Resistant Starch and Health

A Evans, Tate and Lyle, Hoffman Estates, IL, USA

2015 Elsevier Inc. All rights reserved.

Topic Highlights

What is resistant starch?

Resistant starch intake; measurement and consumption
Effect of resistant starch intake on gut health
Metabolic effects of resistant starch intake

Learning Objectives

To get a basic understanding of what resistant starch is and

where it is found
To learn about how its consumption has been linked to a
variety of potential beneficial health outcomes in the area
of gut health and various metabolic effects such as blood
glucose, insulin, and lipid levels

What Is Resistant Starch?

Starch is the major source of carbohydrates in the human diet.
Starch is present in many different fruits, vegetables, roots, and
grains. Starch and starch derivatives are a nutritive, abundant,
and economical food source. Starch can be consumed unprocessed in the form of raw fruits and vegetables or in the form of
more shelf-stable processed foods. Food starches contribute to
the characteristic viscosity, texture, mouthfeel, and consistency
of many food products.
In the human body, starch is digested by a-amylases. First,
salivary a-amylase in the mouth catalyzes the hydrolysis of
amylose to maltose, maltotriose, and maltotetraose and the
hydrolysis of amylopectin to the same products plus two
a-limit dextrins. The partially digested starch then passes into
the stomach. After some resident time in the low pH environment of the stomach, the partially hydrolyzed starch then
passes into the small intestine where it is neutralized. The
majority of hydrolysis of the starch is then accomplished by
pancreatic a-amylase that is secreted from the pancreatic duct
via a multiple attack mechanism. a-Amylases hydrolyze the
starch into small mono-, di-, and oligosaccharides that then
need to be further broken down to be absorbed as glucose. Two
other enzymes are necessary to convert the hydrolysis products
of the a-amylases into glucose, which can be actively transported across the small intestine membrane. These two
enzymes are the brush-border glucogenic enzymes maltase
glucoamylase and sucraseisomaltase. The resulting D-glucose
is then actively transported across the luminal membrane of
the small intestine and passes into the blood via the sodium
glucose cotransporter, which is located at the luminal surface
of enterocytes.
Several factors influence the rate and extent of starch digestion. The main hydrolysis of starch is performed by the
a-amylases. Starch digestion by a-amylases requires a series of

Encyclopedia of Food Grains

steps. First, the enzymes diffuse into the starch matrix of the
food. In the second step, the enzymes bind to the substrate,
and finally, the enzymes cleave the a-1,4-glycosidic linkages of
the substrate (starch). The structure of the food matrix and the
structure of the starch itself influence the kinetics of the amylase hydrolysis.
Resistant starch (RS) has been defined as the starch and
products of starch digestion that are not absorbed in the small
intestine of healthy individuals. Based on the source of the
enzyme resistance, RS has been classified into five different
types (Table 1).
In type 2, type 3, and type 5 RS, the enzyme resistance is due
to the physical structure of the starch molecules. Type 2 RS is
found in raw starch granules and the enzyme resistance is due
to the natural organization of the starch within the starch
granules. Significant amounts of type 2 RS can be found in
green banana, potato, and high-amylose maize.
In type 3 RS, the enzyme resistance is due to the physical
structure of starch chains that have undergone some type of
restructuring due to retrogradation or heat treatment. Different
factors, such as amylose/amylopectin ratio, chain length, lipid
content, and processing conditions, have been shown to influence the amount and quality of type 3 RS. Annealing and heat
moisture treatment are two types of heat treatments that are
often used to create RS. Both of these treatments, as well as
gelatinization, either fully or partially melt crystalline structure
present in the native starch granules. After heat treatment, linear
amylose molecules and linear regions of amylopectin molecules
can organize into a mix of amorphous and crystalline areas with
varying degrees of enzyme resistance. Formation of the crystalline structures usually takes place above the glass transition
temperature and below the melting temperature, and any components present that influence the glass transition temperature
can therefore be expected to influence the formation (yield and
quality) of the formed type 3 RS. The amylose content of starch
has been positively correlated with RS yield and the formation
of type 3 RS is strongly related to the crystallization of amylose.
The amount of RS formed is also dependent on the water
content and temperature used during the heat treatment.
Water does act as a plasticizer in the system and a minimum
water content is necessary to achieve the chain mobility needed
to form crystalline structure resistant to enzyme digestion. At
high-starch concentrations, the starch chains interact more easily, leading to increased crystal and RS formation. The presence
of lipids has been shown to decrease the formation of type 3 RS
due to formation of amyloselipid complexes (type 5 RS).
The enzyme resistance in type 5 RS is due to the molecular
structure of amyloselipid complexes that can be either present in
the native starch or formed by controlled reactions using nongranular starch and lipids to form the resistant amyloselipid
complex.
The enzyme resistance in type 4 RS is due to chemical
modification of the starch. Chemical modification of

