Blackwell Science, LtdOxford, UKNBUNutrition Bulletin1471-98272004 British Nutrition Foundation? 20043012754Review ArticleHealth properties of RSA.

Nugent

R EV IEW

Health properties of
resistant starch
A. P. Nugent
British Nutrition Foundation, London, UK

Summary Resistant starch (RS) refers to the portion of starch and starch products that resist
digestion as they pass through the gastrointestinal tract. RS is an extremely broad
and diverse range of materials and a number of different types exist (RS1–4). At
present, these are mostly defined according to physical and chemical characteristics.
RS may be categorised as a type of dietary fibre, as defined by the American
Association of Cereal Chemists and the Food Nutrition Board of the Institute of
Medicine of the National Academies. RS is measured in part by the methodology
recommended by the Association of Official Analytical Chemists for measuring
dietary fibre. Dietary intakes of RS in westernised countries are likely to be low.
However, accurate comparative assessments of dietary intakes between countries,
and subsequent epidemiological analysis, are absent due to the lack of consensus
over of an agreed, repeatable and simple in vitro method for analysing the RS con-
tent of foods. At present, the recognised method is that of McCleary & Monaghan
(2002). RS appears to confer considerable benefits to human colonic health, but has
a smaller impact on lipid and glucose metabolism. Comparisons between studies are
hampered by differences in study design, poor experimental design and differences
in the source, type and dose of RS in the ingredients or diets used. It is likely that
RS mediates some or all of its effects through the action of short chain fatty acids
but interest is increasing regarding its prebiotic potential. There is also increasing
interest in using RS to lower the energy value and available carbohydrate content of
foods. RS can also be used to enhance the fibre content of foods and is under inves-
tigation regarding its potential to accelerate the onset of satiation and to lower the
glycaemic response. Due to the difficulties in agreeing on a universal definition and
method of analysis for dietary fibre, RS may be included within the term ‘fibre’ on
the nutrition labels in some countries but not in others. Pressure to agree a legal def-
inition and universal method of analysis is likely to increase due to the potential of
RS to enhance colonic health, and to act as a vehicle to increase the total dietary
fibre content of foodstuffs, particularly those which are low in energy and/or in
total carbohydrate content.

Keywords: colonic health, fibre, glucose metabolism, resistant starch

Correspondence: Dr Anne Nugent, Nutrition Scientist, British Nutrition Foundation, High Holborn House, London, WC1V 6RQ, UK.
E-mail: a.nugent@nutrition.org.uk

