMC include cholesterol-lowering
actions and attenuating postprandial glycemic reponses. High-molecular-
weight 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 lipid-
lowering effect in animals and humans.
Cellulose 271
Table 12.2
Food Application of Cellulose and Its Derivatives
Cellulose/Derivatives Application
Powdered cellulose Breads, beef burgers, doughnuts, pasta, imitation
cheese, cereal
Microcrystalline cellulose Dressings, beverages, whipped toppings,
reduced-fat foods, ice cream, tablets
Methylcellulose Sauces, soups, breads, fried foods, reduced-fat
foods, gluten-free bakery products
Sodium carboxymethylcellulose Frozen desserts, dressings, sauces, syrups,
beverages, reduced-fat foods
Hydroxypropylmethylcellulose 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-HPMC-
containing 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 incremen-
tal 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 rheo-
logical 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
Acetobacter xylinum produces bacterial cellulose with a width of approxi-

mately 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 applica-
tions 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.
Significance of Mixing-In Behavior of Nutrients in the Lumen
The physical properties of cellulose and cellulose derivatives are impor-
tant 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 par-
ticles of both smaller and larger (> 1 mm) sizes and microcrystalline cel-
lulose 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 influ-
ences chemical reactions and absorption.88 The extent of nutrient micromix-
ing 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 Turbu-
lence 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 transloca-
tion 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)

Cellulose 273
where a is a constant. This should result

in a homogenous concentration of nutri- Lumen
ents across the intestine. However, in vivo
measurement of the short-chain fatty acid Intestinal wall
concentration across the contents of the
cecum and colon does not support such
homogenous concentration. The short- Lumen (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
epithelium by diffusion in laminar flow Diffusion
(Figure 12.1).85 If the diffusion rate of a
nutrient in the lumen is lower than its
transepithelial absorption rate, the over-
all absorption rate of the nutrient should
be proportional to either its diffusion Trans epithelial
rate in the lumen or its membrane trans- transport
Epithelium
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 epithe-
lium 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 Reyn-
olds 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
a. Laminar flow
Circular tube
Direction of flow No radial mixing

Reynolds number
Poor micromixing <2300
with diffusion
0
Velocity
b. Turbulent flow
Reynolds number
>2300
Quick micromixing
0
Velocity
c. Karman vortex
40< Reynolds number

Moderate micromixing <9600
with folding
Obstruction
d. Low Reynolds number situation
No vortex
Reynolds number
Lumen <10
Poor micromixing
with diffusion
Intestinal wall
Obstruction (constriction)
Figure 12.2
Schematic drawing of flow behavior in a tube. Arrows represent the flow line when (a) Reyn-
olds 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 num-
ber 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, sug-
gesting that diffusion is still important to homogenize the fluid completely.88
A vortex is particularly important in macroscopic mixing in laminar flow.85
Cellulose 275
Table 12.3
Reynolds Numbers of Flows Produced Peristalsis in the Lumen of the
Intestine in the Pig, Chicken, and Human
Velocity of Reynolds
Radius of GI Peristalsis Shear Rate Number
Tract (mm) (mm · s–1) (s–1) (no unit)
Pig
Small intestine 5.0 50 49 4.4
Cecum 15 11 3.8 0.15
Chicken
Cecum 4.0 1.0 1.9 0.00010
Humana
Colon 25 21 4.3 0.52
a Estimated from viscosity of pig.
Source: Takahashi T. and Sakata T., Foods & Food Ingredients J. Jpn. 210, 944, 2005
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. There-
fore, 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 lami-
nar 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).
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 seg-
ment 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 constric-
tion 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 situa-
tion, 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 constric-
tion 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 con-
taining barium sulfate into the ileum or cecum of rats confirmed the poor
macroscopic mixing in the large intestine in vivo (Takahashi et al. unpub-
lished 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 con-
taining microcrystalline cellulose and HPMC may diminish glucose absorp-
tion by depressing the diffusion rate in the lumen.5
Cellulose 277
Safety and Technology

The summary of evaluations performed by the joint FAO/WHO expert com-
mittee on food additives did not specify an acceptable daily intake of pow-
dered 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 cal-
cium 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. Fur-
ther 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.
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13
Oat β-Glucan
Niina Tapola and Essi Sarkkinen
Contents
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
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 Rus-
sia, 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
Oat is a good source of different dietary fibers such as β-glucan, arabi-

noxylans, 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 sub-
aleurone layer of oats.3 Environmental factors and especially genetic vari-
ability 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 con-
tain 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 tetrasaccha-
rides.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 concen-
tration has been also seen in the subaleurone region of those cultivars that
have low β-glucan content.3

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
Oat β-Glucan 285
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 differ-
ences in viscosity between the oat varieties are explained in terms of dif-
ferences in mean molecular weight of β-glucan. The viscosity of β-glucan
preparations decreases when the proteins are removed by trypsin. The vis-
cosity 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 alka-
line 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 dif-
ferent oat ingredients measured by high-performance size exclusion chro-
matography 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
β -Glucan Content Calcofluor Average
Sample (% of Dry Matter) MW (x 10-4 g/mol) Reference
Oats 3.4 225 16
Instant oats 4.5 252 14
Rolled oats 4.2 254 14
Rolled oats 5.0 230 16
Oat bran 8.3 215 16
Oat bran 8.7 296 14
Oat bran 8.8 280 14
Oat bran 13.6 206 16
Oat bran 16.4 216 16
Oat bran 20.0 206 16
Table 13.2
Average Molecular Weight (MW) of β-Glucan in Different Experimental and
Commercial Oat-Based Foods
β-Glucan Calcofluor Average MW (x
Sample (% of Dry Matter) 10-4 g/mol)
Oat ingredients
Oats 3.4 225
Rolled oats 5.0 230
Oat bran 8.3 215
Oat bran 13.6 206
Oat bran 16.4 216
Oat bran 20.0 206
Experimental oat-based foods
Apple juice 2.8 58
Extruded flakes 3.1 189
Fresh pasta 1.4 57
Macaroni 1.6 188
Muffin 1.9 192
Teacake 1.5 45
Commercial oat-based foods
Bread loaf 1.1 63
Crisp bread 2.5 95
Porridge 4.9 201
Pancake batter 0.99 19
Pancake 0.97 20
Extruded oats 3.2 193
Yogurt-like product 2.8 83
Fermented drink 0.24 39
Breakfast cereal 16.6 194
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 temper-
ature and longer the duration time of heating, the more the molecular weight
Oat β-Glucan 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 impor-
tant roles in degradation. Using large oat bran particles and short fermen-
tation 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 pre-
ferred 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 con-
centration 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.
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 con-
tents 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, Gluca-
gel®, and Cerogen®), enzymatic hydrolysis Table 13.3
(Oatrim, OatsCreme™), and alkaline extrac-
tion (OatVantage™, Vitacel®).29 Conventional Different Oat-Based Foods
milling has produced oat brans with 1.28 Bread
to 1.60 times more β-glucan than in groats Hot cereals
and the fractionating process increases the Breakfast cereals
β-glucan content by three- or four-fold.6,12 In Cookies
addition to the method, the cultivars with Cereal bars
high levels of β-glucan are important for Pasta
obtaining high β-glucan contents. Oat fiber Power drink
ingredients have been used in various food Oat milk
Oat ice cream
applications (Table 13.3).
Fermented oat bran porridge
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 concentra-
tions.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 cho-
lesterol 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 cho-
lesterol 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. Accord-
ing 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 concentra-
tions in subjects with low (< 5 mmol/l) serum cholesterol. The largest reduc-
tions 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 peri-
ods compared with high-amylose diet and low-amylose diet. This result
suggested that oat bran can suppress the rise in plasma triglyceride concen-
tration 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 sim-
ilar 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 choles-
terol 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 muf-
fins with oat bran concentrate compared to the white bakery consumption.
Romero et al.50 found oat bran cookies decreased both serum total and LDL-
290
Table 13.4
Human Studies of Effects of Oat in Hot and Cold Cereals on Blood Lipids
Daily
Amount of Study
Oat Beta-Glucan Duration Changes in
Subjects Ingredient (g) (Weeks) Vehicle Blood Lipids References
Parallel Studies
84 Healthy subjects Oat bran N/A 2 Hot and cold cereals ↓TC, LDL-C 35
36 Overweight men Oatmeal + oat bran 5.5 12 Hot and cold cereals ↓LDL-C 36
208 Healthy subjects Oat bran N/A 6 Hot cereals, muffins, recipes for NS 38
Oatmeal N/A use
152 Hypercholesterolemic N/A 3.0 6 Ready-to-eat cereals ↓TC, LDL-C 41
subjects
35 Hypercholesterolemic Oat bran N/A 12 Ready-to-eat cereals NS 43
subjects
20 Hypercholesterolemic Oat bran N/A 3 Hot cereals and muffins ↓TC 90
110 Normo- and mildly Oat bran+ oat meal 7.3 12 Ready-to-eat cereals and muffins NS 91
hypercholesterolemic
subjects
36 Hypercholesterolemic Oat bran 10.3 8 In juice, yoghurt, and as porridge NS 44
subjects
44 Hypercholesterolemic Oat bran N/A 6 Sprinkle on, mixed into foods ↓TC, LDL-C 45
subjects
62 Hypercholesterolemic Oat bran 3.0 8 With yogurt and milk NS 46
subjects concentrate
Crossover Studies
12 Hypercholesterolemic Oat bran + oat bran N/A 2 Ready-to-eat cereals ↓TC, LDL-C 40
subjects concentrate
145 Hypercholesterolemic Oat bran N/A 6 Ready-to-eat cereals ↓TC, LDL-C 39
Oat β-Glucan
subjects
23 Hypercholesterolemic men Oat bran N/A 4 Ready-to-eat cereals ↓TC, LDL-C 37
64 Hypercholesterolemic Oat bran N/A 4 Ready-to-eat cereals ↓TC, LDL-C 42
subjects
8 Hypercholesterolemic Oat bran N/A 1.4 Hot cereals and muffins ↓TC, LDL-C 60
subjects
Notes: NS = not significant, TC = Total Cholesterol, LDL-C = LDL-Cholesterol, N/A = not available.
291
292
Table 13.5
Human Studies on Effects of Oat in Bread and Bakery Applications on Blood Lipids
Daily
Amount of Study
Subjects Ingredient (g) (Weeks) Vehicle Blood Lipids References
Parallel Studies
30 Hypercholesterolemic men Oat bran concentrate 11.2 8 Bread NS 51

66 Normal and Oat bran N/A 8 Cookies ↓TC, LDL-C 50
hypercholesterolemic subjects
48 Hypercholesterolemic Oat bran 5.9 4 Bread and cookies NS 19
subjects
34 Overweight women Oat bran 2.31 4 Muffins ↑HDL-C 54
Crossover Studies
24 Hypercholesterolemic Oat bran N/A 4 Bread and muffins ↓TC, LDL-C 47

subjects
9 Ileostomic subjects Oat bran N/A 3 Bread ↓TC, LDL-C 48
8 Type 2 diabetic subjects Oat bran concentrate N/A 12 Bread, bun and ↓TC, LDL-C 49
muffins
16 Hypercholesterolemic Oat bran N/A 3 Muffins NS 53
subjects
20 Healthy subjects Oat bran N/A 6 Entrees and muffins NS 55
12 Hypercholesterolemic Oat bran N/A 4 Bread NS 52
subjects
Notes: NS = not significant, TC = Total Cholesterol, LDL-C = LDL-Cholesterol, HDL-C = HDL-Cholesterol, N/A = not available
Oat β-Glucan 293
cholesterol concentrations more than wheat bran cookies and similar to psyl-
lium-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 hyper-
cholesterolemia 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 LDL-
cholesterol 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 bever-
age with 10 g of β-glucan did not affect serum lipids significantly in compari-
son 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 cho-
lesterol-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 excre-
tion has been reported after oat fiber intake.48,60–63 Increased bile acid excre-
tion 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 hypo-
cholesterolemic effects of β-glucan have been postulated.64 Soluble viscous
fiber may also alter different steps of fat digestion in the gut and conse-
quently reduce absorption of dietary cholesterol.65 Inhibition of endogenous
cholesterol synthesis is one possible, but not major, mechanism. The inhibi-
tory effect is mediated by increased production of short-chain fatty acids,
which are fermentation products of soluble fiber.64
294
Table 13.6
Human Studies on Effects of Oat in Drinks on Blood Lipids
Daily
Amount of Study
Subjects Ingredient (g) (weeks) Vehicle Blood Lipids References
Parallel Studies
54 Hypercholesterolemic Oat bran 5.0 5 Beverage ↓TC 25

subjects 10.0 NS
Crossover Studies
14 Healthy men Oat gum 9.0 1.4 Instant whip ↑HDL 57

19 Hypercholesterolemic Oat gum 5.8 4 Mixed in non-carbonated diet ↓TC, LDL-C 56
subjects drink
24 Healthy subjects Oat 3.4/4.5 4 Oat milk NS 58
52 Hypercholesterolemic Oat flake and oat bran 3.8 5 Oat milk ↓TC, LDL-C 59
subjects
25 Hypercholesterolemic Oat bran 5.0 2 Mixed with orange juice ↓TC, LDL-C 19
subjects
Notes: NS = not significant, TC = otal Cholesterol, LDL-C = LDL-Cholesterol, HDL= HDL-Cholesteroll.
Table 13.7
Human Studies of Effects of Oat in Various Vehicles on Blood Lipids
Daily
Oat β-Glucan
Amount of Study
Subjects Ingredient (g) (weeks) Vehicle Blood Lipids References
Parallel studies
148 Hypercholesterolemic Oatmeal 1.2 6 Hot cereals, muffins, shakes NS 33

subjects Oat bran 2.0 NS
Oatmeal 2.4 NS
Oat bran 4.0 ↓ TC, LDL-C
Oatmeal 3.6 ↓ TC, LDL-C
Oat bran 6.0 ↓ TC, LDL-C
236 Healthy subjects Oatmeal N/A 8 As itself, muffins and recipes for NS 92
use
48 Hypercholesterolemic Oat bran N/A 12 Recipes for use NS 43
subjects
Crossover studies
29 Hypercholesterolemic Oat bran N/A 6 bread, hot cereals and recipes for NS 93
subjects use
23 Hypertriglyceridemic Oat bran N/A 4 muffins, cereals, bread, pasta ↓TG 34
subjects
40 Hypercholesterolemic Oat bran 1.1–1.3 4 cereals, bread, muffins, chouder NS 94
subjects 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.
295
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 glyce-
mic 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 glu-
cose 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 glu-
cose 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 glyce-
mic 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, Björk-
lund 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 insu-
lin 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 prod-
ucts, 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 inges-
tion 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 consid-
ered safe and non-toxic. As to the microbiological and chemical safety (con-
taminants 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-
ficient amount of water along with the oat fiber product should be empha-
sized, 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 absorp-
tion of minerals such as calcium, magnesium, zinc, and manganese. How-
ever, 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 produc-
tion 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 prod-
ucts totally free from gluten could be considered safe for celiac patients.
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14
Rice Bran: Production, Composition,
Functionality and Food Applications,
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-grow-
ing 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
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 Ban-
gladesh, 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 pro-
duce 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 by-
product 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, success-
fully 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 health-
promoting 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.
Rice Bran 307
Table 14.1
Composition of Rice Bran
Percent of
Stabilized Parboiled
Rice Bran Rice Bran
Total Dietary Fiber 20.9 27.0
Soluble Dietary Fiber 1.9 1.9
Nitrogen 2.4 3.0
Fat 22.4 29.6
Source: [14]
Table 14.2
Composition of Rice Bran Oil
Component %
Unsaponifiable Matter 4.1
Saturated Fatty Acids:
Palmitic 17.0
Stearic 1.7
Arachidic 0.6
Monounsaturated Fatty Acids:
Oleic 39.4
Vaccenic 0.9
Gadoleic 0.6
Polyunsaturated Fatty Acids:
Linoleic 34.3
Linolenic 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 health-
ful 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
Table 14.3
Composition of Rice Bran Oil Unsaponifiable Matter
Sterol %
Plant Sterols 43
Campesterol
Stigmasterol
β-Sitosterol
Triterpene Alcohols 28
24-Methylene Cycloartenol
Cycloartenol
Aliphatic alcohols, hydrocarbons 19
4-Methyl Sterols 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 pre-
school children in the Latin American countries. Rice-bran-containing bev-
erage base can be used for isotonic drinks, iced tea drinks, enhanced juices,
mineral supplements, and sports beverages. “Rice Milk” non-dairy alterna-
tive to milk is made from organically grown rice. Healthy meal replacement
drinks made from stabilized rice bran are being introduced in the market.
Rice Bran 309
Safety
Stabilized rice bran has shown no negative influence on shelf life or organo-
leptic 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].
Cholesterol Lowering with Rice Bran
Hamster Studies
The hamster has become the preferred rodent model for cholesterol stud-
ies, 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 Ameri-
can 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 signifi-
cantly 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 cholesterol-
fed hamsters, diets containing 11%, 22%, 33%, and 44% rice bran resulted in
plasma cholesterol reductions of 8%, 11%, 15%, and 21%, respectively, com-
pared 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.
Table 14.4
Hamster Studies: Plasma and Liver Cholesterol Lowering by Rice Bran
Control Rice Bran Effect Ref.
Plasma cholesterol 402 274 Significant 14
(mg/dL) 327 255 Significant 15
322 237 Significant 5
302 276 Not significant 16
281 266 Not significant 17
Liver cholesterol 57 31 Significant 14
(mg/g) 37 28 Significant 15
36 23 Significant 5
Several fractions of rice bran were evaluated for cholesterol-lowering

properties. Defatted rice bran resulted in a loss of cholesterol-lowering abil-
ity [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 reduc-
tions [5, 15]. However, RBO extracted at 4°C or 54°C and wax and gum frac-
tions 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 com-
pared 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 signifi-
cantly 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 signifi-
cant 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 cel-
lulose (insoluble fiber) control diet (<10 cP over a three-hour period), rather
than to oat bran diet viscosity (104 cP), indicating that cholesterol lowering
Rice Bran 311
by rice bran is related to a mechanism other than gel forming and sequester-
ing 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 signifi-
cantly 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 choles-
terol 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 ele-
vated 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 ani-
mals 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, com-
pared 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, respec-
tively), and by cellulose diets with added U (0.8%). Plasma and liver choles-
terol 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 contain-
ing 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-
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 lipopro-
tein 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 cholesterol-
fed 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); how-
ever, 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 com-
pared with the fiber-free control diet [25]. Topping et al. [26] found signifi-
cantly 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 signifi-
cantly 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
Rice Bran 313
addition of 0.5% oryzanol to RBO diet showed a further significant decrease

in PC. Rice bran oil also lowered liver cholesterol and triglycerides signifi-
cantly. 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% oryz-
anol and 1% cholesterol diet [29]. An additional mechanism for reducing
atherosclerotic risk with oryzanol was suggested by significantly lower ADP-
induced 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 activ-
ity 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 choles-
terol 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 argin-
ine/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) com-
pared 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 signifi-
cantly increased, compared with the 7% fat control diet; however, when diets
were made isocaloric (10.8% fat), LDL-C significantly increased and HDL-C
Table 14.5
Human Studies: Plasma Cholesterol Lowering by Rice Bran (RB) and Rice
Bran Oil (RBO)
Plasma Cholesterol, mg/dL
Control Treatment Effect Ref.
21 days (100g RB) 235 211 Significant 43
21 days (100g RB) 217 208 Not significant 43
15 days (RBO) 247 204 Significant 49
30 days (RBO) 247 183 Significant 49
4 weeks (60g RB) 245 242 Not significant 42
42 days (84g RB) 267 245 Significant 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 trig-
lyceride 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 hypercholes-
terolemic 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% (signifi-
cant) 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-cross-
over design study [44], moderately hypercholesterolemic adults achieved sig-
nificant 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 indi-
viduals 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 normocho-
lesterolemic 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). Sig-
nificant cholesterol-lowering effects of γ-oryzanol were reported in hyperlip-
idemic 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 fiber-
free 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 cholesterol-
lowering 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 nor-
mocholesterolemic 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 sta-
bilized rice bran, rice bran oil, and tocotrienol-rich fraction of rice oil lower
TC, LDL-C, and improve the HDL/TC ratio.
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 doc-
umented by various in vitro, animal and human studies. It would be advis-
able 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 sta-
bilized and sold as health food. Rice bran and its fractions are sold at differ-
ent 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 con-
sumer preference. The stabilized rice bran at $1 per Kg would have a poten-
tial 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
Rice Bran 317
Table 14.6
Stabilized Rice Bran Prices
Source $/Kg
Wholesale
Rice Bran (spot price) 2.92