http://dx.doi.org/10.1016/B978-0-12-394437-5.00097-8

CARBOHYDRATES | Resistant Starch and Health

Classification of resistant starch (RS)

Table 1
RS
type

Source of enzyme resistance

Examples

1
2

Whole grains
Raw starch granule structure

Structures formed on
reassociation or retrogradation
of starch after heat treatment
Chemical modifications of the
starch
Starch lipid complex

Seeds, grains
Green banana, high
amylose, potato
Cooked pasta, cooked
potato

4
5

Modified starch
Amylose-containing starch

starch creates chain irregularities or branches in the starch

chains. Cross-linking of starch covalently links two starch
chains together, in effect creating a branch point on both
chains. Chemical substitution introduces a bulky side group
to the starch chains. The introduction of these chemical groups
may create a steric hindrance to one or more human digestive
enzymes.

RS Intake
Quantification of RS
To determine the effect of RS intake on health, it is important
to determine the amount of RS consumed as accurately as
possible. Ideally, RS consumption would be determined
in vivo by quantification of undigested starch in healthy individuals. This is, however, very difficult to do. Several in vivo
approaches have been used for measurement of RS. These
in vivo methods include the hydrogen breath test, direct collection of ileal effluent from ileostomy patients, and direct collection of the ileal effluent from healthy subjects using a long
triple lumen tube.
The measurement of hydrogen breath to determine the
amount of RS in a diet is based on the concept of fermentation
of dietary fibers including RS. When RS enters the colon, it may
be fermented by the colon microbiota that leads to the production of short-chain fatty acids (SCFAs) (acetate, butyrate,
and propionate) and gases like hydrogen (methane and carbon
dioxide). Most of the gases produced by colonic fermentation
are absorbed into the circulation, but about 10% is present in
the breath on exhalation. Since hydrogen breath is not specific
for only RS fermentation, but does indeed measure fermentation from any dietary fiber source, care has to be taken when
interpreting these results for RS content in a food/diet.
Direct collection of ileal effluents would be expected to give
more accurate results than hydrogen breath measurement
especially when different forms of dietary fibers and RS may
be present in a diet. Analysis of the ileal effluent allows for
quantification of undigested carbohydrate and potential identification of the different sources of dietary fiber within the
effluent. Most ileostomy models are, however, based on the
use of patients that had their colon removed due to health
issues and their digestive patterns may therefore not be representative of a healthy population. Analysis of ileal effluent
from healthy individuals should provide the most accurate

data, but these measurements are difficult and intrusive and

can therefore not be done on large scales.
It is generally accepted that any in vitro method used to
measure RS should give values in line with those obtained
with ileostomy patients. In 1986, Berry developed a new
in vitro method by modification of a method previously developed by Englyst, Wiggins, and Cummings in 1982. This modified method was subsequently confirmed to give results in line
with healthy ileostomy subjects. In 1992, Englyst developed a
method that could measure rapidly digestible starch (RDS),
slowly digestible starch (SDS), and RS. This method employed
incubation of the samples at 37  C with pancreatic amylase
and amyloglucosidase and measures the amount of RS by
subtracting the sum of RDS and SDS from the total starch
present in the sample. Several new methods for the measurement of RS were developed during the European Research
Program EURESTA. Even though many different methods
were developed during the 1990s for the measurement of RS,
none of these methods were successfully subjected to interlaboratory evaluation to be adopted as an official AOAC method
of analysis. In 2002, McCleary and Managhan developed a new
RS method by modifying existing methods to obtain a method
that would yield robust, reproducible results that correlated
with results from ileostomy patients. This method underwent
interlaboratory evaluation and was later adopted as AOAC
Official Method 2002.02. An Integrated method for the measurement of total dietary fiber was later developed and was
published in 2007. This method allows the accurate measurement of all dietary fibers including RS. The enzymatic incubation step uses pancreatic a-amylase and more closely simulates
digestion in the human digestive tract and yields RS values in
line with those obtained with AOAC Official Method 2002.02
and with results from ileostomy patients. This method was
accepted as AOAC Method 2009.01.