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54 27

28 A. Nugent

What is starch? healthy people’ (Asp 1992). RS that reaches the large
intestine can act as a substrate for microbial fermenta-
Starches are one of the main forms of dietary carbohy-
tion, the end-products being hydrogen, carbon dioxide,
drates (the others being sugars). Starchy foods are
methane and short chain fatty acids (SCFA) (Englyst
derived from plant sources such as potatoes and cereal
et al. 1996). However, as the EURESTA definition
products (e.g. breads), and are staple items in the British
describes RS in terms of its physiological functionality,
diet (BNF 1994). In plants, starch occurs as granules
rather than its physical or chemical characteristics, sci-
that provide an economical means of storing carbohy-
entists have defined a number of categories of RS to
drate in an insoluble and tightly packed manner
describe how the starches may escape digestion in upper
(Imberty et al. 1991). The size and shape of these gran-
gastrointestinal tract.
ules varies among plant species and also cultivars of the
same species (Baghurst et al. 1996).
Chemically, starches are polysaccharides, i.e. they are Structure of resistant starch
composed of a number of monosaccharides or sugar
The resistance of starch to digestion is influenced by the
(glucose) molecules linked together with a1–4 and/or
nature of the association between starch polymers, with
a1–6 linkages. Two main structural types of starch
higher amylose levels in the starch being associated with
exist: amylose which is a linear a1–4 molecule and typ-
slower digestibility rates. Both B and C type starches
ically constitutes 15–20% of starch, and amylopectin
appear to be more resistant to digestion with high-amy-
which is a larger branched molecule with a1–4 and a1–
lose maize producing RS which has been particularly
6 linkages and is a major component of starch (BNF
useful in the preparation of foods (Brown 2004).
1990). Two crystalline structures of starch have been
Retrograded starches refer to certain structural forms
identified (an ‘A’ and ‘B’ type), which contain differing
of RS. Retrogradation occurs when starch is cooked in
proportions of amylopectin. A type starches are found
water beyond its gelatinisation temperature and then
in cereals, while B type starches are found in tubers and
cooled. Amylose is found in the amphorous parts of the
amylose-rich starches. A third type called ‘C type’
starch crystal, while amylopectin gives starch its crystal-
appears to be a mixture of both A and B forms and is
line structure. Upon heating with excess water and at
found in legumes (Topping & Clifton 2001). In general,
sufficiently high temperatures, the starch crystalline
digestible starches are broken down (hydrolysed) by the
regions ‘melt’. The starch granules gelatinise and the
enzymes a-amylases, glucoamylase and sucrase-isomal-
starch is subsequently more easily digested. However,
tase in the small intestine to yield free glucose that is
these starch gels are unstable and upon cooling re-form
then absorbed.
crystals that are resistant to hydrolysis by amylases (i.e.
are resistant to digestion). Slow cooling of the gelati-
nised starch favours Type A crystallisation while slow
What is resistant starch?
cooling in excess water favours Type B crystallisation.
In 1982, while developing an in vitro assay for non- This process is known as retrogradation (Topping &
starch polysaccharides (a type of dietary fibre), Englyst Clifton 2001). In general, starches rich in amylose are
and coworkers found that some starch remained after naturally more resistant to digestion and also more sus-
enzymic hydrolysis. Follow-up studies with healthy ileo- ceptible to retrogradation.
stomy subjects confirmed the presence of similar
starches, which resisted digestion in the stomach and
Classification and food sources of
small intestine. Further analysis revealed that these
resistant starch
starches could be fermented in the large intestine in vivo.
The term ‘resistant starch’ (RS) was coined and used to Resistant starch has been classified into four general
describe these starches (Englyst et al. 1982). Although subtypes called RS1–RS4 (Englyst et al. 1992; Brown
the term ‘resistant starch’ is not defined by any govern- et al. 1995). Table 1 outlines a summary of the different
ment agency (Goldring 2004), a group of scientists types of RS, their classification criteria and food sources.
funded by the European Union (EU) in a concerted Briefly, RS1 is the term given to RS where the starch is
action known as EURESTA (FLAIR Concerted Action physically inaccessible to digestion, e.g. due to the pres-
no. 11 Physiological Implications of the Consumption ence of intact cell walls in grains, seeds or tubers. RS2
of Resistant Starch in Man) defined RS as the ‘total describes native starch granules that are protected from
amount of starch, and the products of starch degrada- digestion by the conformation or structure of the starch
tion that resists digestion in the small intestine of granule as in raw potatoes and green bananas. A par-