Rice Bran Deoiled 4.25
Retail
Health Foods Markets

Rice Bran Organic 9:50
Rice Bran Solubles 87.89
Rice Bran 6.14
Rice Bran Syrup 27.48
Rice Bran (low fiber) 55.01
Rice Bran (with fiber) 58.64
Rice Bran (with fiber) 49.50
Rice Bran Beverage 102.65
Rice Bran Oil 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 hypocholes-

terolemic 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 for-
tification 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 inter-
ference 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-
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 rice-
bran-containing foods and food products such as breads, breakfast cereals,
cakes, cookies, extruded snacks, muffins, pies, and snack bars. The popular-
ity 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 incor-
poration into more healthful, value-added foods for human consumption.
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15
Barley Fiber
Christine E. Fastnaught
Contents
Extrusion...................................................................................................... 329
Bakery Products.......................................................................................... 332
Meats.............................................................................................................334
β-glucan Extracts........................................................................................334
Miscellaneous.............................................................................................. 336
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 dis-
tributed throughout the mature seed. The content and balance of these fibers
in the whole grain is effected by genetics and growing environments. Genet-
ics controls the type of hull, cemented or loose, and the subsequent process-
ing 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
Table 15.1
Average Fiber Composition of 14 Covered and 14 Hulless Barley Cultivars2, 5
Component Covered Hulless
Total Fiber 20.03 15.00
Arabinoxylan 7.50 5.01
A-X ratioa 0.44 0.72
Cellulose 4.60 2.39
β-glucan 4.91 5.64
Klason lignin 1.50 0.81
Uronic acid 0.80 0.70
Galactose 0.30 0.30
Mannose 0.40 0.40
a = 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 aleu-
rone and starchy endosperm. The hull fiber is equal parts cellulose and arabi-
noxylan 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 con-
tent 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 associ-
ated 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 cross-
sections of barley and oats show that the oat aleurone cell walls (outer tissue
Barley Fiber 325
Table 15.2
Range of Total and Soluble Dietary Fiber and β-Glucan Content in Diverse Barley
Genotypes6-8
Total
Dietary Fiber (% dry wt) β-Glucan
Genotype Na Total Soluble Nb (% Dry Wt)
Hulled (covered) 126 15.0–24.1 3.3–6.7 243 2.0–5.9
Hulless 19 11.0–15.7 3.0–7.0 55 4.1–6.4
Waxy starch, hulled 3 20.0–21.0 6.4–7.2 10 4.7–7.3
Waxy starch, hulless 20 13.1–20.1 5.2–10.2 35 5.1–11.3
Waxy starch, high 2 33.4–34.0 18.1–19.6 4 14.7–17.5
protein, hulless
High amylose 2 17.2–17.9 6.8–7.5 6 6.0–9.7
starch, hulless
a = number of cultivars/samples reported for range of dietary fiber.
b = 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 con-
tent 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 mill-
ing. 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 solu-
ble 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, ham-
mer 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
from conventional milling are classified as flour, shorts, or bran, depending

on particle size. Often the bran and shorts are combined because the brittle-
ness 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 avail-
able 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 (cel-
lotetraosyl). 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 water-
soluble 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 cul-
tivar genetics and growing environments also affect β-glucan molecular
weight.33 And finally, enzyme activity is a critical factor that must be consid-
ered 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
Barley Fiber 327
Table 15.3
Weight Average and Peak Molecular Weight of β-glucan from Barley and Oats.
Solvent Barley Oat Number of Cultivars
Molecular Weight (weight average g/mol × 106)
Water, 10˚C 1.2–1.6 — 24 barley58

Water 0.67 0.45 1 barley, 1 oat59
Water, 90˚C /enzymes 0.45–1.32 — 6 barley, Greek60
Water, 23˚C 0.72–2.34 — 1 normal, 3 waxy hulless barley33
NaOH-NaBH4 2.92–3.30 — 2 waxy hulless barley33
Water, 23˚C 0.27–0.66 — 1 normal, 2 waxy hulless barley34
NaOH 0.8–1.2 — 1 normal, 2 waxy hulless barley34
NaOH pre- + NaOH 1.32–1.87 — 1 normal, 2 waxy hulless barley34
Water, 100˚C 1.64 2.25 1 barley, 1 oat35
NaOH 173 185 1 barley, 1 oat35
Na2CO3 162 181 1 barley, 1 oat35
Peak Molecular Weight (g/mol × 106)
Water, 90˚C /enzyme 1.32–1.69 2.09–2.51 8 barley, 6 oat39

NaOH 1.26 1.27 1 normal barley, 1 oat39
Water, 40˚C & 65˚C 0.2–0.3 — Sequential extracts, 1 barley61
Water / NaOH 0.4–1.6 — Sequential extracts, 1 barley62
Water, 65˚C 0.58–1.31 — Sequential extracts, 24 barley47
NaOH 1.02–1.6 — Sequential extracts, 24 barley47
Na2CO3, pH 10 3.2 — 1 waxy hulless barley63
Na2CO3, pH 10 1.70–2.66 2.89–3.03 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 bar-
ley 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 thermo-
stable 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
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 meth-
ods) 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 simi-
lar 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 com-
pared to a cellulose control.
Processes to purify β-glucan have developed from the research on molecu-
lar weight and solubility. Various combinations of solvents, pH, temperature,
and enzymes have been utilized in the production of barley β-glucan iso-
lates.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 hav-
ing 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, Mor-
gan and Ofman69 developed a new method of β-glucan isolation using hot
Barley Fiber 329
water extraction followed by freeze-thawing of the extract to precipitate the

β-glucans. The presence of endogenous enzyme resulted in lower molecu-
lar 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-maltodex-
trin product containing 7% to 8% dietary fiber. Patents for barley β-glucan
extraction methods have been reviewed,6 but new processes have been dis-
closed 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 forma-
tion 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 retro-
graded 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.

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 with-
out 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 formu-
lation 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
Table 15.4
Typical β-glucan Soluble Fiber Levels in Barley Food Raw Materials Reported
in Published Articles.
β-glucan % (dwb)a
Barley Raw Material No. Range Mean
Whole berries14,15,20,83,84
Covered-dehulled 6 3.3–4.6 4.2
Hulless 8 4.1–7.3 5.8
Pearl 14,15, 20,83,85
Covered 4 3.4–4.7 4.2
Hulless 6 4.1–6.8 5.7
Flakes22 3 2.8–5.7 4.5
Cracked/Grits86 1 7.1 7.1
Meal83,87,88 6 4.1–6.9 5.6
Flour concentrate –ground and sieved 24,25,83,89 3 9.0–23.0 16.8
Flour – impact milled/air-classified fractions 90
β-glucan enriched 15 8.0–23.0 12.4
Other 27 3.0–9.5 5.4
Flour – roller-milled 45% to 70% flour extraction20,21,84,91,92
Covered 3 2.7–4.2 3.3
Hulless 10 3.0–6.0 3.9
Bran – roller-milled 45% to 70% flour extraction20,21,84,92-94
Covered 4 5.9–8.7 7.2
Hulless 10 5.4–13.4 8.1
Bran – pearled 20% to 32% 14,20,83,85
Covered 2 3.6–4.5 4.1
Hulless 5 2.8–6.6 4.7
a 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%. Mar-
lett98 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 den-
sity 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
Barley Fiber 331
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
β-Glucan/Serving (g)
Serving If Raw Barley Has
Food Product Size (g) 4% 5.5% 7%
Pearl barley, uncooked 48.0 1.7 2.4 3.0
Hot barley cereal (flakes) - uncooked 40.0 1.4 2.0 2.5
Granola 49.0 1.3 1.8 2.3
Tortilla, soft – 50% barley meal or flour 51.0 0.7 0.9 1.2
Tortilla chips – 50% barley meal or flour 28.4 0.6 0.8 1.0
Muffin – 50% barley meal or flour 57 0.5 0.6 0.8
No-bake cookie – 100% barley flakes 90.0 1.2 1.6 2.0
Lemon cookie – 100% barley flour 30.0 0.3 0.6 0.9
Extruded barley/rice crisp – 50% barley 33.0 0.6 0.8 1.1
Extruded barley/corn puff snack – 50% barley 28.4 0.6 0.8 1.0
Turkish flat bread – 40% barley 64.0 0.7 0.9 1.2
Barley waffles a 1 waffle 0.75 1.0 1.3
Spaghetti – 40% barley 56.0 0.8 1.1 1.4
Angel Barley Pilaf a ¼ recipe 1.0 1.3 1.7
Stew with pearl barley a 1/6 recipe 0.9 1.2 1.5
Barley almond vegetable salad a ¼ recipe 1.3 2.0 2.3
Tuna barley garden salad a 1/6 recipe 1.2 1.6 2.0
Barley Caponata a 1/8 recipe 0.7 0.9 1.2
a, 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 contain-
ing 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 accept-
able cooking and sensory qualities and increased β-glucan contents. Baik
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 milled-
fiber-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 develop-
ment time but improved bread grain and texture while maintaining loaf vol-
ume. 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 compo-
nents (i.e., starch, β-glucan, and arabinoxylan) on rheological properties of
wheat dough. They prepared dough with 20% whole meal barley, or 15% iso-
lated barley starch, or 4% isolated barley β-glucan or arabinoxylan made from
four barley cultivars with varying amylose starch contents (waxy, 6% amy-
lase; 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 stabil-
ity, and work input. Conversely, addition of the barley starch increased mix-
ing 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 polysac-
charides canceled themselves out. The authors concluded that the combi-
nation 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 reduc-
tion 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 no-
fat muffin, and quick breads, which were rated by consumer panels as hav-
ing 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 moisture-
absorbing 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 simi-
lar 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
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. Sen-
sory 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 improve-
ments 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 beef-
barley 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 mois-
ture 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 incorpo-
rate β-glucan into products where the other components (starch, protein,
insoluble fiber, and lipids) may present problems in formulation. As men-
tioned previously there are numerous wet milling methods for extracting
β-glucan from barley, thus each β-glucan product has specific characteris-
tics 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 reduc-
ing sugars being released more slowly in an in vitro digestion process. Simi-
lar 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 Ire-
land 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 signifi-
cantly slower than the control bread.
Temelli et al.142 has compared beverages made with 0.3%, 0.5%, or 0.7% pec-
tin or purified β-glucan (85%). Beverages made with 0.5% and 0.7% β-glucan
were more viscous than comparable pectin beverages but consumer accept-
ability 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 pow-
der 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 concen-
tration 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-cook-
ing, 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
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 prod-
uct. Forsberg134 also describes a process for precooking, grinding, and dry-
ing 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 consump-
tion as a rice-like product or formulated in snack foods.
Hulless barley cultivars can be used to produce malt and malt extract con-
taining 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 com-
mercial extracts.150
Brewers’ spent grains have been used as a fiber source in bakery prod-
ucts.3,110 This material has high water-absorption capacity, low fat absorp-
tion, 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 (poly-
phenols, phenolic acids, proanthocyanidins) and enzymes (polyphenoloxi-
dase (PPO), peroxidase) that cause discoloration upon oxidation. Ames et
al.82 reported that infrared heat treatment of barley flour reduced peroxi-
dase activity and improved tortilla brightness. But there is considerable
genetic variation in barley for total phenolics and enzyme levels includ-
ing 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 bright-
ness. 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 neces-
sitate strict definition and characterization of the individual fiber products
by processors. The health benefits associated with barley fiber and whole
Barley Fiber 337
grain barley will generate demand by the medical community and consum-
ers. Development of foods containing barley fiber can increase to meet this
demand when manufacturers understand the benefits, unique attributes,
and impact on specific products.
Digestion
The effect of barley insoluble fiber in the digestive system has been clearly
documented in both animal and human studies. Ingestion of BSG (brew-
ers’ 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 epi-
thelial 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 sepa-
rate 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 fac-
tor 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 signifi-
cant 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.
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 dis-
ease (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 measur-
ing changes in lipid profiles and risk reduction for CHD.6,164,165 These stud-
ies 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 consump-
tion of barley β-glucan soluble fiber is an effective dietary approach for low-
ering 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 con-
suming 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 choles-
terol 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 molecu-
lar 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.
Table 15.6
Summary of Human Clinical Trials Utilizing Barley Foods Containing β-Glucan Soluble Fiber as a Dietary Intervention to Reduce
Risk of Coronary Heart Disease
Barley Fiber
Reference/Subjects Diet Intervention Methods Changes (mg/dl)a

Keenan et al.166 Extracted Barley β-glucan- Randomized, double-blind, controlled, Treatment vs. Control
155 men and women Barliv™ five-arm parallel for 6-week diet period 3 g LMW: TC: – 17.1 (- 7.2%)
1. Low molecular weight 5 treatments: 0, 3 g LMW BG, 3 g HMW LDL: – 13.4 (- 8.7%)
(LMW) BG, 5 g HMW BG, 5 g HMW BG 3 g HMW: TC: – 19.1 (- 8.2%)
2. High molecular weight β-glucans prepared in ready-to-eat corn LDL: – 14.0 (- 9.2%)
(HMW) flakes and juice beverage 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%)
Hinata et al.167 Pearl barley Rice: barley mix at a ratio of 7:3; Barley vs. baseline
52 men SDF intake increased from 3.4 g to 18.7 g; TC: – 16.0 (- 9.7%)
Avg. period of 14 months
Aman135 Aktivated® Barley — 5% BG Randomized, single blind, controlled, Barley 3 g vs. Control -
39 subjects crossover with 4-week diet period; LDL: no data (– 5.0%)
2 treatments: 0 and 3 g BG
Biorkland et al.168 β-glucan extracts: barley Randomized, single blind, controlled, Oat- 5 vs. Baseline -
89 subjects — 36% BG parallel with 5-week diet period; TC: – 12.4 (– 4.8%)
oat — 18% BG 4 treatments: 5 and 10 g of barley or oat LDL: – 9.3 (– 5.5%)
β-glucan Oat- 10, Barley- 5 and Barley- 10 showed
no difference to baseline
Behall et al.169 Barley Randomized, double blind, controlled Barley 3 g vs. Control - All
7 men and 18 women Pearl, Flakes, Sieved Flour crossover with Latin Square design of TC: – 10.3 (– 4.9%)
— 5.0% BG three 5-week diet periods; LDL: – 9.7 (- 6.5%)
3 treatments: 0, 3 g, 6 g barley soluble fiber; Barley 6 g vs. Control - All
all with NCEP Step 1 diet TC: – 12.3 (– 5.8%)
LDL: – 12.4 (– 8.4%)
339
(continued)
340
Reference/Subjects Diet Intervention Methods Changes (mg/dl)a

Behall et al. 170 Barley Randomized, double blind, controlled Barley 3 g vs. Control -
18 men Pearl, Flakes, Sieved Flour crossover with Latin Square design of TC: – 1.0 (– 1.0% ns)
— 5.0% BG three 5-week diet periods; LDL: – 0.4 (– 0.3% ns)
3 treatments: 0, 3 g, 6 g barley soluble fiber; Barley 6 g vs. Control -
all with NCEP Step 1 diet TC: – 17.9 (– 8.8%)
LDL: – 14.3 (– 11.0%)
Keogh et al.171 Barley extract – 12-week crossover; 4-week washout Barley vs. Control -
18 men Glucagel — 75% β-glucan between two 4-week diet periods; TC: – 1.3%, ns
2 treatments: 0 and 9.9 g barley β-glucan as LDL: –- 3.8%, ns
part of a controlled Westernized diet
Li et al.172 Barley — whole grain 12-week crossover; 4-week washout Barley vs. Control -
10 women between two 4-week diet periods; TC: – 20.0 (– 14.5%)
2 treatments: 0 or 89 g barley/day as part LDL: – 11.1 (– 21.0%)
of a controlled Japanese standard diet
Ikegami et al.173 Pearled barley All studies: 280 g/day barley/rice 50:50 Barley vs. baseline -
Trial 1: 5 men 13.6% TDF calculated mix = 6.1 g TDF/day from barley TC: – 11.3 (– 5.4% ns)
Trial 1: 4 weeks LDL: – 11.6 (– 8.2% ns)
Trial 2: 20 men Trial 2: 2 weeks TC: – 27.5 (– 9.9%)
LDL: – 23.9 (– 12.8%)
Trial 3: 7 women Trial 3: 2 weeks TC: – 24.8 (– 9.8%)
LDL: – 23.2 (– 13.4%)
Narain et al.174 Barley flour — whole grain 4 wk crossover, 1 wk rest; Barley vs. baseline -
5 men and 1 woman Barley = 100 g/day TC: +2.0 (+ 0.9%) ns
HDL: +14.8 (+ 29.2%)
McIntosh et al.104 Barley — Randomized crossover, 2–4 week periods Barley vs. wheat -
21 men bran 50% extraction — with no rest; TC: – 15.1 (– 6.0%)
4.9% BG BG g/day: TDF g/day: LDL: – 12.8 (– 6.8%)
flakes — 4.4% BG barley = 8.0 barley = 38.4
wheat = 1.5 wheat = 38.4
Newman et al.175 Barley flour — whole grain Randomized parallel, 4 weeks Barley vs. wheat -
14 men waxy hulless barley — EDF g/day: TC: – 24.3 (– 12.3%)
9.6% BG barley = 42 LDL: – 18.9 (– 14.3%)
32.6% EDF wheat = 42 HDL: – 4.3 (– 10.5% ns)
Newman et al.176 Barley flour — whole grain Randomized parallel, 6 weeks Barley vs. baseline -
Barley Fiber
22 subjects waxy hulless barley TDF intake g/day: TC: – 12.0 (– 4.7%)
barley diet = 40 LDL: – 24.0 (– 13.9%)
oat diet = 27 HDL: + 5.0 (+ 10.2%)
Oat vs. baseline -
TC: – 12.0 (– 4.8%)
LDL: – 11.0 (– 7.0%)
HDL: – 6.0 (– 9.5%)
a All changes reported are significant (p < 0.05) unless followed by ns (nonsignificant).
b Abbreviations: LMW = low molecular weight; HMW = high molecular weight; BG = β-glucan; TC = total cholesterol; LDL = low density lipo-
protein 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.
341
Overall, the scientific evidence has clearly demonstrated the health ben-
efits 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 tri-
als 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 cho-
lesterol reduction. At least one barley β-glucan concentrate, Barliv™ barley
Betafiber, has demonstrated the ability to lower cholesterol in a human clini-
cal 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 posi-
tive 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 gelatiniza-
tion (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 interac-
tion 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
Barley Fiber 343
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 diabet-
ics 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 reduc-
ing 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 consump-
tion 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 non-
diabetic 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 glu-
cose 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 postpran-
dial 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.
In summary, there is considerable evidence showing that consumption

of foods with a low glycemic index may provide considerable health ben-
efits, 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 resis-
tance.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 prod-
ucts 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 con-
sumption 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 dia-
stolic 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 pres-
sure 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 oligosaccha-
rides) 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
Barley Fiber 345
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 anti-
nutrient, 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-molec-
ular-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 mor-
tality 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 bar-
ley 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.
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 gas-
trointestinal 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 flatu-
lence 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 gen-
eral condition and behavior, growth, feed and water consumption, feed
conversion efficiency, red blood cell and clotting potential parameters, clini-
cal chemistry values, and organ weights. Overall, no signs of toxicity were
detected even when large amounts were consumed. In a further study, Dela-
ney 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 immunopathol-
ogy. 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 con-
suming oatmeal, whole wheat or triticale porridges or breads. Harrington
et al.218 reported that calcium absorption in rats was unaffected by a barley
Barley Fiber 347
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 Cash-
man219 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 auto-
immune disease called celiac disease in genetically susceptible individuals.
While barley glutens are very different from wheat glutens, the effect of bar-
ley 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.
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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
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
Extracted Polysaccharides......................................................................... 372
Whole Sugar Beet Fiber.............................................................................. 373
Ready-to-Eat Breakfast Cereals..................................................... 373
Bakery Products.............................................................................. 374
Meat Products.................................................................................. 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
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 con-
flicts seriously disrupted shipping transport with the colonies. The Napole-
onic 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 ter-
ritories. In 1747, a Prussian chemist, Andreas Sigismund Marggraf, had been
successful in recovering crystallized sugar from sugar beet. In France, Benja-
min 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 centri-
fuge 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 extrac-
tion of polysaccharides (pectins, arabinans, cellulose) or monomeric compo-
nents (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: pri-
mary 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
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 Non-Lignified Primary Lignified Secondary
Dicotyledons and Cellulose ~ Pectins > Cellulose > Heteroxylans >
Monocotyledons non- Xyloglucan Glucomannans
commelinid
Monocotyledons commelinid Heteroxylans (+ mixed Cellulose ~ Heteroxylans >>
β-glucans in Poaceae and Glucomannans
other families) > Cellulose
>> Pectins and Xyloglucans
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 solubi-
lized 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-
Table 16.2
Dietary Fiber (Total, Insoluble and Soluble, % Dry Weight) of Native and Modified
Sugar Beet Fiber Preparations
TDF IDF SDF Ref.
Native sugar beet fiber 87.1 71.7 15.4 (9)
Autoclaved at 122°C 78.4 52.5 25.9
Autoclaved at 136°C 78.6 48.9 29.7
Native sugar beet pulp 76.9 52.1 24.8 (10)
Fibrex® 73.0 49.0 24.0 Data provided by the supplier (Danisco)
Native sugar beet fiber 70.0 57.8 12.2 (11)
H2O2-treated 94.3 61.1 33.2
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 alcohol-
insoluble 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 struc-
ture 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).
364
Table 16.3
Sugar Composition of Different Sugar Beet Fiber Preparations (% dry weight)
Yield Total
(%) Rha Ara Xyl Man Gal Glc GalA sugars Ref.
Native pulp 100 1.4 19.1 1.6 1.3 4.6 20.6 20.2 68.8 17
Acid- and alkali-treated pulp 35 1.0 11.0 3.6 2.7 2.3 54.2 4.9 69.8
Native pulp 100 2.4 19.6 1.4 1.3 5.5 21.5 20.6 72.3 18
Acid- and alkali-treated pulp 53 2.3 10.0 2.1 2.1 5.7 38.9 16.0 77.1
Native fiber 100 1.5 23.6 1.4 1.4 5.4 24.3 23.2 80.8 17
Acid- and alkali-treated fiber 46 1.2 5.3 2.5 2.6 4.5 51.0 12.0 79.1
AIS from fresh roots 4 2.0 17.2 1.1 1.0 4.5 18.8 20.0 64.6 19
Water-extraction at 20°C
Residue 82 1.2 19.2 1.4 1.0 4.9 22.2 21.7 71.6 20
Soluble (polymeric) 2 1.2 16.1 tr tr 6.1 1.2 31.6 56.2
IDF 60 1.6 24.6 1.6 1.4 6.1 29.6 19.6 84.5 20
SDF 13 0.9 7.9 tr 4.2 3.1 0.6 43.4 60.1
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 polysaccha-
rides: (1) pectin, rich in GalA, Gal, Ara, and Rha; (2) hemicelluloses, typi-
cally 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 com-
plex 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 methyl-
esterified 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, rhamnogalac-
turonan II, is a highly complex molecule made of a short homogalacturonan
backbone with four conserved side chains consisting of 12 different mono-
saccharides. Sugar beet pectins have distinctive features, notably low aver-
age 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 homoga-
lacturonans is only slightly lower (70–100) than that of citrus or apple
homogalacturonans (100–120). The Rha residues are concentrated in rham-
nogalacturonans 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. Rhamnogalactur-
onan II, a small complex pectic polysaccharide, and its boron-cross-linked
dimer, can be isolated from beet after enzymatic digestion (33).
Table 16.4
366
Extraction Conditions and Characteristics of Sugar Beet Pectins