Sources of RS and Intake Levels

Of all unprocessed foods, the green banana has the highest RS
content of between 47% and 57%. While flour can be prepared
from green bananas and incorporated into different foods as a
source of RS, it is important to keep in mind that food processing methods such as cooking may gelatinize the starch granules and destroy the structures responsible for the enzyme
resistance originally present and responsible for RS formation.
Raw potato starch is also high in RS, but since raw potato starch
is seldom consumed, it is not a good source of RS. However,
cooling of cooked potatoes or potato products can lead to
retrogradation of the starch and may lead to formation of
new RS (type 3) if the right conditions (heat, moisture, time,
and starch concentration) are met. The level of RS in different
legumes can vary widely and RS content in the legumes as
consumed depends on processing and legume variety.
Murphy et al. examined the RS intake in the United States
by comparing reported RS contents of different foods with
dietary recall records from participants in the 19992002
National Health and Nutrition Examination Survey. They
showed that the RS concentration varies greatly, even within
the same food category. This could be due to natural differences (cultivar), differences in food preparation methods, and
also differences in analytic methods used to determine the

CARBOHYDRATES | Resistant Starch and Health

amount of RS present. The RS content of different breads varied

between 0.1% in wheat rolls and 4.5% in pumpernickel bread.
Ready-to-eat breakfast levels contained between 0% (rice
cereal) and 6.2% (puffed wheat) of RS and cookies/crackers
had between 0.2% (oatmeal) and 2.8% (crackers and crisp
bread) of RS. The category of cooked cereal and pastas had
the widest range of RS contents between 0.4% (noodles and
chow mein) and 11.3% (oats and rolled uncooked). Within
the vegetable category, the lowest RS content was shown for
sweet corn (cooked/canned) and potatoes (slow-cooked) with
0.3% while the highest content was observed for fried potatoes
with 2.8%. In the legume category, RS content ranged from
0.6% for chickpeas (cooked/canned) to 4.2% for white beans
(cooked/canned).
Comparison of the RS content of different foods and the
food intake records showed that Americans on average consumed an estimated 38 g of RS per day. In Europe, the intake
of RS has been estimated to be between 3 and 6 g per day while
the intake in developing countries has been estimated to be
between 30 and 40 g per day.

Health Benefits of RS
Gut Health
By definition, RS escapes digestion in the human small intestine. RS therefore passes into the colon where like other dietary
fibers, it may be fermented. Fermentation of carbohydrates in
the colon leads to the production of SCFAs. SCFAs are the
metabolic products of anaerobic bacterial fermentation and
consist of butyrate, propionate, and acetate.
The SCFAs produced by bacterial fermentation in the
human gut are the preferred fuel for the cells lining the colon
(colonocytes) and have been shown to lower luminal pH,
increase the excretion of bile acids, and help prevent the development of abnormal colonic cells. A lower pH has been associated with protection against colorectal cancer and has been
shown to inhibit the conversion of primary to secondary bile
acids. Secondary bile acids are thought to promote tumors as
they are cytotoxic to colonic cells. It is therefore reasonable to
assume that RS may confer health benefits to gut health by
production of SCFA, which in turn have a positive effect on pH
and reduced production of secondary bile acids. A low pH has
also been found to suppress the growth of potentially pathogenic organisms and reduce the absorption of toxic compounds (such as ammonia).
Individual SCFAs have also been shown to have more specific actions in the colon. Most RS is readily fermented into
SCFA and many are a good source of butyrate. Butyrate is a
preferred energy source for colonocytes and helps drive the
uptake of electrolytes and water. Intake of butyrate producing
RS as part of oral rehydration solutions has been shown to
significantly reduce the recovery time for children with watery
diarrhea. Butyrate has also been shown to help maintain barrier function in the gut by enhancing mucin production. The
barrier function is important to reduce bacterial translocation,
which may be a key element in the development of diseases
such as inflammatory bowel disease (IBD). Intake of RS has
been suggested to be beneficial for the reduction of IBD.