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54


Table 1 Classification of types of resistant starch, food sources and factors affecting their resistance to digestion in the colon
Type of RS Description
RS1 Physically protected
RS2 Ungelatinised resistant granules with B-type
crystallinity and are hydrolysed slowly by
a-amylases
RS3 Retrograded starch (i.e. non-granular
starch-derived materials)
RS4 Chemically modified starches due to cross-bonding
with chemical reagents, ethers, esters, etc.
RS, resistant starch.
ticular type of RS2 is unique as it retains its structure
and resistance even during the processing and prepara-
tion of many foods; this RS2 is called high-amylose
maize starch. RS3 refers to non-granular starch-derived
materials that resist digestion. RS3 forms are generally
formed during the retrogradation of starch granules.
Some examples of RS3 are cooked and cooled potatoes
and cornflakes. RS4 describes a group of starches that
have been chemically modified and include starches
which have been etherised, esterified or cross-bonded
with chemicals in such a manner as to decrease their
digestibility. RS4 may be further subdivided into four
subcategories according to their solubility in water and
the experimental methods by which they can be analy-
sed (Brown 2004).
Although RS is found naturally in all starch-contain-
ing foods, factors which influence the net amount of RS
present include the initial quantity and type of starch
present, how the starchy food is processed, cooked and
stored and how it is ingested (Brown 1996). As evident
in Table 1, RS1 is made less resistant to digestion by
milling and chewing, RS2 by food processing techniques
(e.g. cooking) and RS3 by the conditions of food pro-
cessing used (e.g. during the preparation of bread and
cornflakes). RS4, as a result of chemical modification,
can resist hydrolysis after food processing; however, this
is dependent upon the starch base, and the type and level
of modification.
In addition to the structural factors mentioned above
whereby the presence of water and the chemical struc-
ture of starch can influence the amount of RS present,
other factors intrinsic to starchy foods can affect a-
amylase activity and therefore starch breakdown. These
include the formation of amylose-lipid complexes, the
presence of native a-amylase inhibitors and also non-
starch polysaccharides, all of which can directly affect
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 29
Food sources Resistance reduced by
Whole- or partly milled grains and seeds, legumes, Milling, chewing
pasta
Raw potatoes, green bananas, some legumes, high Food processing and cooking
amlyose starches
Cooked and cooled potatoes, bread, cornflakes, Processing conditions
food products with prolonged and/or repeated
moist heat treatment
Some fibre-drinks, foods in which modified starches Less susceptible to digestibility
have been used (e.g. certain breads and cakes) in vitro
a-amylase activity (Englyst et al. 1992). Extrinsic addi-
tives may also bind to starch making it more or less sus-
ceptible to degradation, e.g. phosphorus (Niba 2003). In
addition, physiological factors can impact the amount
of RS in a food – increased chewing decreases particle
size (smaller particles being more easily digested in the
gut), while intra-individual variations in transit time and
biological factors (e.g. menstrual cycle) also affect the
digestibility of starch. At present, it is not known how
the various types of RS4 are affected by digestion
in vivo.
Resistant starch as a component of
dietary fibre
There is no globally agreed definition of dietary fibre.
Problems with defining dietary fibre arise from the lack
of a universally agreed and reliable method to quantify
all of the components of dietary fibre. Various defini-
tions of dietary fibre have been suggested whereby
dietary fibre may be defined as part of a plant, as chem-
ical substances, according to indigestibility in the small
intestine and/or by its beneficial digestive and physio-
logical effects and metabolic fate (Champ et al. 2003a).
However, the American Association of Cereal Chemists
(AACC) proposed one of the most recent definitions in
2000. The AACC defined dietary fibre as ‘the edible
parts of plants or analogous carbohydrates that are
resistant to digestion and absorption in the human small
intestine with complete or partial fermentation in the
large intestine. Dietary fibre includes polysaccharides,
oligosacccharides, lignin and associated plant sub-
stances. Dietary fibres promote beneficial physiological
effects including laxation, and/or blood cholesterol
attenuation, and/or blood glucose attenuation’ (Anon
2000; Jones 2000). Contrary to some earlier definitions,
30 A. Nugent
this description of dietary fibre specifically refers to non-
starch polysaccharides, resistant oligosaccharides and
analogous carbohydrates. It also includes RS, therefore
RS may be considered a component of dietary fibre (De
Vries 2003). More recently, the Food and Nutrition
Board of the Institute of Medicine of the National Acad-
emies has published definition(s) of dietary fibre that
include RS (Institute of Medicine 2002) and the Codex
Alimentarius Committee is also looking at a definition,
but this is in process. Traditionally in the UK, the defi-
nition for dietary fibre accounts for only non-starch
polysaccharides and lignin, and does not include RS
(DH 1991). This definition is based on the method of
Englyst et al. (1992). Although the UK Food Standards
Agency now recommends that manufacturers use the
AOAC method for measuring dietary fibre on all food
products in the UK, difficulties arise as population
dietary fibre recommendations and existing food com-
position tables are still based on the Englyst method (see
labelling section).
Measurement of resistant starch
The main step of any method to measure the content of
RS in foods must first remove all of the digestible starch
from the product using thermostable a-amylases
(McCleary & Rossiter 2004). At present, the method of
McCleary & Monaghan (2002 and AOAC method
2002.02) is considered the most reproducible and
repeatable measurement of RS in starch and plant mate-
rials, but it has not been shown to analyse all RS as
defined (Champ et al. 2003b). It is based on the princi-
ple of enzymic digestion and measures the portions of
starch resistant to digestion at 37∞C that are typically
not quantitated due to the gelatisation at 100∞C fol-
lowed by digestion at 60∞C. A commercial test kit is
available and further details of the method are available
at http://www.megazyme.com/booklets/KRSTAR.pdf.
Table 2 lists the RS contents from a number of sample
foods using this method and sourced from McCleary &
Rossiter (2004).
In the US and some other countries such as Japan
and Australia, the Association of Official Analytical
Chemists (AOAC) method 985.29 for Total Dietary
Fibre Determination in Foods (Prosky et al. 1985; a
gravimetric determination of dietary fibre quantity
after enzymic digestion, mimicking human digestion) is
commonly used to measure total dietary fibre (De Vries
2004). This method accounts for some (i.e. RS3, the
retrograded portion, and RS2 as found in high amylose
maize) RS present as part of the total dietary fibre
value. Therefore, while it does measure some RS as
Table 2 Resistant starch contents of a number of sample foods and
commercially manufactured sources of resistant starch
RS content (as assessed using
Food sample AOAC 2002.02)
Wheat bran 0.42
Rye crispbread 1.2
Kidney beans 5.3
Corn flakes 2.8
Native potato starch 78.1
Cooked and cooled potato starch 3.8
HYLON VII 53.7
Hi-maize 1043 45.7
NOVELOSE 240 46.9
ActiStar 58.0
CrystaLean 40.9
Source: Reprinted with kind permission from McCleary & Rossiter (2004).
Copyright (2004) AOAC INTERNATIONAL.
part of the total dietary fibre figure, additional methods
are needed for quantification of the other categories of
RS (Champ et al. 2003b). Again, this highlights the
need for a universally agreed definition and method of
analysis for all of the components of dietary fibre,
including RS.
Commercially manufactured sources of
resistant starch
In addition to the natural food sources of RS, some com-
mercially manufactured forms of RS are also available
(Table 2). Hi-maize® was originally obtained from a
maize hybrid grown in Australia. It originally contained
80–85% amylose with approximately 30% dietary fibre
when commercially released in 1993 but it has since
been improved to provide ingredients containing
approximately 60% dietary fibre (Brown et al. 1995).
This product, a high-amylose maize starch and categor-
ised as RS2, is now sold throughout the world by
National Starch and Chemical Co. and is used in prod-
ucts including cereals, biscuits, other baked goods, dairy
products, nutrition bars and breads. In particular,
Hi-maize is incorporated into Australian, New Zealand
and Swedish breads, e.g. Wonder-White, Nature’s Fresh
Fibre White and Pagens ‘Bra’.
A number of RS3 ingredients are available with a
dietary fibre content < 30%; in general these are
derived from cooked and recrystallised maize or tapi-
oca starch (Crosby 2003). NOVELOSE 330® (National
Starch and Chemical Limited) and CrystaLean (Opta
Food Ingredients, Inc.) are also examples of commer-
cially developed RS3 which is derived from high amy-
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