Yield GalA Rha Ara Gal DM DAc FeA [] Ref.
Extraction Conditions (%) (%) (%) (mL/g)
Single Extraction
Buffer pH 4.5 20°C 5.6 51.3 1.3 10.1 5.1 63 32 — 187 24

Buffer pH 6.5 80°C 28.9 45.6 1.9 16.4 5.5 52 34 — 70 24
CDTA pH 4.5 20°C 7.1 48.4 1.1 8.2 4.6 52 27 — 257 24
CDTA pH 6.5 80°C 27.5 48.4 1.6 14.3 4.8 55 35 — 100 24
EDTA 2% 85°C 13.6 55.2 1.9 33.7 7.3 — — — — 25
HCl pH 3.0 75°C 2.5 44.5 1.1 11.4 3.3 94 39 0.26 454 19
HCl pH 1.0 75°C 28.0 29.5 2.8 29.4 6.8 34 37 0.80 342 19
HCl pH 3.0 95°C 5.6 44.5 1.4 15.9 2.7 83 36 0.35 351 19
HCl pH 1.0 95°C 35.0 45.5 4.1 3.1 8.5 65 28 0.60 304 19
NaOH 2% 45°C 19.9 42.4 1.9 8.1 3.7 — — — — 26
NaOH 0.05M 4°C — 58.9 2.6 20.1 5.5 16 19 — — 27
Sequential Extraction Scheme
Water 20°C 2.2 54.4 0.9 8.4 6.5 76 31 0.10 259 28

NH4 oxalate 1% 20°C 0.5 77.9 0.9 1.9 2.4 60 15 0.04 57
HCl 0.05M 85°C 19.9 65.1 2.3 10.0 5.9 62 35 0.48 225
NaOH 0.05M 4°C 11.1 54.9 3.2 12.5 8.1 8 4 0.57 181
Water 20°C 6.4 7.6 0.3 7.3 4.0 41 41 0 — 29
Autoclave pH 5.2 121°C 17.8 39.9 2.1 26.7 3.9 70 48 0.61 —
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 pre-
dominantly 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 methy-
lation 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 homogalactur-
onan 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 con-
cluded 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 rham-
nogalacturonan 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
and methyl esterified are rare so that unsubstituted GalA residues are pres-
ent 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 ran-
domly 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 polygalac-
turonase (39, 40, 63), most of the GalA (~90% of the GalA initially present
in pectin) is recovered as oligogalacturonates of low degree of polymeriza-
tion 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 stud-
ied by degradation with dilute acids (34) or specific enzymes (64, 65). Diges-
tion by a mixture of endo-arabinase and arabinofuranosidase can lead to
complete separation of the Ara while the Gal is retained with the rhamnoga-
lacturonan 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.
Efficient extraction can be obtained either by heating or by alkaline treat-

ments (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 degrada-
tion of the pectic backbone through β-elimination and therefore to extrac-
tion. 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. Depend-
ing 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 defini-
tion, 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
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 cation-
exchange 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 diges-
tive 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 condi-
tion 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 fac-
tors, 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 con-
centration. The conditions of hydration also play a role: The presence of shear
Table 16.5
Hydration Properties of Different Sugar Beet Fiber Preparations
Swelling (mL/g) WA (mL/g) WRC (mL/g) Ref.
Beet Pulp (fiber #) in Water
Native 11.0 — 26.6 78

11.5 # — 26.5 # 79
H+-form 25.0 — 22.5 78
17.8 — 23.9 80
Na+-form 32.0 — — 80
32.6 # — — 79
Beet Pulp in Presence of Supporting Salts
Native 10.0 — — 78
H+-form 13.4 — 16.0
80
Na+-form 15.3 — — 80
Saponified Beet Pulp in Water
Native 25.0 — 24.8 78

H+-form 20.0 — 20.7 78
21.9 — 18.3 81
Na+-form 32.4 — — 81
Beet Fiber in Water
Φ 540 µm 21.5 8.5 24.2a 82

12.6b
Φ 385 µm 21.4 8.8 22.6a 82
12.0b
Φ 205 µm 15.9 7.3 19.2a 82
9.2b
Thermomechanically Treated Pulp
Extruded beet pulp 14.4 (native 19.3) — 28.2 (native 32.9) 83

Autoclaved beet pulp
at 122°C 20.0 (native 23.0) — 35.0 (native 34.0) 9
at 136°C 21.0 (native 23.0) —– 38.4 (native 34.0) 9
a Long incubation, heavy stirring.
b 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.
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-bind-
ing 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 inter-
act 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).

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 pec-
tin: 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), treat-
ment with mild acid, alkali, fungus methyl-esterase or plant methyl-esterase
(35). All those treatments led to low-ester pectins, which gelled in the pres-
ence 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 stabiliza-
tion of flavored oil emulsions (94, 95) and stabilization of acidified drinking
yogurt (96). As sugar beet pectins may form gels by an oxidative cross-link-
ing 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
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 mak-
ing 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 tex-
ture 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 enrich-
ment in high-fiber ready-to-eat cereals applications (99). It has been incor-
porated 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.
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 addi-
tion 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 replace-
ment, beet fiber appears to provide beneficial effects on dough textural pro-
file, 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 vol-
ume 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 prod-
ucts, 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).
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 virtu-
ally 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 associ-
ated enzymes to the polymers, may account for this difference (17). Process-
ing of fiber, such as autoclaving or chemical extraction followed by drying,

influenced its fermentability (9, 17). Harsh drying conditions following pec-
tin 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 physico-
chemical 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 evalu-
ated 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 consti-
pated 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 indi-
gestible 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-
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 contrib-
ute, 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 dif-
ferent 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
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 Results Ref.
20 Healthy 16 days No changes in blood 133
fasting Glc and insulin
concentrations.
18 Healthy middle-aged 3 weeks No effect on fasting 134
with risk ischemic plasma Glc and insulin
heart disease Effect on postprandial
parameters.
8 NIDDM 8 weeks Improvement in Glc 135
response to a
standardized breakfast.
40 NIDDM 8 weeks Blood Glc and insulin 136
fasting or postprandial
levels were not
significantly affected.
Table 16.7
Postprandial Responses of Plasma Insulin and Glucose in Volunteers Given Sugar
Beet Fiber Supplements
Intake Carbohydrate
(g/meal) (g/meal) Subjects Results Ref.
20 86 Healthy male No difference in the mean 137
human volunteers blood and plasma insulin
curves at any time
between the control and
fiber diets.
10 100 Healthy male An improved Glc 138
human volunteers tolerance; no change in
insulin level; no decrease
in postprandial insulin.
7 51 (liquid Healthy male Lower postprandial blood 140
formula) human volunteers Glc and serum insulin
response compared with
formula without fiber.
56 653 Pigs No effect on postprandial 139
glycemic and insulinemic
values.
114 446 Pigs No difference in Glc 120
absorption between sugar
beet fiber and wheat bran
supplemented diets.
by slowing the gastric emptying and/or influencing the diffusion and mix-
ing 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 excre-
tion. 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 postpran-
dial 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 insol-
uble 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 effec-
tive 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
Table 16.8
Effect of Sugar Beet Fiber on Lipid Metabolism (Human Studies)
Intake
(g/day/subject) Subjects Duration Results Ref
30 Hypercholester- 2-4 weeks Significant reduction of 143
olemic women LDL cholesterol with no
change in HDL.
8 NIDDM 8 weeks Lower fasting blood Glc; 135
reduction of LDL
cholesterol with no
change in HDL; lower
fasting levels of
triglycerides;
improvements in Glc
response to
standardized breakfast.
40 NIDDM 8 weeks Decrease of 8% in total 136
cholesterol when
compared with the
habitual diet, but no
decrease compared with
the low-fiber diet.
18 NIDDM 6 weeks Decrease of 6.2, 10.6, and 144
6.0% in, respectively,
total cholesterol,
triglycerides, and Apo B
levels.
30 Healthy 3 weeks Decrease of 12 and 15% in 142
volunteers total and LDL
cholesterol; small
changes in HDL;
significant decrease in
serum triglycerides.
20 Healthy 16 days Decrease of 4.6% in total 133
volunteers cholesterol; decrease
more marked with
subject with a high
habitual fat intake.
1 Healthy 3 weeks Decrease of 8 and 9.6% in 134
middle-aged total and LDL cholesterol
volunteers in subjects in whom
fasting plasma
cholesterol was above
normal; no difference in
HDL cholesterol.
Table 16.9
Effect of Sugar Beet Fiber on Lipid Metabolism (Animal Studies)
Level of
Incorporation
(g/kg diet) Animals Duration Results Ref.
100 g/kg Rats 28 days Significant reduction of serum 123
semi- synthetic cholesterol, but less than that of
diet guar gum.
300 g/kg Rats 3 weeks Decrease in plasma triglyceride 147
fructose base and cholesterol concentration in
diet the postprandial as well as the
post-absorptive period.
100 g/kg Rats 28 days Depress of the liver triglyceride 149
semi-synthetic level in concert with decreased
diet liver lipogenesis; no change in
liver cholesterol; animal less fat.
150 g/kg Rats 14 days Lower circulating cholesterol, 150
cholesterol free hepatic cholesterol, and
diet circulating triacylglycerol; no
change in total hepatic lipid
concentrations and hepatic
adipose tissue lipogenesis;
reduced expression of hepatic
lipoprotein A-1gene.
100 g/kg 25% Rats 28 days Lower plasma total cholesterol; 148
casein diet lower HDL cholesterol.
120 g/kg Weaning 4 weeks No change in serum cholesterol and 145
semi-synthetic piglets HDL cholesterol concentrations;
diet lower fasting triacylglycerol due to
reduction in VLDL synthesis.
100 g/kg semi- Rats 40 days Lower plasma total cholesterol, 153
synthetic diet LDL and triglycerides; decrease
±0.3% in HDL phospholipids and total
cholesterol phospholipids in cholesterol
group.
Diet free of cholesterol, no effect
on measured parameters.
100-220 g/kg Growing Fattening Gradual increase in fiber content 146
diet pigs period caused a linear decrease in total
cholesterol and cholesterol
fractions in blood serums;
decrease in adipose tissue
cholesterol.
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 excre-
tion of bile acids, as they are synthesized from cholesterol in the liver (155).
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 repeti-
tion 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. Modifica-
tion 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 cho-
lesterol 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 fermen-
tation 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 low-
ering 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 pro-
tective effect of sugar beet fiber at any stage of the colorectal carcinogenesis
process.
Although the contribution of dietary fiber to cancer protection is not very

clear, several mechanisms by which they can be protective have been sug-
gested. Sugar beet fiber may reduce the risk for colon carcinogenesis through
enhancement of defecation and dilution of carcinogens. They can exert a pro-
tective 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. Gal-
laher 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 antioxida-
tive enzyme systems. Antioxidant properties of sugar beet fiber were inves-
tigated 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 fermenta-
tion may account for the decrease of aberrant crypt foci in 1,2 dimethylhy-
drazine 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 prolif-
eration 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+ intraepi-
thelial lymphocytes that participate in the elimination of abnormal epithelial
cells after initiation (162). Thus, the protective effect of sugar beet fiber on col-
orectal 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
doses were concerned. The form under which fiber was ingested also dif-
fered: it can be included in foods (prepared dishes, bread, biscuits, chocolate
bars), pressed in tablets, or mixed as a powder in water. Generally toler-
ance was good. Only afew studies reported cases of discomfort, abdominal
cramping, and bloating or trouble with flatulence or borborygmi. This gener-
ally 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 compli-
ance 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 find-
ing new end uses to beet fiber. Beet fiber has thereby been extensively stud-
ied 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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17
Psyllium
Seyed Ali Ziai
Contents
P. psyllium L.................................................................................................. 394
P. ovata Forsk................................................................................................ 394
Chemical Constituents............................................................................... 395
Functionality and Food Application................................................................. 395
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 spe-
cies, 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
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 nutraceuti-
cals 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 varia-
tions 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 psyl-
lium, 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 Per-
sian name which means “like the ears of a horse”), Indian plantago, Isfugul,
Pale psyllium, Indian psyllium (Eng.), Indische, Flohsamen, Indisches psyl-
lium (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
Psyllium 395
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 fac-
tor 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 appar-
ent 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 alkali-
insoluble material and non-fermentable. Fraction C, which represented 15%
psyllium seed husk, was viscous and fast fermented. Fraction B, which rep-
resents 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, inflamma-
tion, 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,
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, suspend-
ers, emulsifiers, and thickeners and has wide application in pharmaceuti-
cals 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 experi-
mentally 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 antitus-
sive, 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 (Mere-
col SH), and yogurt (Merecol Y).6 In the United States ready-to-eat (RTE) cere-
als 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 prepara-
tion of pasta, dough with low cholesterol, RTE cereals, baked snacks, and
pharmaceutical composition to reduce cholesterol and improve functional-
ity. Procter & Gamble is second with patents for the use of psyllium in laxa-
tives, food composition with improved palatability, drink composition, and
treatment composition for hypercholesterolemia.17 Psyllium husk in phar-
maceuticals is formulated as effervescent granules, granules, oral powder,
hydrophilic mucilloid for oral suspension, and capsules.18
Psyllium 397
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 treat-
ment 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 sys-
tem. The important part that the intestine plays in this phenomenon
is terminal ileum due to the increased viscosity as water is progres-
sively removed from the luminal contents. By decreasing postpran-
dial serum lipids and glucose, the postprandial insulin response is
blunted, which affects lipids and lipoprotein synthesis.19–21 By bind-
ing 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 diabe-
tes 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 vis-
cosity 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 dis-
order with unsatisfactory defecation characterized by infrequent stools, dif-
ficult stool passage, or both present for at least three months.34
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 short-
chain 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 princi-
pally 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 (psyl-
lium, 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 com-
bination compared to other laxatives44–46 improved stool frequency and stool
consistency (Table 17.1). In one study on both healthy and chronically consti-
pated 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 psyl-
lium 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 high-
fiber 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 diver-
ticular disease patients promote laxation and reduce intra-colonic pressure
resulting in reduction of pain.35
Psyllium 399
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 consti-
pation-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 poly-
carbophil) 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 cat-
egorized 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
400
Table 17.1
Summary of Clinical Trials on Laxative Effects of Psyllium36.
No. of
Intervention Study Design Patients Duration Outcome Results Safety Analysis Ref.
Lactoluse 30 mL/ Open, randomized 30 1-wk run in The Agiolax produced 4.5 BM/week No sig. adverse 44
day or Agiolax and controlled followed two (in both periods) compared with 2.2 effect noted
(psyllium & senna) crossover 5-wk treatment and 1.9 per week for lactoluse
periods separated
by 1 wk
Lactoluse 30-60 mL/ Multicenter double 85 Two 2-wk periods SF was greater with the Agiolax No difference in 45
day Agiolax blind crossover Agiolax or (0.8/day) than lactoluse (0.6/day, adverse effects
(psyllium & senna) lactoluse with p < 0.001), scores for SC and EOD
10–20 mL/day matching placebo were sig. higher for the Agiolax
with 3–5 days than for lactoluse
before and
between
treatments
Lactoluse 30 mL/ Open, randomized 112 4 wk Both treatments resulted in sig. No serious 40
day or psyllium parallel group (p < 0.0001) increase in SF, SC adverse effects
7g/day study (p = 0.027) over baseline but not
between the treatment groups
No sig. difference in straining and
global improvement
Lactoluse 15 mL/ Randomized double 77 Two 2-wk Sig. increase in SF by Agiolax than No difference in 46
day or Agiolax blind, crossover treatment periods lactoluse (0.8/day vs. 0.6/day, adverse effects
(psyllium & senna) with 3–5 days p < 0.001) between the
10 mL/day laxative free Improvement in SC (p < 0.005) and treatment
period before and EOD (p = 0.02) by agiolax groups
between
treatments
Psyllium (P) and Open, randomized 40 1-wk placebo and Both increased stool frequency (P 3.6 P group 3/22 41
psyllium with single blind 1-wk treatment BM/wk vs. PS 6.8 BM/wk cramping and
senna (PS) controlled p < 0.001) gas
Both increased wet and dry stool PS group 7/22
Psyllium
weights cramping,
Only PS increased stool moisture unfavorable
Both improved SC and provided a diarrhea,
high degree of subjective relief bloating, gas
and nausea
Psyllium 3.6 g tid or Multicenter 201 2 wk SF increased sig. from 2.3/wk to 7/ 39
placebo randomized wk with psyllium and 4.5/wk with
placebo controlled placebo
single blind Stool consistency, sig. decreased and
parallel 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
Psyllium (P) 3.5 g/ Open, multicenter 224(P) 4 wk GPs assessed P superior to other No sig. adverse 49
day or another randomized 170 (other) treatments in improving basal effects
laxative (lactoluse, controlled function and in overall effectiveness
bisacodyl, docusate, with a higher percentage of normal,
senna, and well-formed stools and fewer hard
magnesium sulfate) 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
(continued)
401
402
No. of
Intervention Study Design Patients Duration Outcome Results Safety Analysis Ref.
Psyllium 24 g/day Single blind 10 4 wk each arm Sig. decrease in gut transit time (53.9 No sig. adverse 37
or placebo randomized h in placebo to 30.0 h p < 0.05) effects
placebo controlled Stool weight, SC not sig. improved
with crossover by P
A trend in stool frequency increase in
P (from 0.8 to 1.3 BM/day)
Psyllium 10g/day or Double blind 22 8 wk with 4-wk SF increased sig. after 8-wk psyllium No sig. adverse 38
placebo randomized run in on placebo (3.8 vs. 2.9 BM/wk, p < 0.05) effects
placebo controlled and 4-wk Subjects reported improvement in
washout 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
Psyllium (P) 5.1 g Multicenter 170 1-wk washout Compared to baseline P increased 42
bid and docusate randomized followed by 1-wk stool water content vs. D (2.33% vs.
(D) 100 mg bid double blind baseline (placebo) 0.01%, p = 0.007)
parallel followed by 2-wk Stool wet weight also increased (84.9
treatment 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
Psyllium (P) 2 Open label 32 Two consecutive No sig. changes in SF (C 7.20 vs. P Not mentioned 43
teaspoons/day or randomized 3-wk treatment 7.22)
calcium controlled periods No difference in EOD, SC
Psyllium
polycarbophil (C) 2 crossover More patients seemed to favor C