Butyrate has been shown to induce apoptosis, decreasing

the risk of cancer development. Animal studies have shown
that an increased supply of butyrate to the large bowel
decreases the induction of large bowel tumors in rats. However, despite the fact that the data strongly suggest the link
between butyrate and reduced risk of colonic cancer, studies
examining the link between RS intake and colonic cancer have
not been able to prove such a relationship. One reason for this
may be the importance of RS intake levels. Studies examining
the butyrate production from RS intake have shown significant
increase in fecal butyrate when 22 g of RS was consumed per
day, but no changes in butyrate or pH levels were observed
when 12.5 g of RS was consumed per day. The level of butyrate
produced may also depend on the type of RS consumed.
Another aspect of gut health often linked to dietary fibers is
laxation and fecal bulk. An increase of fecal bulk is thought to
be beneficial and is often reported as a potential health benefit
of different dietary fibers. Increases in fecal mass are important
for relief of constipation and prevention of diverticulosis and
other disorders such as hemorrhoids. The effect of RS on fecal
bulk has been studied and an increase of fecal output was
reported from different studies. Phillips et al. reported an
average increase in fecal output of 42% and also showed that
the fecal output increased with increased RS intake. This
increase fecal output could be due to increased water in the
fecal material, undigested and unfermented starch and dietary
fibers, or possible bacteria from the digestive tract. Increased
fecal nitrogen was observed in diets high in RS indicating either
an increase in bacterial mass or protein excretion.

Metabolic Effects
Several studies have shown that replacement of digestible carbohydrate with RS leads to a reduced blood glucose response.
This has formed the basis for approval of a European Food
Safety Authority (EFSA) claim for RS (EFSA, ID 681, April
2011). While this claim was granted, there was insufficient
evidence for the effects of RS when the glycemic load (amount
of digestible carbohydrate) remains constant. In 2012,
Robertson reviewed several studies on the effect of RS addition
to the diet when the available carbohydrate load was held
constant and noted a significant inconsistency between the
studies reviewed. While some found no effect of RS on glycemia and significant reduction in insulin secretion, others
found the opposite, that is, a reduction in glycemia and an
elevation in postprandial insulinemia. The difference in these
results could be due to differences in the RS tested or simply be
due to the difficult relationship between glucose absorption,
clearance, and hepatic release, which makes accurate measurements and conclusions difficult. Another important factor to
consider is the sources of RS used in different studies. RS can
come from foods such as beans, high-amylose corn starch, or
potatoes, and these foods all have different physiochemical
properties that can affect the response to RS ingestion. The fat
content of the diets is also important as fat is known to have a
significant impact on the glycemic response to a meal. A careful
review of studies with appropriate fat and protein levels
showed that RS consumption does indeed lead to a small
decrease in postprandial glycemia and a larger attenuation of
postprandial insulinemia. These acute changes in plasma

CARBOHYDRATES | Resistant Starch and Health

glucose and insulin concentrations caused by the addition of

RS to the diet could have important metabolic implications.
Both hyperglycemia and hyperinsulinemia are affected in the
development of insulin resistance. Increases in plasma glucose
concentrations have been linked to increased concentrations of
free fatty acids. Glucose uptake in the muscles and increased
glucose uptake in the adipose tissue have been linked to
hyperinsulinemia.
The potential chronic effects of RS intake on metabolism
and associated diseases are even more interesting than the
acute effects discussed earlier. There are animal data showing
a significant relationship of RS inclusion in the diet and
improved insulin sensitivity. Decreased insulin sensitivity, or
insulin resistance, has severe metabolic consequences as it is
strongly associated with several diseases known as metabolic
syndrome. Metabolic syndrome describes diseases such as type
2 diabetes, obesity, coronary heart disease, hypertension, and
dyslipidemia.
Even if RS only leads to reduction in blood glucose
response when digestible carbohydrates are replaced, such an
effect may have significant benefits to human health. Diabetes
affects about 8% of US population and is increasing globally.
Diabetes is characterized by hyperglycemia that can subsequently lead to systemic tissue toxicity. Risk factors for diabetes
include increased glucose response (both fasting and postprandial), decreased insulin sensitivity, and obesity. These risk
factors may be reversible with lifestyle modifications that
have been shown to be effective in delaying the onset of type
2 diabetes. One lifestyle change could be to reduce the glycemic load of the diet that could be achieved by replacing ordinary starch in foods with RS.
RS has been shown to have significant effects of serum
triglyceride and cholesterol concentrations. Several animal
studies have shown significantly lower plasma cholesterol and
triglyceride concentrations when RS is included in the diet in
replacement of digestible starch. A decrease in fasting cholesterol and triglycerides was observed when RS was consumed
chronically (514 weeks). The mechanism responsible for
these effects seems to be increased bile acid excretion caused
by consumption of RS, but some study showing reduced
plasma cholesterol and triglyceride concentrations even compared to the bile acid sequestrant cholestyramine suggests that
the effects of RS extend beyond just bile acid secretion. The
effects of RS on cholesterol and blood triglyceride levels seem
to be mediated through a combination of enhancement of bile
acid secretion, a significant decrease in cholesterol absorption,
and an increase in hepatic LDL receptor expression. Both high
blood lipid and cholesterol levels are associated with coronary
heart disease and the effects of RS consumption may therefore
have important health ramifications.
The effects of RS consumption on satiety and weight management are not as clear. One major reason for the current
global obesity epidemic is the overconsumption of energy, and
therefore, strategies that can manage the energy intake may be
successful in reducing obesity. Dietary fiber is one way to
decrease the energy value of foods if it is used to replace
digestible carbohydrates that have a higher caloric value.
Some dietary fibers have also been linked to increased satiety
and lower BMI, but not all fibers have the same effects. RS is a
type of dietary fiber and it would therefore be reasonable to

expect some effect on satiety and/or total energy intake when

RS is used to replace digestible starch in the diet. Animal
studies have shown the production of satiety hormones
GLP-1 and PYY when RS was added to the diet, which suggests
an effect of RS on satiety. However, only a few human studies
have been conducted to examine the effect of RS on satiety and
the results were mixed. Some studies have shown an increase in
satiety after RS consumption, but others have shown little or
no effect. Satiety seems to be linked to changes in plasma
glucose concentrations and studies that showed a decrease in
plasma glucose/insulin response to a high RS meal also
showed an increase in satiety while those studies that showed
no change in plasma glucose also showed no difference in
satiety. Overall, there is indication that there is at least a weak
association between RS consumption and satiety. Some animal
studies have shown reduced energy intake when RS was added
to the diet. Aziz et al. showed that body weight was reduced by
40% in obese rats that were fed with a diet high in RS compared with rats fed with a low-RS diet. While this study seems
to indicate a real positive effect of RS on energy intake and
potentially obesity management, the levels of RS used for this
study (23.4%) may not be realistic in a human diet. Long-term
studies in humans with realistic RS inclusion levels are
required to get a better understanding of the potential for RS
to help in the management and reduction of the current obesity epidemic.

Summary/Conclusions
RS is a dietary fiber and can be used to replace digestible starch
in foods. Many animal studies have been conduced to examine
the effect of RS consumption. RS may be fermented in the
colon and the resulting SCFA production has been linked to a
number of health benefits such as reduced pH, which has been
associated with the suppression of growth of potentially pathogenic organisms and reduction of the absorption of toxic
compounds. Fermentation of RS has been shown to produce
relatively high levels of the SCFA butyrate that has been linked
to reduced risk of colon cancer. RS fermentation has also been
linked to benefits in the risk reduction of IBD by strengthening
of the gut barrier via increased production of mucin. RS has
been shown to increase fecal bulk, which is important for relief
of constipation and prevention of diverticulosis and other
disorders such as hemorrhoids.
An EFSA claim was granted in 2011 for reduced blood
glucose response when RS is used to replace digestible carbohydrate in the diet (EFSA, ID 681, April 2011). The effect of RS
on glycemia and insulinemia is less clear, and studies have
shown that different effects are possible due to study designs
(e.g., amount of fat and protein in diets) and amount of RS
tested. Overall, it does seem that RS consumption does indeed
lead to a small decrease in postprandial glycemia and a more
significant attenuation of postprandial insulinemia that could
have important metabolic implications. Both hyperglycemia
and hyperinsulinemia are affected in the development of
insulin resistance, which in turn has been linked to several
diseases known as metabolic syndrome, for example, type 2
diabetes, obesity, coronary heart disease, hypertension, and
dyslipidemia.