tabs/day
1,2,or 4 g Two phase 50 healthy 1-wk run in taking Healthy subjects: No difference in 47
methylcellulose (M) 59 placebo then 10- 4 g M sig. increased SF, fecal water, the incidences
or 3.4 g psyllium chronically day treatment and fecal solids. of abdominal
(P) constipated period with one Chronically constipated: camps,
of the M or P All doses of M & P sig. increased SF, flatulence, or
water content, and fecal solids. No abdominal
increase in stool weight by both pain between
the treatment
and placebo
periods
Note: bid: Twice daily, EOD: ease on defecation, SC: stool consistency, SF: stool frequency, sig.: significant/significantly, tid: three times daily, wk:
week,
403
404
Table 17.2
Trials of Psyllium on Irritable Bowel Syndrome
Duration
Year Country Dose (per day) Study Design (weeks) Outcome Ref.
73
1979 UK 1 Sachet (5 g) DB 12 Improved: IBS symptoms 74
1981 US 6.4 g DB 8 No benefit: IBS symptoms, abdominal pain, 70
bowel habit
1982 India NA DB 3 Improved: IBS symptoms 75
1983 Ireland 2 Sachets DB 4 No benefit: IBS symptoms 76
1984 India NA DB NA Improved: IBS symptoms 77
1987 UK 1 Sachet (5 g) DB 12 Improved: IBS symptoms, constipation, 71
Not abdominal pain
1987 India 20 g O 2 Improved: IBS symptoms, abdominal pain 78
1990 India 30 g DB 4 Improved: IBS symptoms, bowel habits, 72
Not abdominal pain
Note: DB: Double blind trial, O: Open trial.
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 colono-
cytes 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 random-
ized 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 abdomi-
nal 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 occur-
rence of colorectal cancer itself as an end point.79 Specific interventions have
failed to affect particular events within carcinogenesis; for example, in the
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 meta-
analysis 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 short-
chain fatty acids in the distal colon.80,90 Butyrate is the preferred oxida-
tive 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 dis-
ease (CHD). CHD may represent itself as angina pectoris or MI. The major
risk factors are hypertension, hyperlipidemia, and smoking, as well as dia-
betes. Other conditions such as fat intake, lack of physical activity, stress, and
Psyllium 407
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 asso-
ciation 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 lifestyle-
related 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 compre-
hensive 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 choles-
terol 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 inter-
ruption 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 syn-
thesis 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-regulat-
ing 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 choles-
terol 7-α-hydroxylase (CYP7) (the rate limiting enzyme in the bile acid syn-
thesis 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 result-
ing in lowering plasma LDL cholesterol.113 In one study in rats, investigators
found that psyllium improved the serum lipid profile by decreasing trans-
fatty acid absorption, especially hypercholesterolemic effect. Hydrogena-
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 proper-
ties 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 contain-
ing 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 choles-
terol, may reduce the risk of CHD.16 This claim was based on scientific evi-
dence 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 accompa-
nied 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 con-
sumption 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 psyl-
lium 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 diges-
tive system (e.g., flatulence, abdominal pain, diarrhea, constipation, dyspep-
sia, 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 hypercholes-
terolemic 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 cross-
over 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 modifi-
cations 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 concentra-
tions.133 Based on this effect the recommendations for the diabetic diet have
changed from a low-carbohydrate, high-fat, high-protein diet to one moder-
ately low in fat and high in starch and NSP.134,135 Diabetes is a chronic condi-
tion and needs maintenance therapy with chronic use of medications, and
fibers as functional foods could be formulated best for long-term compli-
ance. 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 Psyl-
lium 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
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 reten-
tion 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 experi-
mentally 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 com-
mon 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 epidemiologi-
cal 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 exam-
ple 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 psyl-
lium has been documented by other scientific groups, including the FDA.164
Psyllium 411
The adverse effects of psyllium have been relatively uncommon; how-

ever, 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 hyper-
sensitivity reaction. In one survey of 130 pharmaceutical workers, the preva-
lence 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 swal-
lowed, 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
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 ispa-
ghula was discontinued. Four days subsequently, lithium concentration
reached to 0.76 mmol/L.184
In an experiment psyllium increased the extent of ethinylestradiol absorp-
tion 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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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 superflu-
ous 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 sen-
sory 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 matu-
427
Table 18.1
Composition of Edible Parts of Fruits
Water
Available Binding of
Carbo- Dietary Dietary
Fruit Water (%) hydrates Protein Fat Fiber Fiber
Apple 85.3 12.4 0.3 0.4 2.3 31.5
Apricot 85.3 9.4 0.9 0.1 2.0 37.5
Mango 82.0 12.8 0.6 0.5 1.7 40.3
Strawberry 89.5 6.5 0.8 0.4 2.0 41.1
Pineapple 85.3 13.1 0.5 0.2 1.4 51.2
Orange 86.7 9.2 1.0 0.2 2.2 34.7
Plum 83.7 11.4 0.6 0.2 1.7 42.2
Peach 87.5 9.4 0.8 0.1 1.7 45.5
Source: Souci-Fachmann-Kraut, Food Composition and Nutrition Tables 1989/90, and theo-
retical water binding of dietary fiber.
ration of a plant and increases with the need of a tissue for structural stabili-
zation [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 pro-
tective 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 respon-
sible 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 com-
position 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 accumu-
lation 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.
Fruit Fibers 429
In the case of citrus processing [11] of juices and essential oils, the remain-
ing 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-soften-
ing, the production of fiber is economically not of interest. Therefore, a dry-
ing 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 function-
ality, 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 stir-
ring 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 meth-
ods [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
25
Water Binding (g water/g Fiber)
20
15
10
0
an
ls)
er
r
be
be
be
be
ib
ul
Br
Fi
Fi
Fi
Fi
F
(H
at
at
le
on
us
ul
he
er
pp
he
tr
m
eP
ib
W
Ci
W
Le
aF
ng
sic
us
sic
Pe
ra
Pl
as
as
O
Cl
Q
Cl
A
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 concep-
tions, 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 appli-
cations 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 pre-
vent syneresis (see Table 18.2). Especially those fruit fibers that are produced
Fruit Fibers 431
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 Fig-
ure 18.3) visualize the mechanism responsible for the superior water bind-
ing. 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 bind-
ing) 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 sug-
gested 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
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 com-
ponents that may be considered as less healthy are carbohydrates, mainly
sugars. According to a recent WHO report [53] “benefits of fruits and veg-
etables cannot be ascribed to a single mix of nutrients and bioactive sub-
stances” 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
Fruit Fibers 433
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 compara-
tive 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 laryn-
geal cancer. A Harvard research group [61] analyzed whether the source of
dietary fiber has an influence on the reduction of heart disease risk by pool-
ing 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 80 100 120 140

Faecal Bulking Index
Figure 18.2
Faecal Bulking Index (FBI) (according to [63]) reflects non-digested food matter, hindgut bacte-
rial biomass, and the water-holding capacity of the whole. Reference was 12.5% wheat bran
(100) to the normal diet (bases = 0).
2 mm 2 mm
200 µm 200 µm
Herbacel AQ Plus Citrus Fiber powder 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.
Fruit Fibers 435
40
6% Starch
1,8% Starch + 1,2% Citrus fiber
30
Viscosity (Pa s)
20
10
0
0 10 20 30 40 50 60 70 80 90 100
Shear Rate (1/s)
“Starch” “Starch + Citrus Fiber”

Ingredients [%] [%]
Water 68 71,0
Vegetable Oil 9 9
Modified Waxy Maize 6 1,8
Citrus Fiber (Herbacel AQ Plus ) 0 1,2
Vinegar (5% acid) 6 6
Egg Yolk 3 3
Sugar 3 3
Mustard 2 2
Salt 1,5 1,5
Lemon Juice 1 1
Spices 0,5 0,5
Figure 18.4
Flow behavior of low-fat mayonnaise on basis of starch versus starch and citrus fiber.
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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
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
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
Pericarp Pericarp
seed coat Aleurone 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 inter-
nationally 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 sta-
tus, 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 stud-
ies on fermentation and colon cancer prevention will be briefly discussed.
Aleurone Flour 441
Table 19.1
Wheat Aleurone Micronutrient Compositiona
Constituent Unitb Contentb
Crude Protein g/100 g 20.8
Crude Fat g/100 g 5.7c
Water insoluble dietary fiber g/100 g 43.0
Water soluble dietary fiber g/100 g 4.1
Crude Ash g/100 g 11.3
Phosphorous g/Kg 25.4
Potassium g/Kg 22.5
Magnesium g/Kg 10.3
Calcium mg/Kg 930
Iron mg/Kg 260
Zinc mg/Kg 139
Sodium mg/Kg 21
Vitamins
B1 (Thiamin) mg/100 g 1.4
B2 (Riboflavin) mg/100 g 0.2
B6 (Pyridoxine) mg/100 g 1.3
Niacin mg/100 g 32.9
Folic acid μg/100 g 158.0
Pantothenic Acid mg/100 g 4.9
E (DL-α-tocopherol) mg/100 g 1.2
Phytic Acid (inositol 4,5,6 triphosphate) g/100 g 8.4
a Data from Earling et al. [3] (analyses performed by Buhler laboratory, 2004).
b Dry matter basis.
c 66% polyunsaturated, 18% monounsaturated, 16% saturated fat.
Table 19.2
Proximate Analysis of Wheat Bran Flour and Aleurone Flour1
Wheat Bran Flour Aleurone Flour
Constituent (g/100 g) (g/100 g)
Total Starch 21.6 36.5
Total Dietary Fiber 31.6 15.4
Total Fat 5.2 6.5
Total Protein 17.8 23.6
Total Free Sugars 6.2 7.2
Total Ash 3.5 4.1
Total Moisture 10.4 5.1
Sum Total 96.3 98.4

Note: Values are means of duplicate analyses.
Source: Data from Fenech et al. [1].
Pericarp Seedcoat
Wheat Grain (Pericarp Seedcoat Flour)
Wheat Bran
(Wheat Bran Flour)
Starchy Endosperm Aleurone Cells

(White Flour) 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 micron-
ized aleurone for their free-radical scavenging properties against 2,2-diphe-
nyl-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 availabil-
ity 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 con-
taining 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, con-
centrations 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 pro-
portional 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 short-
chain 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 preven-
tion 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 car-
diovascular 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 pre-
vent 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 per-
formed a randomized, controlled intervention trial to compare the change in
plasma folate after consumption of (a) a cereal made from ALF, (b) a cereal
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 posi-
tive 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 con-
sisted 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 fol-
lowing 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 propor-
tion 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-
Aleurone Flour 445
30 WB cereal
ALF cereal
25 0.5mg folic acid

Plasma Folate, nmol/L
+ WB cereal
20
15
10
0 1 2 3 4 5 6 7 8
Time Relative to Cereal Intake, h
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 fol-
lowing 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 gen-
ders) 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
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 lev-
els 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 free-
living 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:
Aleurone Flour 447
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., Sum-
merhill, 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 com-
parison 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 pro-
vided. 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 compli-
ance 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 interven-
tion was 25, 25, and 18 for the ALF, PCS, and FA groups, respectively. The
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 ALF group FA group ANOVA
N = 25 N = 25 N = 18 Pa
Tabletsb 25 (24, 26)a 25 (25, 26)a 633 (625, 641)b < 0.0001
Bread 198 (182, 215)b 590 (533, 647)a 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 incre-
ments 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 sig-
nificantly 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 differ-
ences observed at 16 weeks between groups were statistically significant for
Aleurone Flour 449
ANOVA P < 0.0001
FA c
ALF b
PCS a
0 25 50 75 100 125 150 175 200 225

% Plasma Folate Change Relative to Baseline
(a)
ANOVA P < 0.0001
FA c
ALF b
PCS a
0 10 20 30 40 50 60 70 80 90 100 110
% RBC Folate Change Relative to Baseline
(b)
ANOVA P = 0.0034
Figure 19.4
FA b Percentage change in (a) plasma
folate, (b) RBC folate and (c) plasma
homocyst(e)ine at 16 weeks relative
ALF b to baseline. Percentage change was
adjusted for baseline value. Mean val-
ues that do not share a common letter
are significantly different from each
PCS a
other. FA, ALF, and PCS refer to the
treatment groups. FA group: PCS bread
–40 –30 –20 –10 0 + folic acid tablet (high folate control, N
% Plasma Homocyst(e)ine Change = 18); ALF group: ALF bread + placebo
Relative to Baseline tablet (N = 25); PCS group: PCS bread
+ placebo tablet (low folate control,
(c)
N = 25).
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 mag-
nitude 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 treat-
ment [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 esti-
mated 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 sec-
tions 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–for-
tified 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 tis-
sue 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 ham-
burger 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 inter-
vention 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 stud-
ies was there any evidence of toxicity. Unpublished data from the long-
term study showed a reduction in DNA damage in lymphocytes measured
using the cytokinesis-block micronucleus assay, which suggested a protec-
tive 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 bacte-
rial populations remains unknown. The safe upper limit of ALF consump-
tion has not been determined yet.
Summary
In summary, aleurone flour has a strong potential as an important ingredi-
ent in functional foods from the baking industry because of its high micro-
nutrient density as well as high fermentable fiber content. The bioavailability
and bioefficacy of nutrients in aleurone flour deserve further attention as it
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 grate-
fully 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; Rod-
ney Trimble for sample processing, total dietary fiber and free sugar mea-
surements; 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 measure-
ments. Rosemary McArthur and Clare Aitken are acknowledged for their
important role in blood collections and blood sample preparation for analy-
sis, 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.
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risk factor for occlusive vascular disease. Annu. Rev. Nutr. 12:279–298.
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masinghe SN, Everson RB, and Ames BN (1997) Folate deficiency causes uracil
misincorporation into human DNA and chromosome breakage: implications
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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: info.finechemicals@wacker.com
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 concen-
trated source of vitamins, minerals, and fiber
www.horizonmilling.com/products/products_GWwheataleurone.
shtml
E-mail: kyle_marinkovich@cargill.com
Physical address: 15407 McGinty Road W. MS 61, Wayzata MN 55391
455
456 Appendix
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: fortefiber@dow.com
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
Appendix 457
www.ifcfiber.com; info@ifcfiber.com
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
jdv@ife-fiber.be
Tom Yu
Shanghai, 200040
China
Tel: +86-21-6249-6576
Fax: +86-21-6249-4459
tyu@ifcfiber.com
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 min-
imal 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
458 Appendix
Gum Arabic (Acacia gum)

Colloïdes Naturels International
FORTEFIBER™ and its organic-certified versions, FIBREGUM™ BIO & FIB-
REGUM™ BIO L, are all-natural soluble dietary fibers (guaranteed 90% min-
imum level) from Acacia Gum.
Website address: www.cniworld.com

E-mail: information@cniworld.com
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)
Appendix 459
BENEO™ HSI (high-soluble inulin)

BENEO™ Synergy1 (Oligofructose-enriched inulin): The products are pre-
biotic dietary fibers and have been shown to contribute to gut health, better
calcium absorption and immunity.
Website address BENEO: www@beneo.com

www.orafti.com
E-mail: afi@orafti.com
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: info.sensus@sensus.nl
www.sensus.nl
460 Appendix
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: contact@sensus.us
www.sensus.us
Cargill
Oliggo-Fiber™ Instant (Native)
Oliggo-Fiber™ XL (Fat mimetic properties)
Oliggo-Fiber™ F97 (High solubility)
www.cargill.com
E-mail: www.hft@cargill.com
Physical address: 15407 McGinty Road West, Wayzata, MN 55391
Oat Beta Glucan

Foodfiles
www.foodfiles.com
E-mail: foodfiles@foodfiles.com
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.
Appendix 461
Website address: www.jrsusa.com

www.jrs.de
E-mail: info@jrsusa.com
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 main-
tain 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: sales@taiyoint.com
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
scott@taiyoint.com
From Europe:
Call +49-711-779-8291
Fax +49-711-779-8292
462 Appendix
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
info@herbstreith-fox.de
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
Appendix 463
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: roquettejapan@roquette.com
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 regu-
larity 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: webmaster@matsutani.com
Resistant Starch
National Starch
Hi Maize 5 in 1 fiber and Novelose
Benefits range from weight management, glycemic (blood sugar) manage-
ment, energy management, and digestive health. More than 40 studies in
humans using natural Hi-maize and Novelose provide a high level of confi-
dence that the benefits are reliable and real.
National Starch and Chemical Company

10 Finderne Ave
Bridgewater, NJ 08807
1-800-743-6343
464 Appendix
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
Appendix 465
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
industrialsales@ifcfiber.com
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 Acute postprandial glycemic responses,

86–87
Abdominal pain Adamii studies, 277
partially hydrolyzed guar gum, 96 Adequate intake, vii
psyllium, 405, 409 Adverse effects
Abscesses, 395 partially hydrolyzed guar gum,
Absorption, 27–29 107–108
Acacia gum psyllium, 411
bakery products, 130 Aerated desserts, 55
beverages, 129 Aftertaste, 45
breakfast cereals, extruded, 130 Agama-Acevedo studies, 208
cereal bars, 130 Ahotupa, Vasankari and, studies, 179
characteristics, 121–123 Ahrens, Scholz and, studies, 102
cholesterol, 127–128 Aitken, Clare, 452
confectionery, 130–131 Alam studies, 87, 89, 91, 93–94
constipation, 125–126 Aleurone flour, 442
defined, 121–122 Aleurone flour (ALF)
diarrhea, 125–126 characteristics, 439–440
extruded snacks and breakfast folate levels, 443–451
cereals, 130 food applications, 440–451
food product applications, 128–131 functionality, 440–451
health benefits, 125–128 fundamentals, 451–452
hypoglycemic effect, 127–128 human studies, 443–451
metabolism, 123 physiological benefits, 440–451
nitrogen excretion, 126–127 rat studies, 442–443
nutritional aspects, 123–125 safety, 451
prebiotic effect, 123–125 suppliers, 455–456
safety, 122–123 toxicity, 451
snacks, extruded, 130 Alginates, 54, 81
suppliers, 458 Allergies, 396
tolerance, 123 Alles studies, 237
Acesulfame K, 75 Alpha-cell, 456–457
Acetate, 91, see also Short-chain fatty Alpha-cyclodextrin (α-CD)
acids (SCFA) characteristics, 9–10
Acetic acids, 91, see also Short-chain fatty food applications, 11
acids (SCFA) functionality, 11
Acetobacter xylinum, 271 fundamentals, 14–15
Acidic conditions physiological benefits, 11–13
acacia gum, 129 safety and toxicity, 13–14
inulin, 46 suppliers, 455
Nutriose soluble fiber, 35 Aman studies, 286, 336
Activated Barley, 336 American Heart Association Step 1 diet,
Acute intestinal infections, 148–149 89
467
468 Index
Ames studies, 333, 336 Apple pectin

Amino acids, 313 cholesterol reduction, 151
Analysis sources, 140–141
polydextrose, 184 texture, 157
resistant starch, 216–217, 222–223 Approved health claims, see Health
Anderson studies, 250, 254, 257, 408 claims
Animal studies, see also specific animal AQ Plus citrus fiber, 430
barley fiber, 337, 342, 346–347 Arabinogalactan, 94
guar gum, 82 Arcot, Jayashree, 452
hydroxypropylmethylcellulose, 270 Arginine levels, 105
partially hydrolyzed guar gum, 104 Aro studies, 98
psyllium, 408 Arteriosclerosis, 142
resistant starch, 222, 238 Artificial sweeteners, 110
rice bran, 315–316 Artiss studies, 12
Annison and Topping studies, 206, 208 Aruga studies, 106
Annison studies, 208 Asp, Nyman and, studies, 375
Anorectal surgery, 410 Asparagus, 43
Antibacterial activity, 451 Aspartame, 75
Anti-caking effect, 110 Aspergillus niger
Anticarcinogenic properties and effects partially hydrolyzed guar gum, 84
partially hydrolyzed guar gum, sugar beet fiber, 372
108 Asp studies, 209
psyllium, 405–406 Atherosclerosis, 149–150
Anti-inflammatory effects, 405, see also Auerbach studies, 175, 183, 197
Inflammation Available calories, 237, see also Caloric
Anti-neoplastic effects, 405
value
Antioxidation
Avicel, 271
aleurone flour, 439
Ayano studies, 312
partially hydrolyzed guar gum, 110
sugar beet fiber, 382
Antitussive effects, 396 B
AOAC methods
definition of fiber, 2 Bacterial adaptation, 91, see also specific
pectin, 136 type
polydextrose, 184 Bacterial biomass
resistant maltodextrin, 75–76 acacia gum, 124
resistant starch, 222–223 inulin, 47, 48
sugar beet fiber, 363 polydextrose, 178
Apoptosis resistant starch, 227
psyllium, 406 Bacterial overgrowth, 107–108
resistant starch, 231 Bacteroides spp.
Appearance, 36 acacia gum, 124
Appetite modulation, see also Satiety Nutriose soluble fiber, 33
guar gum, 82 pectin, 142
inulin, 51–52 resistant maltodextrin, 65, 67
polydextrose, 183 resistant starch, 230
Apple fiber, 430 Bacteroides ovatus, 142
Apple juice Bacteroides succinogenes, 265
fruit fiber, 428 Bacteroides thetaiotaomicron, 143
oat beta-glucan, 286 Bacteroidetes spp., 34
Index 469
Baik and Czuchajowska studies, 331–332 polydextrose, 195