CARBOHYDRATES | Resistant Starch and Health

RS has been shown to have significant effects on serum

triglyceride and cholesterol concentrations. The effects of RS
on cholesterol and blood triglyceride levels seem to be mediated through a combination of enhancement of bile acid secretion, a significant decrease in cholesterol absorption, and an
increase in hepatic LDL receptor expression. Both high blood
lipid and cholesterol levels are associated with coronary heart
disease and the effects of RS consumption may therefore have
important health ramifications.
The effects of RS consumption on satiety and weight management are not as clear. RS is a type of dietary fiber and it
would therefore be reasonable to expect some effect on satiety
and/or total energy intake when RS is used to replace digestible
starch in the diet. Only a few human studies have been conducted to examine the effect of RS on satiety and the results
were mixed. Overall, there is indication that there is at least a
weak association between RS consumption and satiety, but
long-term studies in humans with realistic RS inclusion levels
are required to get a better understanding of the potential for
RS to help in the management and reduction of the current
obesity epidemic.

Exercise for Revision

What are the different types of resistant starch?

What is the link between resistant starch consumption and
colon cancer?
How does resistant starch affect insulin sensitivity and why
is this important?

Exercises for Readers to Explore the Topic Further

While many animal studies have been conducted examining
the relationship of resistant starch intake and various health
benefits, a more limited number of human clinical studies
have been conducted. The results of these clinical studies are
sometimes contradictory, and strong conclusions on the health
benefits of resistant starch are therefore difficult in some areas.
More human studies with careful study designs are needed in
the future.

See also: The Basics: The Grains that Feed the World; Grains
around the World: Grain Production and Consumption, Overview;
Food Grains and the Consumer: Grains and Health; Food Grains
and Well-being: Functional Foods, Overview; Food Grains and
the Consumer: Consumer Trends in Consumption; Grains and Health
Misinformation and Misconceptions; ; Carbohydrates:
Carbohydrate Metabolism; Beta glucans and health.

Further Reading
Abell GCJ, Cooke CM, Bennett CN, Conlon MA, and McOrist AL (2008) Phylotypes
related to Ruminococcus bromii are abundant in the large bowel of humans and
increase in response to a diet high in resistant starch. FEMS Microbiology Ecology
66: 505515.
Asp N-G (1992) Resistant Starch. Proceedings from the second plenary meeting of
EURESTA: European FLAIR concerned action no. 11 on physiological implications

of the consumption of resistant starch in man. European Journal of Clinical

Nutrition 46: S1S148.
Aziz AA, Keeney LS, Goulet B, and Abdel-Aal ES (2009) Dietary starch type affects body
weight and glycemic control in freely fed but not energy-restricted obese rats.
Journal of Nutrition 139: 18811889.
Berry CS (1986) Resistant starch: Formation and measurement of starch that survives
exhaustive digestion with amylolytic enzymes during the determination of dietary
fibre. Journal of Cereal Science 4: 301314.
Bird AR, Colon MA, Christophersen CT, and Topping DL (2010) Resistant starch, large
bowel fermentation and a broader perspective of prebiotics and probiotics.
Beneficial Microbes 1(4): 423431.
Birt DF, Boylston T, Hendrich S, et al. (2013) Resistant starch: Promise for improving
human health. Advances in Nutrition 4: 587601.
Brayer GD, Sidhu G, and Maurus R (2000) Subsite mapping of the human pancreatic
alpha-amylase active site through structural, kinetic, and mutagenesis techniques.
Biochemistry 39: 47784791.
Brown IL, Yotsuzuka M, Birkett A, and Henriksson A (2006) Prebiotics, synbiotics and
resistant starch. Journal of the Japanese Association of Dietary Fiber Research
10: 19.
Cummings JH, Beatty ER, Bingman SM, Bingham SA, and Englyst HN (1996) Digestion
and physiological properties of resistant starch in the human large bowel. British
Journal of Nutrition 75: 733747.
Cummings JH, Macfarlane GT, and Englyst HN (2001) Prebiotic digestion and
fermentation. American Journal of Clinical Nutrition 73(supplement 2): 415S420S.
Czuchajowska Z, Sievert D, and Pomeranz Y (1991) Enzyme-resistant starch. IV. Effects
of complexing lipids. Cereal Chemistry 68: 537542.
Davie JR (2003) Inhibition of histone deacetylase activity by butyrate. Journal of
Nutrition 133: 2485S2493S.
Dysseker P and Hoffem D (1994) Estimation of resistant starch intake in Europe.
In: Proceedings of the Concluding Plenary Meeting of EURESTA. Wageninger,
pp. 8485. European FLAIR-Concerted Action No. 11 (COST 911).
Eerlingen RC and Delcour JA (1995) Formation, analysis, structure and properties of
type III enzyme resistant starch. Journal of Cereal Science 22: 129138.
Englyst HN, Kingman SM, and Cummings JH (1992) Classification and measurement of
nutritionally important starch fractions. European Journal of Clinical Nutrition
46: S33S50.
Finnie IA, Dwarakanath AD, Taylor BA, and Rhodes JM (1995) Colonic mucin synthesis
in increased by sodium-butyrate. Gut 36: 9399.
Ghodke SK and Ananthanarayan L (2008) Health benefits of resistant starch. Agro Food
Industry Hi-Tech 19: 3739.
Giczewska A and Borowska J (2003) Nutritional value of broad bean seeds. Part 1:
Starch and fibre. Food 47(2): 9597.
Gork AS, Usui N, Ceriati E, et al. (1999) The effect of mucin on bacterial translocation in
I-407 fetal and Caco-2 adult enterocyte cultured cell lines. Pediatric Surgery
International 15: 155159.
Hasjim J, Lee S-O, Hendrich S, Setiawan S, Ai Y, and Jane J (2010) Characterization of
a novel resistant starch and its effects on postprandial plasma glucose
and insulin responses. Cereal Chemistry 87: 257262.
Higgins JA (2004) Resistant starch: Metabolic effects and potential health benefits.
Journal of AOAC International 87: 761768.
Jacobasch G, Schmiedl D, Kruschwski M, and Schmel K (1999) Dietary resistant starch
and chronic inflammatory diseases. International Journal of Colorectal Disease
14: 201211.
Jenkins DJA, Vuksan V, and Kendall CWC (1998) Physiological effects of resistant
starches in fecal bulk, short chain fatty acids, blood lipids and glycemic index.
Journal of the American College of Nutrition 6: 609616.
Keenan MJ, Zhou J, and McCutcheon KL (2009) Effects of resistant starch, a
non-digestible fermentable fiber, on reducing body fat. Obesity (Silver Spring)
14: 15231534.
Knowler WC, Barrett-Connor E, Fowler SE, et al. (2002) Reduction in the incidence of
type 2 diabetes with lifestyle intervention or metformin. New England Journal of
Medicine 346: 393403.
Mazur AK and Nakatani H (1993) Multiple attack mechanism in the porcine pancreatic
alpha-amylase hydrolysis of amylose and amylopectin. Archives of Biochemistry
and Biophysics 306: 2938.
McCleary BV (2007) An integrated procedure for the measurement of total dietary fibre
(including resistant starch), non-digestible oligosaccharides and available
carbohydrates. Analytical Bioanalytical Chemistry 389: 291308.
McCleary BV and Monaghan DA (2002) Measurement of resistant starch. Journal of the
Association of Official Analytical Chemists 85: 665675.
Moore CO, Tuschhoff JV, Hastings CW, and Schanefelt RV (1984) Applications of
starches in foods. In: Whistler RL, BeMiller JN, and Paschall EF (eds.) Starch:
Chemistry and Technology, pp. 575590. New York: Academic Press.