Bakery products and applications Beer studies, 287, 293
acacia gum, 130 Beet fiber, see Sugar beet fiber
aleurone flour, 451 Behall and Howe studies, 237
alpha-cyclodextrin, 11 Behall studies, 234, 237, 338, 343–344
barley fiber, 332–335 Benefits, physiological
fruit fiber, 431–432 alpha-cyclodextrin, 11–13
guar gum, 81 Nutriose soluble fiber, 28–29
inulin, 50, 54 Beneo
Nutriose soluble fiber, 28, 35, 36, 37 appetite and food intake modulation,
oat beta-glucan, 287, 289, 292 52
oat fiber, 250, 252–253 suppliers, 458–459
partially hydrolyzed guar gum, Berglund studies, 331, 333
109–110 Beringer and Wenger studies, 51
pectin, 159 Berry studies, 217, 254
polydextrose, 187, 189, 194 Betafiber, 378
sugar beet fiber, 373–374, 383 Beta-glucan extracts, see also Oat beta-
Baltes, Stumm and, studies, 175 glucan
Bamboo fiber, 465 barley fiber, 334–335
Bananas (green), 149 characteristics, 284
Baray studies, 121–131 Beverages
Barley fiber acacia gum, 129
bakery products, 332–334 barley fiber, 335–336
beta-glucan extracts, 334–335 cellulose, 271
blood pressure, 344 Nutriose soluble fiber, 28, 37
cancer, 344–345 oat beta-glucan, 287
cardiovascular disease, 338–342 partially hydrolyzed guar gum, 92,
characteristics, 323–329 98–99, 110
digestion, 337 pectin, 158–159
extrusion, 329–332 polydextrose, 193, 195
food applications, 329–337 psyllium, 396
functionality, 329–337 resistant starch, 216
glucose response, 342–344 Bhatty, Vasanthan and, studies, 329
immune response, 344–345 Bhatty studies, 326, 328, 332
insulin response, 342–344 Bifidobacteria spp.
meats, 334 acacia gum, 123–124
miscellaneous, 336–337 inulin, 49–50, 52
physiological benefits, 337–345 partially hydrolyzed guar gum,
safety, 346–347 95–96
toxicity, 346–347 pectin, 143
Barley oil, 342 polydextrose, 182
Barliv Barley Betafiber, 335 resistant starch, 230
Basman studies, 333 Bifidobacteria adolescensis, 124
Beauty supplementation, 103–104 Bifidobacteria longum, 124
Becker, Siddhuraju and, studies, 209 Bifidobacterium spp.
Bednar studies, 209 barley fiber, 337
Beef, beef patties, and beef burgers partially hydrolyzed guar gum, 95
barley fiber, 334 pectin, 142, 144
cellulose, 271 resistant maltodextrin, 65, 67
oat fiber, 253 Bifidobacterium angulatum, 144
470 Index
Bifidobacterium bifidum, 144 Body composition, 238

Bifidobacterium infantis, 144 Body fat
Bifidobacterium pseudolongum, 143 alpha-cyclodextrin, 12–13
Bifidogenic effect, 49 resistant maltodextrin, 71–72
Bile acids Body weight, see also Weight
cellulose, 267 management and control
guar gum, 82 hydroxypropylmethylcellulose, 270
oat beta-glucan, 293 inulin, 48
partially hydrolyzed guar gum, partially hydrolyzed guar gum, 89
88–89 Bologna
pectin, 149, 151 barley fiber, 334
psyllium, 395, 397, 407, 408 oat fiber, 253–254
rice bran, 316 Bond studies, 334
rice bran oil, 312–313 Bone mineral content
sugar beet fiber, 372, 376, 378, 382 inulin, 52–53
Binders/extenders, 252 polydextrose, 182
Binders (tablets) Borborygmi, 383
acacia gum, 131 Bosscher studies, 41–55
cellulose, 271 Bourquin studies, 258
polydextrose, 196 Bowel function, see also Intestinal
Bingham studies, 1 regularity; Stools
Biorklund studies, 338, 343 partially hydrolyzed guar gum, 93
Bird studies, 227, 230, 452 polydextrose, 178
Birkett studies, 205–239 resistant maltodextrin, 65
Birkitt studies, 266 Braaten studies, 293, 296
Biscuits, see also Bakery products and Bran Buds, 396
applications Breads, see also Bakery products and
barley fiber, 332, 333–334 applications
Nutriose soluble fiber, 28 aleurone flour, 440, 446–451
sugar beet fiber, 373, 383 barley fiber, 332, 333, 335, 343, 346
Bjorck, Liljeberg and, studies, 342 inulin, 50
Björklund studies, 287, 293, 296 Nutriose soluble fiber, 28, 36
Blake studies, 89 oat beta-glucan, 287, 289, 289, 292, 296
Blanchet studies, 86 oat fiber, 253
Bloating partially hydrolyzed guar gum,
alpha-cyclodextrin, 13, 14 98–99
barley fiber, 346 psyllium, 396
Nutriose soluble fiber, 25, 28 resistant starch, 208, 234
partially hydrolyzed guar gum, 86, sugar beet fiber, 373–374, 383
92, 96 Breakfast cereals
Blockages, 107 acacia gum, 130
Blood cholesterol concentration levels, aleurone flour, 444–446
see Cholesterol barley fiber, 329
Blood glucose, see Glucose metabolism inulin, 54
and response oat beta-glucan, 286, 296
Blood lipids, see Lipid metabolism Breath freshener, 11
Blood pressure Brennan, Symons and, studies, 334
barley fiber, 344 Brewer’s spent grain (BSG), 342
psyllium, 395 Brinkman, Ben, 452
Bodner studies, 249–259 Brouns studies, 5
Index 471
Brownies, 431–432, see also Bakery oat beta-glucan, 298

products and applications partially hydrolyzed guar gum,
Brown studies, 206–210, 216, 230–231, 102–103
234, 288 pectin, 139, 145, 147
BSG, see Brewer’s spent grain (BSG) polydextrose, 182
Buckley studies, 9–15 psyllium, 411
Bulking effect sugar beet fiber, 376
barley fiber, 331 Caloric value
inulin, 48–49 acacia gum, 123
sugar beet fiber, 374 inulin, 47
Bulking ingredient Nutriose soluble fiber, 34–35
cellulose, 271 partially hydrolyzed guar gum, 107
inulin, 45 polydextrose, 183
Bulman, Felicia, 452 resistant maltodextrin, 75
Buns, see also Bakery products and resistant starch, 237
applications Calorie-reduced foods, see Low-calorie
aleurone flour, 451 products
oat beta-glucan, 289 Calories, available, 237
Burdock and Flamm studies, 184 Calvert studies, 100
Burgers, see Beef, beef patties, and beef Cameron studies, 250, 257–258
burgers Cancer
Burkitt and Trowell studies, 1–2 alpha-cyclodextrin, 12
Burkitt studies, 2 approved health claims, 3
Butyrate, see also Short-chain fatty acids barley fiber, 344–345
(SCFA) inulin, 52
aleurone flour, 443 pectin, 154–156
sugar beet fiber, 381–382
Candida albicans, 50
psyllium, 406
Canine studies, see Dog studies
resistant starch, 230
Capsules, 159
Carbohydrates
Butyric acid, see Short-chain fatty acids
alpha-cyclodextrin, 11
(SCFA)
cellulose functionality, 267, 269
Butyrivibrio fibrisolvens, 143
resistant starch comparison, 229
Byrnes studies, 236
Carcinogenesis, 266
Cardiovascular disease, see also
C Coronary heart disease; Heart
disease
Cadmium aleurone flour, 443
barley fiber, 347 alpha-cyclodextrin, 11, 12
pectin, 146 barley fiber, 338–342
Cakes, see also Bakery products and psyllium, 406–409
applications Carrageen gum, 81
polydextrose, 187 Carriers, 11
sugar beet fiber, 373 Caseinate replacement, 54
Calcium Cashman, Kennefick and, studies, 347
aleurone flour, 439 Cataracts, 395
barley fiber, 346–347 Cat studies, 266
cellulose, 277 Cattle studies, 257, 258
inulin, 53 Cavallero studies, 343
472 Index
CAVAMAX W6, 455 oat beta-glucan, 289

Cecal enlargement, 14 oat fiber, 251
Celiac disease pectin, 159
barley fiber, 347 psyllium, 396
oat beta-glucan, 298 resistant starch, 209
Cell proliferation, 266 sugar beet fiber, 373–374
Cellulose Cereals
blood glucose, 268 aleurone flour, 444–446
carbohydrates, 267, 269 oat beta-glucan, 286, 289, 290–291, 296
carcinogenesis, 266 sugar beet fiber, 373
cell proliferation, 266 Cergen, 288
characteristics, 263–264 Champ studies, 217, 222
constipation, 264–265 Characteristics
dilution effect, 266 acacia gum, 121–123
fats, 267 aleurone flour, 439–440
fermentation, 265 alpha-cyclodextrin, 9–10
flow behavior, 275–276 barley fiber, 323–329
food applications, 271–272 cellulose, 263–264
functionality, 264–271 oat beta-glucan, 283–284
gastric emptying blood glucose, 268 oat fiber, 252
hydroxypropylmethylcellulose, psyllium, 393–395
270–271 sugar beet fiber, 361–372
insulin, 268 Cheese and cheese products, see also
intestines, water absorption, 269–270 Dairy products
large intestine fermentation, 265 cellulose, 271
mixing-in behavior, 272–275 inulin, 54
nutrients interrelationship, 276 pectin, 158
oat fiber, 251 Chemically modified starch, 210, 216
peristalsis, 275 Chemical properties and structure
physiological benefits, 270–271, inulin, 42, 45–46
272–276 pectin, 136–138
proteins, 270 psyllium, 395
psyllium comparison, 411 resistant starch, 206
resistant starch, 232 Cheng studies, 442
safety, 277 Cherbut studies, 378
segmentation, 276 Chicken products, 334
stool output, 264–265 Chicks and chicken studies
sugar beet fiber, 369–370 cellulose, 272, 275
suppliers, 456–457 oat fiber, 255, 256
technology, 277 partially hydrolyzed guar gum, 103
water absorption, intestines, 269–270 rice bran, 313–314
Ceolus, 271 Chicory, 43, 45
Cereal products Chilling, 395, see also Freezing
acacia gum, 130 Chiu, Henley and, studies, 208–209
aleurone flour, 440 Chiu studies, 208–209
barley fiber, 335 Cho and Prosky studies, 2
cellulose, 271 Chocolate confectionery
fruit fiber, 429 polydextrose, 194
inulin, 54 Chocolate products, 383
Nutriose soluble fiber, 36 Choe studies, 178
Index 473
Cholera toxin, 125 Coffee, 11

Cholesterol, see also Lipid metabolism; Cold-stage scanning electron
Triglyceride levels microscopy (CryoSEM),
acacia gum, 127–128 189–190
alpha-cyclodextrin, 13 Colitis, 442
barley fiber, 337–338 Colon cancer, see also Colorectal cancer
guar gum, 82 aleurone flour, 442–443
hydroxypropylmethylcellulose, 270 pectin, 154
inulin, 48 psyllium, 406
oat beta-glucan, 289, 293 resistant starch, 231
partially hydrolyzed guar gum, 85, Colonic cell health, 231
88–90 Colonic motility
pectin, 150–152 cellulose, 265
polydextrose, 178–179 sugar beet fiber, 376
psyllium, 407, 409 Colon tumorigenesis, 265
resistant maltodextrin, 70–71 Colorectal cancer, see also Colon cancer
rice bran, 309–315, 312 alpha-cyclodextrin, 11
rice bran oil, 310, 312–313 polydextrose, 181
sugar beet fiber, 378, 381 psyllium, 405–406
viscous dietary fiber, 20 resistant starch, 231
Cholestyramine, 378 sugar beet fiber, 381–382
Cho studies, 1–5, 249–259 Colors
Chromatography alpha-cyclodextrin, 11
inulin, 44 barley fiber, 335–336
Nutriose soluble fiber, 21 Commercial developments and
Chromium, 146 applications
Cichorium intybus, 45 partially hydrolyzed guar gum,
Cigar wrappers, 81 109–110
Cihan studies, 108 resistant starch, 209–210, 216
Citracel, 100 Compositae spp., 43
Citrobacter spp., 148 Composition
Citrus pectin Nutriose soluble fiber, 27
cancer, 155–156 rice bran, 307–308
sources, 140–141, 429 sugar beet fiber, 362–364
texture, 157 Condiments, 159, see also specific type
Ciukanu and Kerek studies, 176 Confectionery
Classification, resistant starch, 206–208 acacia gum, 130–131
Clifton studies, 439–452 alpha-cyclodextrin, 11
Clostridia spp., 49 Nutriose soluble fiber, 36, 37
Clostridium spp., 124 partially hydrolyzed guar gum,
Clostridium butyricum 110
inulin, 50 pectin, 158
resistant starch, 230 polydextrose, 189, 193–194
Clostridium difficile, 50 Constipation, see also Intestinal
Clostridium lochhradii, 265 regularity; Stools
Clostridium perfringens acacia gum, 125–126
inulin, 52 cellulose, 264
Nutriose soluble fiber, 31, 34 cellulose functionality, 264–265
Coates studies, 9–15 fruit fiber, 434
Cobalt, 146 inulin, 48
474 Index
partially hydrolyzed guar gum, 86, Creatinine, 126

90–93 Crispiness
psyllium, 395, 398, 409 inulin, 54
Continuing Survey of Food Intakes by oat fiber, 252
Individuals, ix polydextrose, 186
Contraindications, psyllium, 411 Crohn’s disease
Conventional fibers inulin, 50
barley fiber, 323–347 psyllium, 405
cellulose, 263–277 CryoSEM, see Cold-stage scanning
oat beta-glucan, 283–298 electron microscopy
oat fiber (oat hull), 249–259 (CryoSEM)
psyllium, 393–412 Cultured dairy products, 194
rice bran, 305–318 Culture protagonist, 228
sugar beet fiber, 359–383 Cummings studies, 178, 237
Cook, Caroline, 452 Cyamopsis tetragonolobus, 83
Cookies, see also Bakery products and α-cyclodextrin, see Alpha-cyclodextrin
applications (α-CD)
barley fiber, 333 Cynomolgus monkey studies, 313
Nutriose soluble fiber, 28 Czuchajowska, Baik and, studies,
oat beta-glucan, 287, 289 331–332
oat fiber, 251, 252, 253
polydextrose, 187 D
Copper Daas studies, 84
barley fiber, 347 Dahlia, 43, 45
cellulose, 277 Dairy desserts, 54
pectin, 145–147 Dairy drinks, 195, see also Beverages
sugar beet fiber, 376 Dairy products, see also Cheese and
Corn bran cheese products; Milk and
oat fiber comparison, 249 milk products
rice bran comparison, 312 barley fiber, 335
suppliers, 457 guar gum, 81
Corn flakes, 335 inulin, 46, 54
Cornstarch, 81 Nutriose soluble fiber, 28, 36, 37
Coronary heart disease, see also oat beta-glucan, 293
Cardiovascular disease; Heart oat fiber, 254
disease partially hydrolyzed guar gum, 109
approved health claims, 3 pectin, 158
fruit fiber, 434–435 resistant starch, 216
Cosmetics, 81 Dalidowicz, Wendy, 240
Cottonseed fiber, 465 Danisco Sweeteners, 175
Cough, 395, 396 DASH Study Group, 344
Cow’s milk, 293 Davidson, Peters and, studies, 87
Cow studies, 257, 258 Davidson studies, 288
Crackers, 252, see also Bakery products Dea and Madden studies, 363
and applications De Cassia Freitas studies, 103
Craig studies, 175, 197 Delaney studies, 346
Cramping, 92 Delessert, Benjamin, 360
Cream cheese, 54 Demark-Wahnefried studies, 289
Index 475
De Mateo Silleras, Mijan de la Torre Nutriose soluble fiber, 22–25

and, studies, 91 potential health claim, 4
Den Hond studies, 230 potential structure function claims,
Desserts, frozen 4–5
inulin, 46, 54 recommended daily amounts, vii, x,
oat fiber, 250, 254 1, 398, 433–434
Detection methods, resistant starch, sources of in diet, ix
220–221 stool softening, 53
Detoxification, 127 Dietary gums, 80–81, see also Partially
Developments hydrolyzed guar gum (PHGG)
aleurone flour, 439–452 Dietary supplements, 11, see also
fruit fibers, 427–435 Vitamins; specific types
DeVries studies, 222 Digestible carbohydrates, 229
Dextrin, indigestible, 94 Digestion and digestive tract function
Diabetes, see also Glucose metabolism barley fiber, 337
and response; Glycemic Nutriose soluble fiber, 28–29
management and response resistant maltodextrin, 68
alpha-cyclodextrin, 12 resistant starch, 227–232
inulin, 50–51 sugar beet fiber, 374–375
oat fiber, 257 Dikeman studies, 81
partially hydrolyzed guar gum, Dilution effect, 266
86–87 Dinand studies, 370
potential health claim, 4 Direct methods, resistant starch, 217
psyllium, 397, 407, 409 Diverticular disease
resistant maltodextrin, 70 partially hydrolyzed guar gum, 97
resistant starch, 234, 236 psyllium, 398–399
sugar beet fiber, 376, 378 DNA protection, 451
Diarrhea, see also Intestinal issues; Dog studies
Intestinal regularity alpha-cyclodextrin, 9, 14
acacia gum, 125–126 cellulose, 265–266
alpha-cyclodextrin, 13, 14 partially hydrolyzed guar gum, 103
inulin, 50, 54 psyllium, 410
Nutriose soluble fiber, 25, 27, 28 Dongowski studies, 383
oat fiber, 255 Dongowsky studies, 378
partially hydrolyzed guar gum, 86, Dougherty studies, 249–250, 253
89–94, 102 Dressings
pectin, 148 cellulose, 271
psyllium, 405, 409–410 fruit fiber, 431–432
resistant maltodextrin, 65 guar gum, 81
resistant starch, 232 partially hydrolyzed guar gum,
Diet and food, resistant starch, 208–209 109
Dietary Approaches to Stop Drinks and beverages, 293, 294
Hypertension (DASH) Study Drug delivery systems, 410
Group, 344 Drug interaction, 412
Dietary fiber Dry food mixes, 11
approved health claims, 3 Dry-substance conditions, 46
defined, x–xi, 2, 20 Dumping syndrome, 148
historical developments, 19–20 Dysentery, 395, 396
intake, global levels, 1–2 Dyspepsia, 409
mean intake, x Dysuria, 395
476 Index
E sugar beet fiber, 373

Extrusion
Edema, 395 barley fiber, 329–332
Electrolyte balance resistant starch, 209
acacia gum, 125 rice bran, 312
partially hydrolyzed guar gum, 90, Eye disorders, 395
96
Electronic speakers, 272
Ellis studies, 82 F
Embryonic safety, 13–14
Emollient effects, 396 Falk, Sundberg and, studies, 329
Emulsions Fares studies, 363, 368–369
dietary gums, 81 Fässler studies, 222
fruit fiber, 432 Fastnaught studies, 323–347
inulin, 46 Fat-free products
pectin, 159 oat fiber, 253–254
psyllium, 396 pectin, 158
Endress studies, 135–159 Fat mass, 48
Energy contribution, 183 Fat metabolism, 70–71
Energy partitioning, 238–239 Fats
Englyst’s classification, 10 barley fiber, 334–335, 337
Englyst’s method, 222 cellulose functionality, 267
Englyst studies, 216–217, 222 gums as mimetics, 81
Enteral nutrition formula and feeding pectin, 147
guar gum, 82–83 polydextrose, 179
oat fiber, 256 Fatty acids, 407–408
partially hydrolyzed guar gum, 86, Favier studies, 88
87, 93, 102, 107–108 Fecal issues, see Constipation; Diarrhea;
pectin, 148 Intestinal issues; Stools
resistant maltodextrin, 68 Feeding tubes, see Enteral nutrition
Enterobacter spp., 148 formula and feeding
Entner-Doudoroff pathway, 143 Fenech studies, 439–452
Escherichia spp., 230 Fermentation
Escherichia coli acacia gum, 123
inulin, 49 aleurone flour, 443
partially hydrolyzed guar gum, alpha-cyclodextrin, 9, 10, 11
106 cellulose functionality, 265
pectin, 142–143 inulin, 47, 49, 53
psyllium, 410 Nutriose soluble fiber, 20, 25, 27, 33
Eubacteria spp., 230 oat beta-glucan, 298
Eubacterium, 337 oat fiber, 258
Evans studies, 82 partially hydrolyzed guar gum, 92,
Extensible products, 287 94, 107, 108
Extracted polysaccharides, 372–373 pectin, 142–143
Extruded snacks and breakfast cereals, polydextrose, 182
see also Cereal products psyllium, 397
acacia gum, 130 resistant maltodextrin, 66, 67–68
inulin, 54 resistant starch, 227, 230, 232
Nutriose soluble fiber, 36 sugar beet fiber, 374–375, 382
oat beta-glucan, 286, 296 Fernandez-Garcia studies, 254
Index 477
Fetal safety, 13–14 partially hydrolyzed guar gum, 92,

Fever, 395 93, 96
Fiber content, see Dietary fiber; Total psyllium, 409
dietary fiber (TDF) sugar beet fiber, 383
Fibersol-2 resistant maltodextrin Flavors
body fat ratio decreases, 71–72 alpha-cyclodextrin, 11
bowel movements, 65 inulin, 54
cholesterol levels, 70–71 partially hydrolyzed guar gum, 109
digestive tract function maintenance, Flood studies, 184
68 Flow behavior, 275–276
fat metabolism, 70–71 Flu, 395
food applications, 74–75 Foams
fundamentals, 61–64 inulin, 46, 55
gastrointestinal functions, 64–68 partially hydrolyzed guar gum,
historical developments, 61–63 109–110
intestinal environments, 65–68 Foehse studies, 331
measuring method, total dietary Folate levels, 440–451
fiber, 75 Food and food product applications
physiological effects, 64–72 acacia gum, 128–131
postprandial blood glucose level aleurone flour, 440–451
attenuation, 69–70 alpha-cyclodextrin, 11
prebiotic effects, 65, 67 barley fiber, 329–337, 346
production, 63–64 cellulose, 271–272
resistant starch, 216 fruit fibers, 430–432
safety applications, 72, 74 inulin, 54–55
short-chain fatty acids, 67–68 Nutriose soluble fiber, 35–36
sugar metabolism, 70–71 oat beta-glucan, 287–293
suppliers, 462–463 oat fiber, 252–254
triglyceride levels, 70–71 pectin, 156–159
Fibregum, 123–124, 128, 458, see also polydextrose, 193–196
Acacia gum psyllium, 395–396
Fibrex, 361, 373, see also Sugar beet fiber resistant maltodextrin, 74–75
Film-coating agents resistant starch, 224
dietary gums, 81 rice bran, 308
polydextrose, 196 sugar beet fiber, 372–374, 383
psyllium, 396 Food characteristics, effects on, 287
Filter paper, 272 Food grade specifications, 85
Finocchiaro studies, 205–239 Food intake modulation, 51–52
Firmness, 109 Food matrix, inclusion in, 28
Fischer, Marlett and, studies, 395 Forsberg studies, 336
Fischer studies, 427–435 FORTEFIBER products, 456, 458
Fish oil supplementation, 150 Fouache studies, 207–208, 216
Fish studies, 345 Fox studies, 336
Flamm, Burdock and, studies, 184 Franck studies, 41–55
Flatbreads, 332 Frankfurters, 253–254
Flatulence Freezing, see also Chilling
alpha-cyclodextrin, 13 barley fiber, 335
barley fiber, 346 oat beta-glucan, 287
inulin, 53–54 Fried products, 36
Nutriose soluble fiber, 25, 27, 28 Frozen products
478 Index
inulin, 54 large intestine fermentation, 265

Nutriose soluble fiber, 36 physiological benefits, 270–271
oat fiber, 250, 254 proteins, 270
polydextrose, 194 stool output, 264–265
Fructooligosaccharides (FOS) water absorption, intestines, 269–270
acacia gum comparison, 124–125 Fussell studies, 93
suppliers, 458–460
Fruit fibers G
food product applications, 430–432 Galdeano and Grossmann studies, 251,
fundamentals, 427–430 253
intestinal regularity, 5 Galdeano studies, 253
physiological benefits, 433–435
Gallaher studies, 382
Fruit fillings
Gallstones, 410
Nutriose soluble fiber, 36
Galvin studies, 2
polydextrose, 195
Garleb studies, 257
Fruit juices, 35
Garlic, 43
Fruits
Gases, see also Flatulence
inulin, 47
recommended daily amounts,
433–434
pectin, 143
Fruit spreads
pectin, 157
Gastric emptying
polydextrose, 195
Frutafit products, 459–460 cellulose functionality, 268
Frutalose products, 459–460 oat beta-glucan comparison, 297
Fulcher, Miller and, studies, 325 psyllium, 397
Fullness, feeling of, 82, see also Satiety Gastrointestinal functions, see also
Functionality Intestinal issues
aleurone flour, 440–451 alpha-cyclodextrin, 14
alpha-cyclodextrin, 11 partially hydrolyzed guar gum, 89
barley fiber, 329–337 resistant maltodextrin, 65–68
oat beta-glucan, 284–287 Gatlin, Jaramillo and, studies, 345
psyllium, 395–396 Gee studies, 82
resistant starch, 224 Gelatin
sugar beet fiber, 372–374 partially hydrolyzed guar gum
Functionality, cellulose comparison, 100
blood glucose, 268 replacement, inulin, 54
carbohydrates, 267, 269 Gelation
carcinogenesis, 266 inulin, 54
cell proliferation, 266 pectin, 138–139
constipation, 264–265 psyllium, 397
dilution effect, 266 sugar beet fiber, 372–373
fats, 267 Gene expressions, 48
fermentation, 265 Genotoxicity, 106
gastric emptying blood glucose, 268 Gerbil studies, 179
hydroxypropylmethylcellulose, Giaccari studies, 96
270–271 Giannini studies, 96
insulin, 268 Gibson, Rastall and, studies, 96
intestines, water absorption, 269–270 Gibson, Wang and, studies, 182
Index 479
Gibson and Roberfroid studies, 180 Greenberg and Sellman studies, 84

Gill studies, 333, 335 Grossmann, Galdeano and, studies, 251,
Glass beads, 266 253
Glass transition temperature (Tg), Guar gum, see also Partially hydrolyzed
186–187, 193 guar gum (PHGG)
Glucagel, 288, 335 fundamentals, 81–82
Glucose metabolism and response, glucose effects, 269
see also Diabetes; Glycemic glycemic control, 5
management and response pectin comparison, 150–151
barley fiber, 342–344 psyllium comparison, 409
cellulose, 267–268 sugar beet fiber comparison, 378
cellulose functionality, 268 Guillon studies, 359–383
oat beta-glucan, 296–297 Gulliford studies, 102
partially hydrolyzed guar gum, 85 Gum arabic, 458, see also Acacia gum
pectin, 152–154, 267–268 Gu studies, 86
polydextrose, 179–180 Gut function, effects on, 48–49
psyllium, 397 Gut microflora, 49, see also Microflora
resistant maltodextrin, 70–72 Gut well-being, 31–34
Glycemic index (GI)
acacia gum, 127–128 H
alpha-cyclodextrin, 12
Hagen-Poiseuille law, 269
barley fiber, 342–343
Hallfrisch studies, 344
CAVAMAX W6, 455
oat beta-glucan, 296 Hamberg studies, 378
partially hydrolyzed guar gum, Hamster studies
97–100, 105 cellulose, 267, 270
pectin, 153 inulin, 48
polydextrose, 179–180 psyllium, 407
resistant starch, 232–233 rice bran, 309–312
Glycemic management and response, Hanai studies, 337
see also Diabetes; Glucose Hara, Suzuki and, studies, 88, 105
metabolism and response Haralampu studies, 206, 209
alpha-cyclodextrin, 12 Hara studies, 102, 182, 381
Nutriose soluble fiber, 29 Harland studies, 375
oat fiber, 250, 254–255 Harrington studies, 346
potential structure function claims, 5 Hashizume studies, 61–75
resistant starch, 228, 232, 234–236 Hawrysh studies, 343
Golay studies, 86 Hayes, Pronczuk and, studies, 179
Goni studies, 217 Health benefits, see Physiological
Gonorrhea, 395 functions and benefits
Gordon and Okuma studies, 223 Health claims
Gould studies, 249–250 approved, 3
Gout, 396 barley fiber, 323–324, 338
Graham studies, 100 no-sugar(s)-added, 37
Grainwise, 455–456 Nutriose soluble fiber, 37
Granfeldt studies, 342 potential, 4
Granola bars, 251 potential structure function, 4–5
Grape juice, 28 psyllium, 396, 408
Green bananas, 149 resistant maltodextrin, 74
480 Index
sugar(s)-free claims, 37 aleurone flour, 443–451

Heart disease, see also Cardiovascular barley fiber, 337–338, 346–347
disease; Coronary heart cellulose, 264–265, 275, 277
disease fruit fiber, 434–435
approved health claims, 3 guar gum, 82
psyllium, 395, 406–409 hydroxypropylmethylcellulose,
Heifer studies, 257, 258 270–271
Heijnen studies, 237 inulin, 47–49
Heini studies, 100 Nutriose soluble fiber, 33, 34
Helianthus tuberosus, 45 oat beta-glucan, 289, 293
Hematologic parameters, 105 oat fiber, 255–256, 257, 258
Hemicelluloses partially hydrolyzed guar gum, 92,
oat fiber, 251 94–96, 103
sugar beet fiber, 369 pectin, 155
Hemodialysis, 126 polydextrose, 178–179
Hemorrhoids, 410 psyllium, 407–408
Henley and Chiu studies, 28, 209 resistant maltodextrin, 70
Henningsson studies, 209 resistant starch, 222, 230, 232, 238
Hepatic parameters, 105 rice bran, 314–316
Hetland and Svihus studies, 255–257 sugar beet fiber, 376
Hetland studies, 255 Humectant, 186, 188, see also Hydration
Heyl, Wise and, studies, 51 Hunger, reduced, 51–52, see also Satiety
Higgins studies, 232, 234, 238 Hydration
High amylose corn starch, see Resistant fruit fiber, 430–431
starch (RS) polydextrose, 188–190
High-density lipoprotein (HDL), see sugar beet fiber, 370–371
Cholesterol; Lipid metabolism Hydrocolloid properties, 410
High-fiber foods, potential structure Hydroxycellulose, 100
function claims, 4–5 Hydroxymethylpropyl cellulose
High-intensive sweeteners, 75 (HMPC)
High-moisture systems, 224 glycemic control, 5
High-protein diet, 126 suppliers, 456
Hi-Maize products Hydroxypropylmethylcellulose
resistant starch, 210, 234 (HPMC), 269, 270–271
suppliers, 463–464 Hygroscopicity, 131
Hinata studies, 343 Hylla studies, 237
HIV-positive patients, 144 Hyperglycemia, 70, see also Glycemic
HMPC, see Hydroxymethylpropyl management and response
cellulose (HMPC) Hyperlipidemia, see also Lipid
Homann studies, 93 metabolism
Honey, 396 pectin, 142
Hong studies, 345 polydextrose, 179
Hordeins, 347 Hypersensitivity, see Adverse effects
Hormone status, 48 Hypertension, see Blood pressure
Hot dogs, see Frankfurters Hypoglycemia and hypoglycemic
Howe, Behall and, studies, 237 effects
Howe studies, 9–15 acacia gum, 127–128
Hudson studies, 333 pectin, 148
Human studies psyllium, 409
acacia gum, 125–128 resistant maltodextrin, 70
Index 481
I Intestinal helminth infections, 250, 259

Intestinal issues
IBS, see Irritable bowel syndrome (IBS) acceptability, inulin, 53–54
Ice cream acute infections, pectin, 148–149
fruit fiber, 431 bowel function, polydextrose, 178
inulin, 46 environments, 65–68, 228, 231–232
Nutriose soluble fiber, 28 function, resistant starch, 228
psyllium, 396 Nutriose soluble fiber, 28
Ice cream cones, 252 psyllium, 395, 396
Ice crystals, 159 resistant maltodextrin, 65–68
Ide studies, 88 resistant starch, 228
Ikegami studies, 100 stool output, sugar beet fiber, 375–376
Ileal morphology, 147 transit time, sugar beet fiber, 375–376
Immune response, 344–345 water absorption, cellulose, 269–270
Immunological effects, 101 Intestinal microflora, 94–96, see also
Immunostimulation, 396 specific type
IMT, see Intima-media thickness (IMT) Intestinal regularity
Indirect methods, resistant starch, 217 bowel movements, resistant
Industrial fruit preparations, 157 maltodextrin, 65
Industrial processing resistance, 35–36 diarrhea, acacia gum, 125–126
Infection, resistance to, 49–50 oat fiber, 250, 255–256
Inflammation partially hydrolyzed guar gum, 96
inulin, 49–50 potential structure function claims, 5
psyllium, 395, 396 stool output, cellulose, 264–265
Inflammatory bowel disease (IBD) Intima-media thickness (IMT), 149
inulin, 50 Intoxication, 395
psyllium, 405 Inulin
Inglett, Lee and, studies, 335 appetite modulation, 51–52
Inglett studies, 251, 335 caloric value, 47
Instant teas and coffees, 11 cancer risk reduction, 52
Insulin response and insulin resistance, chemical properties, 45–46
see also Glycemic management chemical structure, 42
and response diabetes suitability, 50–51
alpha-cyclodextrin, 13 food applications, 54–55
barley fiber, 342–344 food intake modulation, 51–52
cellulose, 267–268 fundamentals, 41–42
guar gum, 82 gut function, effects on, 48–49
oat beta-glucan, 296 gut microflora, modulation of, 49
partially hydrolyzed guar gum, infection, resistance to, 49–50
86–87, 105 inflammation, resistance to, 49–50
pectin, 149 intestinal acceptability, 53–54
psyllium, 397 lipid metabolism, improvement,
resistant maltodextrin, 72 47–48
resistant starch, 234 material properties, 46–47
sugar beet fiber, 376, 381 mineral absorption increase, 52–53
Intake native, 42
mean intake, x natural occurrence, 42–43
recommended daily amounts, vii, x, non-digestibility, 47
1, 398, 433–434 nutritional properties, 47–54
sources of in diet, ix outlook and perspectives, 55
482 Index
physical properties, 45–46 Kahlon studies, 305–318

production, 45 Kaolin, 266
properties, 45–54 Kapoor studies, 79–112
quantitative determination, in food, Karman vortex, 274
43–44 Kasai, Ishizuka and, studies, 382
sources, 42, 43 Kay studies, 88
stability, 109 Keenan studies, 237–238, 338, 367
suppliers, 458–460 Kelleher studies, 265
Ions/organic molecules, 372 Kellogg cereals, 396
Iron Kendall studies, 209, 227
aleurone flour, 439 Kennefick and Cashman studies,
barley fiber, 346 347
cellulose, 277 Keogh studies, 338
oat beta-glucan, 298 Kerek, Ciukanu and, studies, 176
partially hydrolyzed guar gum, 103 Keycel, 456–457
pectin, 145–146 Keys studies, 407
psyllium, 412 Kidneys, see also Renal issues
sugar beet fiber, 376 acacia gum, 126
Irritable bowel syndrome (IBS) resistant maltodextrin, 71
partially hydrolyzed guar gum, King studies, 183
96–97 Klebsiella spp., 148
psyllium, 399, 404–405 Knoblock, Ken, 197
Ishizuka and Kasai studies, 382 Knuckles studies, 328, 332
Ishizuka studies, 181 Kokke studies, 1
Isoleucine, 313 Koksel studies, 331
Iyengar studies, 208–209 Kondo studies, 89
Izydorczk studies, 332 Koujitani studies, 106
Kouwijzer studies, 367
Krüger, Chris, 197
J Kulp and Ponte studies, 208
Jam, 50 Kunkel, Lucia and, studies, 411
Jaramillo and Gatlin studies, 345
Jaskari studies, 287
Jejunal morphology, 147 L
Jenkins studies, 237, 296, 409 Labeling, see Health claims
Jerusalem artichokes, 43, 45 Lachnospira multiparus, 144
Jiang and Vasanthan studies, 326 Lactate, 47
Jie studies, 178, 180, 182 Lactation, 412
Johnson studies, 266, 375 Lactobacilli spp.
Juices acacia gum, 123–124
fruit fiber, 428 inulin, 49–50, 52
Nutriose soluble fiber, 28, 35 Nutriose soluble fiber, 31, 33
oat beta-glucan, 286 oat fiber, 254
Juneja studies, 79–112 polydextrose, 182
JustFiber products, 465 resistant starch, 230
Lactobacilli acidophilus, 144
Lactobacilli casei Shirota, 144
K
Lactobacilli plantarum, 144
Kabir studies, 238 Lactobacillus spp.
Index 483
partially hydrolyzed guar gum, oat fiber, 251

95–96 pectin, 146
pectin, 142 Liliacea spp., 43
Lactobacillus acidophilus, 345 Liljeberg and Bjorck studies, 342
Lairon studies, 2 Liljeberg-Elmstahl studies, 209
Lampe studies, 91 Liljeberg studies, 343
Large intestine fermentation, see also Lina studies, 14
Fermentation Lindstrom studies, 4–5
alpha-cyclodextrin, 9, 10, 11 Lipid metabolism, see also Cholesterol;
cellulose functionality, 265 Triglyceride levels
Large intestine morphology, 259 alpha-cyclodextrin, 11
Larrauri studies, 361 barley fiber, 338
Larrea studies, 251 hydroxypropylmethylcellulose, 270
Laxation inulin, 47–48
partially hydrolyzed guar gum, 85, oat beta-glucan, 288–293, 295
90–94 oat fiber, 257
resistant maltodextrin, 68 partially hydrolyzed guar gum, 88,
resistant starch, 227 96
Laxative effects pectin, 142, 150–152
acacia gum, 123 polydextrose, 178–180
Nutriose soluble fiber, 27 psyllium, 407
polydextrose, 184 sugar beet fiber, 378–381
psyllium, 396 Lipodystrophy, 144
Laxative effects, psyllium Lipolysis, 265
anti-carcinogenic effects, 405–406 Lipoproteins, 150
anti-inflammatory effects, 405 Liquid food products, 28, 37
diverticular disease, 398–399 Listeria spp., 49
fundamentals, 397–398 Listeria monocytogenes, 50
heart disease risk, 406–409 Li studies, 343
irritable bowel syndrome, 399, Litesse and Litesse Ultra, 175, 179–180,
404–405 183
Lead, 146–147 Lithium citrate, 412
Le Bihan studies, 19–37 Liu and Tsai studies, 178
Lee and Inglett studies, 335 Liver
Lee and Prosky studies, 2 pectin, 141, 149
Lee and Schwarz studies, 330 resistant maltodextrin, 71
Leeks, 43 Livesey studies, 342
Lee studies, 223, 254, 332 Locust (carob) bean gum, 81
Lefranc-Millot studies, 19–37 Lopez-Guisa studies, 255, 257
Le Leu studies, 230–231 Lopez-Miranda studies, 1
Lemon fiber, 430 Lopez studies, 232
Le Quéré studies, 363 Lorenz, Vis and, studies, 336
Leucine, 313 Low-calorie products
Levigne studies, 363 fruit fiber, 431
Lewis studies, 51 resistant maltodextrin, 75
Lia studies, 337 Low-density lipoprotein (LDL), see
Light bologna, 253–254 Cholesterol; Lipid metabolism
Light microscopy, 189 Low-fat foods and products
Lignin fruit fiber, 431–432
blocking iron absorption, 103 inulin, 54
484 Index
pectin, 158, 159 McIntosh studies, 345, 443

potential structure function claims, McLean Ross studies, 125
4–5 MCS, see Material with cellular
Low-moisture systems, 224 structure (MCS)
Lucia and Kunkel studies, 411 Measuring method
Lung disorders, 395 barley fiber, 327
Lyly studies, 335 resistant maltodextrin, 75
Lysine, 313 Meat and meat products
barley fiber, 334
fruit fiber, 431–432
M inulin, 54
Madden, Dea and, studies, 363 oat fiber, 250, 252
Magnesium polydextrose, 189, 195
aleurone flour, 439
Medical aspects, pectin
barley fiber, 346
acute intestinal infections, 148–149
cellulose, 277
atherosclerosis, 149–150
oat beta-glucan, 298
cancer, 154–156
cholesterol, 150–152
pectin, 145–146
dumping syndrome, 148
glucose metabolism, 152–154
Maize, 37
intestinal infections, acute, 148–149
MaizeWise corn bran, 457
lipid metabolism, 150–152
Maki studies, 271
short bowel syndrome, 148
Mäkivuokko, Harri, 197
short gut syndrome, 148
Mäkivuokko studies, 182 Medications, 410, 412, see also
MALDI-TOF mass spectrometry, 176 Pharmaceuticals
Maltodextrin replacement, 54 Megazyme, 335
Manganese, 298 Meier studies, 91
Manufacturing, see Production and Melting properties, 54
processing Mesalamine, 405
Marggraf, Andreas Sigismund, 360 Metabolic functions, 85–104
Market potential, rice bran, 316 Metabolic syndrome
Marlett and Fischer studies, 395 psyllium, 407
Marlett studies, 1, 5, 330 resistant starch, 234
Marmalade, 396 Metabolism
Mateos studies, 255 acacia gum, 123
Material properties, inulin, 46–47 pectin, 141–142
Material with cellular structure (MCS), Metal ions, 145–147
429 Metamucil, 100
Matsuoka, Tokunaga and, studies, 69 Methylcellulose
Mattes studies, 135–159 partially hydrolyzed guar gum
Mayonnaise, 432, see also Emulsions comparison, 94
May studies, 124 psyllium comparison, 411
McArthur, Rosemary, 452 Mice studies
McCleary and Monaghan studies, 208, alpha-cyclodextrin, 13–14
217 inulin, 50–51
McCleary and Neukom studies, 84 partially hydrolyzed guar gum, 106
McCleary studies, 208, 217, 222 pectin, 155
McGuffin, Anne, 452 resistant starch, 231
Index 485
Michel studies, 124 Murakami studies, 2, 4–5