CARBOHYDRATES | Resistant Starch and Health

Murphy MM, Spungen Douglass J, and Birkett A (2008) Resistant starch intakes in the
United States. Journal of the American Dietetic Association 108: 6778.
Nichols BL, Avery SE, Sen P, Swallow DM, Hahn D, and Sterchi EE (2003) The maltaseglucoamylase gene: Common ancestry to sucrase-isomaltase with
complementary starch digestion activities. Proceeding of the National Academy
of Sciences in the United States of America 100: 14321437.
Nugent A (2005) Health properties of resistant starch. Nutrition Bulletin 30: 2754.
Pencek RR, Koyama Y, and Lacey DB (2002) Transporter-mediated absorption
is the primary route of entry and is required for passive absorption of intestinal
glucose into the blood of conscious dogs. Journal of Nutrition 132: 19291934.
Phillips J, Muir JG, Birkett A, Lu ZX, Jones GP, and ODea K (1995) Effect of resistant
starch of fecal bulk and fermentation-dependent events in humans. American
Journal of Clinical Nutrition 62: 121130.
Ramakrishna BS, Venkataraman S, Srinivasan S, Dash P, Young GP, and Binder HJ
(2000) Amylase-resistant starch plus oral rehydration solution for cholera.
New England Journal of Medicine 342: 308313.
Robertson MD (2012) Dietary-resistant starch and glucose metabolism. Current
Opinion in Clinical Nutrition and Metabolic Care 15: 362367.
Robyt JF (1984) Enzymes in the hydrolysis and synthesis of starch. In: Whistler RL,
BeMiller JN, and Paschall EF (eds.) Starch: Chemistry and Technology, pp. 87118.
New York: Academic Press.
Rodriguez S, Islas JJ, Agama E, Tovar J, and Bello LA (2008) Characterization of a
fibre-rich powder prepared by liquefaction of unripe banana flour. Food Chemistry
107: 15151521.
Roediger WEW (1989) Short chain fatty acids as metabolic regulators of ion
absorption in the colon. Acta Veterinaria Scandinavica. Supplementum
86: 116125.
Rumessen JJ (1992) Hydrogen and methane breath tests for evaluation of resistant
carbohydrates. European Journal of Clinical Nutrition 46(supplement 2): S77S90.
Sharma A and Yadav BS (2008) Resistant starch: Physiological roles and food
applications. Food Reviews International 24: 193234.

Sievert C and Pomeranz Y (1990) Enzyme-resistant starch. II. Differential scanning

calorimetry study on heat-treated starches and enzyme-resistant starch residues.
Cereal Chemistry 68: 8691.
Silvester KR, Englyst HN, and Cummings JH (1995) Ileal recovery of starch from whole
diets containing resistant starch measured in vitro and fermentation of the ileal
effluent. American Journal of Clinical Nutrition 62: 4034113.
Smirnov A, Perez R, Amit-Romach E, Sklan D, and Uni Z (2005) Mucin dynamics and
microbial populations in chicken small intestine are changed by dietary probiotic
and antibiotic growth promoter supplementation. Journal of Nutrition
135: 187192.
Swallow DM, Poulter M, and Hollox EJ (2001) Intolerance to lactose and other dietary
sugars. Drug Metabolism and Disposition 29: 513516.
Swinburn B, Sacks G, and Ravissin E (2009) Increased food energy supply is more than
sufficient to explain the US epidemic of obesity. American Journal of Clinical
Nutrition 90: 14531456.
Tester RF, Karkalas J, and Qi X (2004) Starch Composition, fine structure and
architecture. Journal of Cereal Science 39: 151165.
Topping DL, Bird AR, and Young GP (2009) Effect of aspirin or resistant starch on
colorectal neoplasia in the Lynch syndrome. New England Journal of Medicine
360: 1462.
Wanders AJ, van den Borne J, and de Graaf C (2011) Effects of dietary fibre on
subjective appetite, energy intake and body weight: A systematic review of
randomized controlled trials. Obesity Reviews 12: 724739.
Wolever TM, Robb PA, and Thomas MS (1992) Effect of guar, pectin, psyllium, soy
polysaccharide, and cellulose on breath hydrogen and methane in healthy subjects.
American Journal of Gastroenterology 87: 305310.
Worthley DL, Le Leu RK, and Whitehall VL (2009) A human, double-blind,
placebo-controlled, crossover trial of prebiotic, probiotic, and synbiotic
supplementation: Effects on luminal, inflammatory, epigenetic, and epithelial
biomarkers of colorectal cancer. American Journal of Clinical Nutrition
90: 578586.