Microcrystalline cellulose, 266–267 Mutagenicity
Microflora, see also specific type alpha-cyclodextrin, 14
inulin, 49 partially hydrolyzed guar gum, 106
partially hydrolyzed guar gum, Myers, Weibel and, studies, 370
94–96
Mijan de la Torre and de Mateo Silleras
studies, 91 N
Milk and milk products, see also Cheese Naito studies, 101
and cheese products; Dairy Nakagawa studies, 178
products Nakao studies, 91
guar gum, 81 Naokes studies, 439–452
Narain studies, 343
National Data Laboratory, ix
Miller and Fulcher studies, 325
National Nutrient Databank
Miller-Fosmore studies, 96
Conference, ix
Minekus studies, 222
Natural occurrence, 42–43
Minerals, see also specific type
Natureal, 288
barley fiber, 346–347
Nausea
inulin, 52–53
alpha-cyclodextrin, 13, 14
partially hydrolyzed guar gum,
psyllium, 409
102–103, 105
NCEP step-1 diet, 315
Nephrotoxicity, 126
Mint sauces, 159
Misra studies, 345 Neukom, McCleary and, studies, 84
Mitchell, Helen, 197 Neural tube defects, 443
Mitsuyama studies, 337 Newman and Newman studies, 324
Mixing-in behavior, 272–275 Nichols, Chuck, 197
Modak studies, 345 Nitric oxide (NO) metabolism, 125
Moisture management, 186 Nitrogen excretion, 126–127
Molecular weight, 285 Nitrogen metabolism, 258–259
Monaghan, McCleary and, studies, 208, NO, see Nitric oxide (NO) metabolism
217 Noakes studies, 289
Morgan, Wendy, 452 Nondigestibility, 47
Morgan and Ofman studies, 328 Nontraditional resistant starch, 210, 216,
Morgan studies, 378 218–219
Morita studies, 227, 231–232, 238, 313 Noodles, see Pasta and noodles
Mousses, 55 No-sugar(s)-added claims, 37, see also
Mouthfeel, 36–37 Sugar(s)-free food products
Mucin, 231 Novelose products, 463–464
Muesli Nugent studies, 230
oat beta-glucan, 296 Nurture 1500, 288
sugar beet fiber, 373 Nutraceutical products, 159
Muffins Nutrient interactions and
aleurone flour, 451 interrelationships
barley fiber, 333, 343 cellulose benefits, 276
oat beta-glucan, 287, 289 resistant starch, 232
sugar beet fiber, 374 Nutrim-OB, 288
Muir and O’Dea studies, 217 Nu-trim X, 343
Muir studies, 237 Nutriose soluble fiber
486 Index
absorption in small intestine, 28–29 metal ions, 145–147

caloric value, 34–35 prebiotic nature, 143–144
composition of fiber, 27 toxic metals excretion, 145–147
description, 21–22 weight management, 144–145
dietary fiber content, 22–25 Nuts, 110
digestion in small intestine, 28–29 Nyman and Asp studies, 375
digestive tolerance, 25, 27–28
food applications, 35–36
food matrix, inclusion in, 28 O
fundamentals, 19–21, 37 Oat beta-glucan
glycemic response, 29 bakery applications, 289, 292
gut well-being, 31–34 breads, 289, 292
industrial processing resistance,
cereals, 289, 290–291
35–36
characteristics, 283–284
intestinal bacterial adaptation, 28
drinks and beverages, 293, 294
labeling, 37
food applications, 287–293
mouthfeel, 36–37
food characteristics, effects on, 287
physiochemical properties, 35–36
functionality, 284–287
physiological benefits, 28–29
fundamentals, 284
powder’s properties, 35
glucose metabolism, 296–297
production, 21–22
glycemic control, 5
regulation, 37
lipid metabolism, 288–293, 295
mechanism, 293
safety, 37
sources, 37 molecular weight, 285
suppliers, 462–463 physiological benefits, 288–297
taste, 36–37 postprandial effects, 296–297
technical properties, 35–36 processing, effects on, 285–287
Nutritional aspects, acacia gum, randomized studies, 289–293
123–125 safety, 297–298
Nutritional aspects, inulin suppliers, 460
appetite modulation, 51–52 viscosity, 284–285
caloric value, 47 Oat bran
cancer risk reduction, 52 barley fiber comparison, 342, 345,
diabetes suitability, 50–51 347
food intake modulation, 51–52 intestinal regularity, 5
gut function, effects on, 48–49 psyllium comparison, 409
gut microflora, modulation of, 49 rice bran comparison, 315
infection, resistance to, 49–50 sugar beet fiber comparison, 382
inflammation, resistance to, 49–50 Oat fiber (oat hull)
intestinal acceptability, 53–54 bakery products, 252–253
lipid metabolism, improvement, body weight, 256
47–48 characteristics, 252
mineral absorption increase, 52–53 fat-free frankfurters, 253–254
non-digestibility, 47 fermentability, 258
Nutritional aspects, pectin food applications, 252–254
fermentation, 142–143 frozen desserts, 254
ileal morphology, 147 fundamentals, 249–250
jejunal morphology, 147 glycemic control, 254–255
metabolism of, 141–142 intestinal regularity, 255–256
Index 487
large intestine morphology, 259 P

light bologna, 253–254
nitrogen metabolism, 258–259 Painter studies, 399
pasta shells, 252–253 Palacio and Rombeau studies, 102
pectin comparison, 150–151 Pancakes, 333
pork products, 253–254 Pancreas, 71
Pancreatic amylase activity, 11
production, 250–252
Pancreatic enzymes, 141–142
serum lipids, 257
Paper manufacturing
suppliers, 460–461
cellulose, 272
yogurt, 254
guar gum, 81
Oatmeal, 342
Parisi studies, 97
Oatrim, 288
Park, Matthew R., 240
OatsCreme, 288
Partially hydrolyzed guar gum (PHGG)
OatVantage, 288
acute postprandial glycemic
Oatwell, 288
responses, 86–87
Obesity
adverse effects, 107–108
fruit fiber, 434
anticarcinogenic properties, 108
pectin, 142
beauty supplementation, 103–104
psyllium, 407
blood cholesterol concentration
O’Dea, Muir and, studies, 217
levels, 88–90
Ofloxacin, 410 commercial applications, 109–110
Ofman, Morgan and, studies, 328 dietary gums, 80–81
Ohkuma studies, 207–208, 216 food grade specifications, 85
Oil replacement, 271, see also Fats fundamentals, 80, 82–83, 110–112
Okoniewska studies, 205–239 glycemic index, 97–100
Okubo studies, 95 guar gum, 81–82
Okuma, Gordon and, studies, 223 immunological effects, 101
Okuma studies, 61–75 insulin response, 86–87
Oliggo-Fiber, 460 intestinal microflora balance, 94–96
Oligosaccharides irritable bowel syndrome, 96–97
dietary fiber content, 22–23 laxation improvements, 90–94
introduction in foods, 20 metabolic functions, 85–104
Olson studies, 409 mineral absorption, 102–103
Onions, 43 physiochemical properties, 85
Önning studies, 293 physiological functions, 85–104
Oosterveld studies, 365, 369 postprandial glycemic responses,
Orafti products, 45, see also Synergy 1 86–87
Oral health, 183 prebiotic effects, 94–96
Oral medication, 412, see also processing, 83–85
Medications; Pharmaceuticals regulatory status historical
Oral Rehydration Solution (ORS), background, 108–109
93–94 safety issues, 104–107
Oral rehydration solutions, 129 satiety, 100–101
Orange pulp fiber, 430 suppliers, 461–462
Organic molecules, 372 toxicological behavior, 104–107
Ostergard studies, 330 weight control, 100–101
Ostman studies, 343 Partially methylated alditol acetates
O’Sullivan, Geoff, 197 (PMAAs), 175–176
Outlook and perspectives, inulin, 55 Pasta and noodles
488 Index
aleurone flour, 440, 451 jejunal morphology, 147

barley fiber, 331–332 lipid metabolism, 150–152
cellulose, 271 medical aspects, 148–156
oat beta-glucan, 286 metabolism of, 141–142
oat fiber, 252–253 metal ions, 145–147
partially hydrolyzed guar gum, 109 nutraceutical products, 159
pectin, 159 nutritional aspects, 141–147
polydextrose, 195 partially hydrolyzed guar gum, 90
sugar beet fiber, 373 physical properties, 138–140
Pastries, see also Bakery products and prebiotic nature, 143–144
applications psyllium comparison, 409
inulin, 50 short bowel syndrome, 148
polydextrose, 189–191, 194 short gut syndrome, 148
sugar beet fiber, 373 sorbet, 158–159
Pâtés, see also Meat and meat products sources, 140
inulin, 54 spreads, 157, 159
sugar beet fiber, 374 sugar beet fiber, 363, 365–369
Pawlak studies, 238 suppliers, 462
Pea fiber technological aspects, 136–141
inulin, 52 toxic metals excretion, 145–147
oat fiber comparison, 258 weight management, 144–145
water-binding properties, 430 Pediatric care, 396
Pearled barley, 325, 342 Pender, Kay, 452
Pectin Peristalsis, 275
acacia gum comparison, 124 Peritoneal dialysis, 126
acute intestinal infections, 148–149 Persia studies, 51
apple juice, 428 Persson studies, 347
atherosclerosis, 149–150 Peters and Davidson studies, 87
bakery products, 159 Petruziello studies, 399
barley fiber comparison, 335 Pharmaceuticals, see also Medications
beverages, 158–159 acacia gum, 131
cancer, 154–156 guar gum, 81
capsules, 159 polydextrose, 196
cereal products, 159 psyllium, 396
chemical structure, 136–138 Phenylalanine, 313
cholesterol, 150–152 PHGG, see Partially hydrolyzed guar
commercial type, 140–141 gum (PHGG)
condiments, 159 pH levels, see also Prebiotic
confectionery articles, 158 characteristics and effects
dairy products, 158 acacia gum, 129
dumping syndrome, 148 aleurone flour, 443
fermentation, 142–143 alpha-cyclodextrin, 10
food product applications, 156–159 barley fiber, 335
fruit spreads, 157 inulin, 46, 48
fundamentals, 136 Nutriose soluble fiber, 20, 31–32, 34,
glucose metabolism, 152–154, 267–268 36
glycemic control, 5 partially hydrolyzed guar gum, 84,
ileal morphology, 147 91–92, 94
industrial fruit preparations, 157 pectin, 138–140, 145, 157
intestinal infections, acute, 148–149 polydextrose, 192–193
Index 489
resistant starch, 227 Phytates

Phosphorus pectin, 146
cellulose, 277 sugar beet fiber, 374
oat beta-glucan, 298 Phytic acid, 345–346
Photosensitivity, 395 Pick studies, 289, 343
Physical characteristics and properties Pie crusts, 451
inulin, 45–46 Pig studies
pectin, 138–140 cellulose, 270, 272, 275
polydextrose, 186–190 oat fiber, 250, 255–257, 259
resistant starch, 211 resistant starch, 231–232
Physiochemical properties sugar beet fiber, 375, 378, 381–382
Nutriose soluble fiber, 35–36 Pi-Sunyer, Wursch and, studies, 343
partially hydrolyzed guar gum, 85 Pizza crust, 451
sugar beet fiber, 370–372 Plantago ovata Forsk, 394, see also
Physiological functions and benefits Psyllium
acacia gum, 125–128 Plantago psyllium, 394, see also Psyllium
aleurone flour, 440–451 Plantains (green), 90
alpha-cyclodextrin, 11–13 PMMAs, see Partially methylated alditol
barley fiber, 337–345 acetates (PMAAs)
cellulose functionality, 270–271 Poksay and Schneeman studies, 100
fruit fibers, 433–435 Polydextrose
Nutriose soluble fiber, 28–29 affinity for water, 188–190
oat beta-glucan, 288–297 analysis of, 184
partially hydrolyzed guar gum, baked goods, 194
85–104 beverages, 195
polydextrose, 183–184 blood glucose responses, 179–180
psyllium, 397 blood lipids, 178–180
resistant maltodextrin, 64–72 bowel function, 178
sugar beet fiber, 374–383 chocolate confectionery, 194
Physiological functions and benefits, confectionery items, 193–194
resistant starch (RS) cultured dairy products, 194
available calories, 237 dairy drinks, 195
body composition, 238 energy contribution, 183
colonic cell health, 231 as fiber, 177–180
culture protagonist, 228 food applications, 193–196
digestible carbohydrates comparison, frozen dairy desserts, 194
229 fruit spreads and fruit fillings, 195
digestion, 227–232 fundamentals, 174, 196
energy partitioning, 238–239 glass transition temperature, 186–187
fermentation, 227, 230 manufacture of, 175
fundamentals, 226–227 meat applications, 195
glycemic management, 228, 232, moisture management, 186
234–236 oral health, 183
intestinal environment and function, partially hydrolyzed guar gum
228, 231–232 comparison, 94
nutrient interactions, 232 pasta and noodles, 195
prebiotic benefits, 228, 230–231 pharmaceuticals, 196
satiety hormone production, 238 physical nature, 186–190
tolerance, 228 physiological aspects, 183–184
weight management, 228, 237–239 prebiotic properties, 180–182
490 Index
regulatory status, 196 pectin, 143–144

safety, 184 polydextrose, 180–182
satiety, 183 psyllium, 411
specification, 177 resistant maltodextrin, 65, 67, 68
stability, 109, 191–193 resistant starch, 228, 230–231
structure, 175–177 Pregnancy
sweetness and sweetness alpha-cyclodextrin, 13–14
enhancement, 185 psyllium, 410, 412
technological functionality, 185–193 Pretzels, 252
toleration, 183–184 Prevotella ruminicola, 143–144
Polysaccharides Printing, 81
acacia gum comparison, 124 Probiotics, 52
sugar beet fiber, 365–370, 372–373 Processed cheese, 54, see also Cheese
Pomeranz, Szczodrak and, studies, 329 and cheese products
Ponte, Kulp and, studies, 208 Processing, see Industrial processing
Pork products resistance; Production and
barley fiber, 334 processing
oat fiber, 253–254 Proctor & Gamble, 396
Porridge, 346 Product attributes, resistant starch, 226
Postage stamps, 81 Production and processing
Postmenopausal women, 52 guar gum, 83–85
Postprandial blood glucose level, see inulin, 45
also Glucose metabolism and Nutriose soluble fiber, 21–22
response oat beta-glucan, 285–287
cellulose, 267 oat fiber, 250–252
guar gum, 82 partially hydrolyzed guar gum,
partially hydrolyzed guar gum, 105 83–85
resistant maltodextrin, 69–70, 72 polydextrose, 175
sugar beet fiber, 376 resistant maltodextrin, 63–64
Postprandial effects rice bran, 305–306
alpha-cyclodextrin, 12 sugar beet fiber, 361
oat beta-glucan, 296–297 Pronczuk and Hayes studies, 179
psyllium, 407 Propionate, 91, see also Short-chain fatty
sugar beet fiber, 381 acids (SCFA)
Postprandial glycemic responses, 86–87, Propionic acids, 91, see also Short-chain
see also Glycemic management fatty acids (SCFA)
and response Prosky, Cho and, studies, 2
Postprandial hypertriglyceridemia, 179 Prosky, Lee and, studies, 2
Potatoes, 208 Prosky studies, 208, 223
Potential health claim, 3–4, see also Proteins
Health claims aleurone flour, 439
Pouchitis, 50 cellulose functionality, 270
Powder properties, 35 partially hydrolyzed guar gum, 107
Prebiotic characteristics and effects Proteus spp., 148
acacia gum, 123–125 Protopectin, 136
barley fiber, 337 Psyllium
fruit fiber, 434 acacia gum comparison, 124
Nutriose soluble fiber, 31 anorectal surgery, 410
partially hydrolyzed guar gum, anti-carcinogenic effects, 405–406
94–96 anti-inflammatory effects, 405
Index 491
blocking iron absorption, 103 Ramaswamy studies, 250

characteristics, 393–395 Ranald studies, 9–15
chemical constituents, 395 Randomized studies, 289–293
contraindications, 411 Rashes, 86
diarrhea, 410 Rastall and Gibson studies, 96
diverticular disease, 398–399 Rat studies
drug delivery systems, 410 acacia gum, 124–126, 129
drug interaction, 412 aleurone flour, 442–443
food applications, 395–396 alpha-cyclodextrin, 11–14
functionality, 395–396 barley fiber, 345–346
gallstones, 410 cellulose, 265–266, 269–272, 275–277
glycemic control, 5 inulin, 47–48, 51–52
heart disease risk, 406–409 Nutriose soluble fiber, 29, 32–34
hemorrhoids, 410 oat fiber, 255, 258
hydrocolloid properties, 410 partially hydrolyzed guar gum, 88,
irritable bowel syndrome, 399, 90–91, 100–106
404–405 pectin, 142–147, 150, 154–155
lactation, 412 polydextrose, 178, 181–182
laxative effect, 397–410 psyllium, 407
oat beta-glucan comparison, 293 resistant maltodextrin, 68–71
partially hydrolyzed guar gum resistant starch, 231–232, 236, 238
comparison, 94, 100, 103 rice bran, 312–313
pectin comparison, 150–151 sugar beet fiber, 375, 381–383
physiological benefits, 397 Rautonen, Nina, 197
Plantago ovata Forsk, 394 RBO, see Rice bran oil (RBO)
Plantago psyllium, 394 Read, Tomlin and, studies, 178
pregnancy, 410, 412 Ready-to-drink beverages, 216
resistant starch, 232 Ready-to-eat cereals
safety, 410–412 barley fiber, 330
summary of, 400–403 oat beta-glucan, 289
toxicity, 410–412 psyllium, 396
Pylkas studies, 94 sugar beet fiber, 373
Pyroconversion, 21 Recommended intake, vii
Reformed meat products, 189, 195, see
Q also Meat and meat products
Regulation
QualFlo, 456–457 Nutriose soluble fiber, 37
Quinde studies, 336 partially hydrolyzed guar gum,
108–109
polydextrose, 196
R Renal issues, see also Kidneys
Rabbani studies, 90 acacia gum, 126
Rabbit studies oat fiber, 250, 259
alpha-cyclodextrin, 13 partially hydrolyzed guar gum, 105
rice bran, 313 psyllium, 395
Raghupathy studies, 232 Renard and Thibault studies, 363
Raghuram studies, 315 Renard studies, 359–383
Ralet studies, 359–383 Resistant dextrin, 109, see also Nutriose
Ramakrishna studies, 232 soluble fiber
492 Index
Resistant maltodextrin, see also types, 206–207

Fibersol-2 resistant weight management, 228, 237–239
maltodextrin; Nutriose soluble Reynolds number, 272–276
fiber Rhazes studies, 396
glycemic control, 5 Rheumatism, 396
suppliers, 462–463 Rice
Resistant starch (RS) barley similarity, 329
alpha-cyclodextrin comparison, 10 brown, cooking time, 316
analysis, 216–217, 222–223 partially hydrolyzed guar gum,
available calories, 237 98–99
background, 206 pectin, 149
barley fiber, 329 resistant starch, 208
body composition, 238 Rice bran
chemically modified starch, 210, 216 bile acid binding, 316
chemistry, 206 chick studies, 313–314
classification, 206–208 cholesterol, 309–315
colonic cell health, 231 composition, 307–308
commercial developments and cynomolgus monkey studies, 313
applications, 209–210, 216 food applications, 308
culture protagonist, 228 fundamentals, 316–318
detection methods, 220–221 hamster studies, 309–312
diet and food, 208–209 human studies, 314–315
digestion, 227–232 market potential, 316
energy partitioning, 238–239 oat beta-glucan comparison, 289, 297
fermentation, 227, 230 physiological benefits, 309–315
food applications, 224 production, 305–306
functional properties, 224 rabbit studies, 313
fundamentals, 226–227, 239 rat studies, 312–313
glycemic control, 5 safety, 309
glycemic management, 228, 232, whole grain recommendation, 316
234–236 Rice bran oil (RBO)
health benefits, 226–236 cholesterol, 311, 312–313
high-moisture systems, 224 substituting cooking oil, 315
intestinal environment and function, Rice milk, 293, 308
228, 231–232 Rinaldi, Josephine, 452
low-moisture systems, 224 Ripsin studies, 288
non-traditional form, 210, 216, Roberfroid, Gibson and, studies, 180
218–219 Roberfroid studies, 34, 47
nutrient interactions, 232 Robertson studies, 227, 234, 333, 337
physical comparisons, natural Rochat studies, 125
commercial, 211 Roland studies, 258
prebiotic benefits, 228, 230–231 Rolls studies, 183
product attributes, 226 Rombeau, Palacio and, studies, 102
RS vs. digestible carbohydrates, 229 Romero studies, 289
satiety hormone production, 238 Rong studies, 312
soluble dextrins, 210, 216 Rose studies, 98
sources, commercial, 212–215 Roturier studies, 19–37
suppliers, 463–464 Royle, Peter, 452
tolerance, 228 Ruminococcus albus, 265
traditional forms, 212–215 Rushdi studies, 93
Index 493
Rye and rye products viscous dietary fiber, 20

barley fiber comparison, 347 Sato, Suzuki and, studies, 12
oat beta-glucan, 296 Sauces
sugar beet fiber comparison, 382 cellulose, 271
fruit fiber, 431
guar gum, 81
S inulin, 46, 54
Saccharomyces cerevisiae, 36 partially hydrolyzed guar gum,
Safety issues and applications 109–110
acacia gum, 122–123 pectin, 159
aleurone flour, 451 Sausages
alpha-cyclodextrin, 13–14 barley fiber, 334
barley fiber, 346–347 fruit fiber, 431
inulin, 54
cellulose, 277
polydextrose, 195
oat beta-glucan, 297–298
SCFA, see Short-chain fatty acids (SCFA)
Scherer, Ben, 452
104–107
Schneeman, Poksay and, studies, 100
polydextrose, 184
Scholz and Ahrens studies, 102
psyllium, 410–412
Schwab studies, 179
resistant maltodextrin, 72, 74
Schwarz, Lee and, studies, 330
rice bran, 309
Seaweed extracts, 81
Segmentation, 276
Sajilata studies, 206–207
Seib and Woo studies, 208
Saku studies, 178 Sellman, Greenberg and, studies, 84
Salad dressing, 432, see also Dressings Sensitization, see Adverse effects
Salisbury, Carolyn, 452 Sepsis and septic shock, 93
Salmonella spp. Serum lipids, 257, see also Lipid
inulin, 49 metabolism
pectin, 148 Shah studies, 100
Salmonella typhimurium Shamai studies, 208
inulin, 50 Shand studies, 334
partially hydrolyzed guar gum, Shao, Yokoyama and, studies, 344
105–106 Shi and Trzasko studies, 210
Salty goods, 36 Shigella spp.
Salyers studies, 94 inulin, 49
Sandstrom studies, 346 pectin, 148
Saniez-Degrave studies, 19–37 Shimomura studies, 180
Sarkkinen studies, 283–298 Shinnick studies, 328
Satiety, see also Appetite modulation Shi studies, 210
guar gum, 82 Short bowel syndrome, 148
inulin, 52 Short-chain fatty acids (SCFA), see also
partially hydrolyzed guar gum, Prebiotic characteristics and
100–101 effects
polydextrose, 183 acacia gum, 124
potential structure function claims, aleurone flour, 443
4–5 alpha-cyclodextrin, 11
psyllium, 397 cellulose, 265, 269
resistant starch, 238 guar gum, 82
494 Index
inulin, 47 alpha-cyclodextrin, 11
Nutriose soluble fiber, 27, 32, 34, 35 oat beta-glucan, 293
oat fiber, 258 Soy fiber, 465
partially hydrolyzed guar gum, 87, Spaghetti, 332
90, 91, 94 Spapen studies, 93
pectin, 142–143, 147 Speakers, electronic, 272
polydextrose, 178–179 Specifications, 177
psyllium, 398, 405–406 Spina bifida, 443
resistant maltodextrin, 67–68, 68 Sponsors, 455
resistant starch, 227, 236 Sports drinks, 129, see also Beverages
sugar beet fiber, 375, 381–382 Spreads and spreadable products
Shortcrust pastry, 189–191, see also inulin, 46, 54
Pastries pectin, 157, 159
Short gut syndrome, 148 Stability
Siddhuraju and Becker studies, 209 barley fiber, 334
Skin gums, 81
partially hydrolyzed guar gum, 86, inulin, 46, 54, 109
103 partially hydrolyzed guar gum,
psyllium, 396 109–110
Slimy products, 287 pectin, 159
Snack foods polydextrose, 109, 191–193
acacia gum, 130 psyllium, 396
barley fiber, 336 resistant dextrin, 109
oat beta-glucan, 286 sugar beet fiber, 372
resistant starch, 209 Staphylococcus aureus, 230
sugar beet fiber, 373 Starch replacement, 54
Snart studies, 345 Steatosis, 48
Softness, 36 Steenblock studies, 253
Soluble cellulose, 456 Stenvert, Nick, 452
Soluble dextrins, 210, 216 Step 1 diet (AHA), 89
Soluble fibers Stephen studies, 255
acacia gum, 121–131 Sterilization, 20, 35
alpha-cyclodextrin, 9–15 Stevia, 75
inulin, 41–55 Stickiness, 131
Nutriose, 19–37 Stool bulk
partially hydrolyzed guar gum, alpha-cyclodextrin, 11
79–112 inulin, 48–49
pectin, 135–159 Stool consistency
polydextrose, 173–196 acacia gum, 126
resistant maltodextrin, 61–75 partially hydrolyzed guar gum,
Sorbet, 158–159 90–91
Soups psyllium, 398
barley fiber, 329, 335, 346 Stool frequency
inulin, 54 cellulose, 264
Nutriose soluble fiber, 37 inulin, 48–49
oat beta-glucan, 287 partially hydrolyzed guar gum,
partially hydrolyzed guar gum, 109 91–92
psyllium, 396 polydextrose, 178
sugar beet fiber, 373 psyllium, 398, 399
Soya milk Stool incontinence, 126
Index 495
Stool output, see also Intestinal food applications, 372–374

regularity functionality, 372–374
cellulose functionality, 264–265 fundamentals, 360–361, 383
inulin, 48–49 glucose metabolism, 376–378
partially hydrolyzed guar gum, 94 hemicelluloses, 369
sugar beet fiber, 375–376 hydration properties, 370–371
Stool softening lipid metabolism, 378–381
inulin, 53–54 meat products, 374
partially hydrolyzed guar gum, 105 mineral adsorption, 376
polydextrose, 178 molar mass, 368–369
sugar beet fiber, 375 non-sugar substituents, 367–368
Stool straining, 399 pectin structure, 365–369
Stool transit time physiochemical properties, 370–372
cellulose, 264–265 physiological benefits, 374–383
oat fiber, 255–256 production, 361
partially hydrolyzed guar gum, safety, 383
90–91 side chains, 367
polydextrose, 178 stool output, 375–376
psyllium, 398 structure of polysaccharides, 365–370
sugar beet fiber, 378 tolerance, 382–383
Stool weight toxicity, 383
cellulose, 264 transit time, 375–376
inulin, 48–49 whole fiber, 373–374
oat fiber, 255–256 Sugar cane fiber, 465
partially hydrolyzed guar gum, Sugar metabolism, see Glucose
90–91 metabolism and response
psyllium, 399 Sugar(s)-free food products
resistant starch, 227 acacia gum, 128, 130
Stowell studies, 173–196 claims, 37
Strauss studies, 51 Nutriose soluble fiber, 37
Streptococcus spp., 230 polydextrose, 175, 196
Streptococcus bovis, 144 Sundberg and Falk studies, 329
Streptococcus iniae, 345 SunFiber, 461–462, see also Partially
Strontium, 146–147 hydrolyzed guar gum (PHGG)
Stumm and Baltes studies, 175 Sunitha studies, 313
Sucralose, 75 Sunvold studies, 255–257
Sugar beet fiber Suppliers
adsorption/binding of ions/organic acacia gum, 458
molecules, 372 aleurone flour, 455–456
backbone, 365, 367 alpha—cyclodextrin, 455
bakery products, 374 bamboo fiber, 465
cellulose, 369–370 cellulose, 456–457
cereals, 373 corn bran, 457
characteristics, 361–372 cottonseed fiber, 465
colorectal cancer, 381–382 Fibersol-2, 462–463
composition, 362–364 fructo-oligosaccharides, 458–460
digestability, 374–375 gum arabic, 458
extracted polysaccharides, 372–373 hydroxymethylpropul cellulose, 456
extraction, 368–369 inulin, 458–460
fermentability, 374–375 Nutriose soluble fiber, 462–463
496 Index
oat beta glucan, 460 Tea, 11

oat fiber, 460–461 Teacakes, 286
partially hydrolyzed guar gum, Technology
461–462 cellulose, 277
pectin, 462 Nutriose soluble fiber, 35–36
resistant maltodextrin, 462–463 polydextrose, 185–193
resistant starch, 463–464 Temelli studies, 328, 335
soluble cellulose, 456 Temperatures
soy fiber, 465 acacia gum, 129
sugar beet fiber, 464 alpha-cyclodextrin, 10
sugar cane fiber, 465 barley fiber, 330
Surimi, 195 Nutriose soluble fiber, 20
Suspension, 396 pectin, 140
Suzuki and Hara studies, 88, 105 polydextrose, 192–193
Suzuki and Sato studies, 12 Textiles, 81
Svihus, Hetland and, studies, 255–257 Texture
Sweetness and sweet products barley fiber, 334
alpha-cyclodextrin, 11 cellulose, 271
inulin, 45 inulin, 54
Nutriose soluble fiber, 36 oat fiber, 251
polydextrose, 185 partially hydrolyzed guar gum, 109
Symons and Brennan studies, 334 pectin, 156
Synergy 1 Tg, see Glass transition temperature (Tg)
cancer risk reduction, 52 Thibault, Renard and, studies, 363
fundamentals, 45 Thibault studies, 359–383
gut microflora modulation, 49 Thickeners
guar gum, 81
mineral absorption, 52–53
oat beta-glucan, 287
ulcerative colitis, 50
psyllium, 396
Szczodrak and Pomeranz studies, 329
Thomsen studies, 250, 259
Thorup studies, 381
T Tiihonen, Kirsti, 197
Timing of medications, 412
Table spreads, 46, 54, see also Spreads Tissue damage, 127
and spreadable products Titgemeyer studies, 258
Tablet binders Toden studies, 231
acacia gum, 131 Tokunaga and Matsuoka studies, 69
pectin, 159 Tolerance, see also Digestion
polydextrose, 196 acacia gum, 123
Takahashi studies Nutriose soluble fiber, 25, 27–28
cellulose, 263–277 polydextrose, 183–184
partially hydrolyzed guar gum, 88, resistant starch, 228
92, 95, 100, 103, 106 sugar beet fiber, 382–383
Takeno studies, 88, 90 Tomato sauces, 159
Tapola studies, 283–298 Tomlin and Read studies, 178
Tappy studies, 296 Tooth-friendly properties, 183
Tartness, 109 Topping, Annison and, studies, 206, 208
Taste Topping studies, 329, 439–452
inulin, 54 Tortillas
Nutriose soluble fiber, 36–37 barley fiber, 333, 336
Index 497
resistant starch, 208 Tube-feeding formulas, see Enteral

Total dietary fiber (TDF) nutrition formula and feeding
barley fiber, 330, 333–334 Tuohy studies, 95
maltodextrin, 23
measuring method, 75
rice bran, 307, 309, 311, 312 U
Tovar studies, 207 Udon noodles, 332
Toxicity Ulcerative colitis, 50
aleurone flour, 451 Urea
alpha-cyclodextrin, 13–14 acacia gum, 126
barley fiber, 346–347 oat fiber, 250, 259
partially hydrolyzed guar gum, 100, Uremia, 395
104–107 Urine
psyllium, 410–412 acacia gum, 126
sugar beet fiber, 383 pectin, 141
Toxic metals excretion, 145–147 Uronic acids, 141
Traditional resistant starch, 212–215 Usher, Sylvia, 452
Tragacanth gum, 81
Transit time
cellulose, 264–265 V
dietary fiber, 5 Vahouny Fiber Symposium, x
oat fiber, 255–256 Valine, 313
partially hydrolyzed guar gum, Vasankari and Ahotupa studies, 179
90–91 Vasanthan, Jiang and, studies, 326
polydextrose, 178 Vasanthan and Bhatty studies, 329
psyllium, 398 Vegetables and vegetable juices
sugar beet fiber, 375–376, 378 Nutriose soluble fiber, 35
Treponema saccharophilum, 143 recommended daily amounts,
Triacylglycerides, 96 433–434
Trichuris suis, 259 Veillnella spp., 49
Triglyceride levels, see also Cholesterol; Velazquez studies, 94
Lipid metabolism Vis and Lorenz studies, 336
alpha-cyclodextrin, 13 Viscosity
barley fiber, 338 acacia gum, 128
inulin, 47–48 alpha-cyclodextrin, 10
partially hydrolyzed guar gum, 88 barley fiber, 335
pectin, 150 guar gum, 82
polydextrose, 178–179 inulin, 46
resistant maltodextrin, 70–71 oat beta-glucan, 284–285, 298
Trimble, Rodney, 452 partially hydrolyzed guar gum,
Trinidad studies, 98 99–100
Trogh studies, 333 pectin, 151, 156
Trowell, Burkitt and, studies, 1–2 psyllium, 396
Trowell studies, 427 Vitacel Oat Fibers, 288, 460–461
Trowel studies, 409 Vitamins
Tryptophan, 313 aleurone flour, 439
Trzasko, Shi and, studies, 210 alpha-cyclodextrin, 11
Tsai, Liu and, studies, 178 barley fiber, 346–347
Tsuda studies, 86 partially hydrolyzed guar gum, 107
498 Index
psyllium, 411 Wils studies, 19–37

Wise and Heyl studies, 51
Wisker studies, 346
W Wolf studies, 208
Waalkens-Berendsen studies, 13 Woo, Seib and, studies, 208
Wang and Gibson studies, 182 Wood studies, 286, 296, 343
Wang studies, 230–231, 255–256 Woo studies, 210
Watanabe studies, 102 Wounds, 395
Water absorption, intestines, 269–270, Wursch and Pi-Sunyer studies,
see also Hydration 343
Water binding property, 429–430
Wattle blossom model, 122
Weaver studies, 108
X
Weber studies, 347 Xerophthalmia, 395
Weibel and Myers studies, 370 Xylitol, 183
Weibel studies, 370 Xylooligosaccharides, 124
Weickert studies, 250, 254
Weight management and control, see
also Body weight Y
alpha-cyclodextrin, 12–13
Yacon, 43
oat fiber, 256
Yamada studies, 88, 101
Yamatoya studies, 87, 89, 92, 98
100–101
Yeast fermentation, 129
pectin, 144–145
Yeast-leavened bread, 287
potential structure function claims,
Yogurt, see also Dairy products
4–5
barley fiber, 335
resistant starch, 228, 237–239
inulin, 54
Wells studies, 107–108
Wenger, Beringer and, studies, 51
oat fiber, 250, 254
Wheat, 37
partially hydrolyzed guar gum, 89,
Wheat bran
109
acacia gum, 124
pectin, 158
aleurone flour comparison, 444
polydextrose, 194
barley fiber comparison, 347
intestinal regularity, 5 psyllium, 396
oat beta-glucan comparison, 289, 293, sugar beet fiber, 372
297 Yokoyama and Shao studies, 344
oat fiber comparison, 249, 258 Yokoyama studies, 343
resistant starch, 232 York studies, 175
rice bran comparison, 312 Younes studies, 250, 258
water-binding properties, 430 Yu studies, 257
Wheat fiber, 430
Whipped cream Z
cellulose, 271
partially hydrolyzed guar gum, 110 Zarling studies, 253, 255–256
Whole fiber, 373–374 Zervas and Zijlstra studies, 256, 259
Whole grain recommendation, 316 Zhang studies, 1, 345
Williams studies, 1 Zheng studies, 335
Index 499
Zhou studies, 238, 442 cellulose, 277

Ziai studies, 393–412 oat beta-glucan, 298
Zijlstra, Zervas and, studies, 256, 259 partially hydrolyzed guar gum
Zinc comparison, 103
aleurone flour, 439 pectin, 145–147
barley fiber, 346–347 sugar beet fiber, 376

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FIBER

Boca Raton London New York

CRC Press is an imprint of the

© 2009 by Taylor and Francis Group, LLC

No claim to original U.S. Government works

Printed in the United States of America on acid-free paper

International Standard Book Number: 978-1-4200-4384-6 (Hardback)

Library of Congress Cataloging‑in‑Publication Data

Visit the Taylor & Francis Web site at

and the CRC Press Web site at

1 Functional and Dietary Fibers: An Introduction........................... 1

Section I Soluble Fibers

3 Nutriose ® Soluble Fiber............................................................... 19

5 Fibersol® -2 Resistant Maltodextrin: Functional Dietary

6 Partially Hydrolyzed Guar Gum Dietary Fiber............................ 79

7 Acacia Gum...................................................................................... 121

Section II Resistant Starch

10 Resistant Starch (RS)...................................................................... 205

Section III Conventional Fibers

11 Oat Fiber from Oat Hull................................................................. 249

13 Oat β-Glucan.................................................................................... 283

14 Rice Bran: Production, Composition, Functionality

15 Barley Fiber...................................................................................... 323

16 Sugar Beet Fiber: Production, Characteristics, Food

Section IV New Development

18 Fruit Fibers....................................................................................... 427

19 Aleurone Flour: A Novel Wheat Ingredient Rich in

Appendix: Suppliers of Dietary Fiber Ingredients............................. 455

Susan Cho, Ph.D., M.B.A., is the President of NutraSource, a nutrition and

Priscilla Samuel, Ph.D., is Director of Nutrition Sciences, Scientific & Reg-

Anne Birkett Christine E. Fastnaught

Jon Bodner Michael Fenech

Sebastien Baray Jürgen Fischer

Jonathan David Buckley Anne Franck

Peter Clifton Chieko Hashizume

Hans Ulrich Endress Peter Howe

Lekh R. Juneja Kazuhiro Okuma

Talwinder S. Kahlon Marie-Christine Ralet

Mahendra P. Kapoor Catherine Renard

Julian D. Stowell David Topping

Dietary Fiber Intake Levels around the World

day (Cho et al. unpublished data). Approximately 75% of Americans do not

What Is Dietary Fiber?

Approved Health Claims

Potential Health Claim

Potential Structure Function Claims

High-Fiber Foods/High-Fiber, Low-Fat Foods and Glycemic Control

Dietary Fiber and Intestinal Regularity

Jonathan David Buckley, Alison Mary Coates,

As a result of α-CD’s chemical structure (i.e., α-glucan), combined with its

large intestine mean that it is by definition a form of soluble, fermentable,

Functionality and Food Applications

Area under Plasma Glucose Curve

as well as dogs [49], with no evidence of any maternal toxicity, fetotoxicity,

Catherine Lefranc-Millot, Daniel Wils, Jean-Michel Roturier,

• A decrease of the colon pH, limiting the growth of potentially harm-

As soluble dietary fibers are fermented in the colon, particular attention

The particular profile of NUTRIOSE® confers to this dietary fiber an out-

Production and Description

Dietary Fiber Content

CH2OH CH2OH CH2OH

In 2001, an enzymatic-gravimetric-HPLC method was proposed to the

105 104 103

105 104 103