lose maize (Yue & Waring 1998). Research is
intensifying regarding RS4 chemically modified
starches; RS4 which have been created using difunc-
tional phosphate reagents are available for inclusion in
foods; however, as yet there is a lack of information
regarding their potential clinical and physiological
effects (Brown 2004).
There are a number of advantages to using commer-
cially manufactured sources of RS in food products.
Unlike natural sources of RS (e.g. legumes, potatoes,
bananas), commercially manufactured resistant starches
are not affected by processing and storage conditions.
For example, the amount of RS2 in green bananas
decreases with increasing ripeness, however, a commer-
cial form of RS2, Hi-maize, does not experience these
difficulties. As RS is included within the definitions of
dietary fibre by the AACC (Anon 2000; Jones 2000),
and the Institute of Medicine of the National Academies
(Institute of Medicine 2002), and is measured within the
remit of the AOAC method (Prosky et al. 1985) which is
used in the US, UK, Australia and Japan, commercially
manufactured sources of RS can be used as vehicles to
increase the total dietary fibre content of foods and food
products without affecting taste and texture (Liversey
1994). They may also be used to provide fibre in some
commercially available low-carbohydrate foods mar-
keted for those following low-carbohydrate dieting reg-
imens. Table 3 lists some of the advantages and
functional properties of commercial sources of RS2 and
RS3.
Table 3 Functional properties and advantages of commercial
sources of RS2 and RS3
Natural sources
Bland in flavour
White in colour
Fine particle size (which causes less interference with texture)
High gelatinisation temperature
Good extrusion and film-forming qualities
Lower water-holding properties than traditional fibre products
Allows the formation of low-bulk high fibre products with improved texture,
appearance and mouthfeel (i.e. better organo-leptic qualities) compared
with traditional high-fibre products
Increases coating crispness of products
Increases the bowl life of breakfast cereals
Functional food ingredient
May lower the calorific value of foods
Can be used to reduce oil pick-up in expanded snacks
Useful in products for coeliacs, bulk laxatives and in products for oral
rehydration therapy
Source: Adapted from Liversey (1994), Brown et al. (1995) and Yue & Waring
(1998).
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 31
Calorific value and dietary intakes of
resistant starch
Experimentally, the energy value of RS has been calcu-
lated as approximately 8 kJ/g (2 kcal/g). This is consid-
erably lower than the energy value for completely
digestible starch 15 kJ/g (4.2 kcal/g) (Liversey 1994).
However, at present in Europe this energy value is not
accounted for during nutritional labelling of foodstuffs
(see labelling and legislation section).
Several studies have attempted to quantify population
dietary intakes of RS. However, a number of different
methods of analyses of RS were used in these studies and
this makes any real comparisons between countries and/
or studies difficult. From population studies, it has been
calculated that intakes of non-starch polysaccharides
are approximately < 20 g/day (Baghurst et al. 1996).
The last national survey of dietary intakes in the UK
revealed that intakes of non-starch polysaccharides were
approximately 12 g/day for women and 15 g/day for
men (Henderson et al. 2003). However, it is believed
that approximately 60–80 g of substrate is needed per
day to sustain the 1013-1014 organisms found in the
human large bowel. It is thought that RS contributes to
this ‘carbohydrate gap’ (Topping et al. 2003). RS has
been reported to constitute up to 15% of the dry matter
of a food product (Champ et al. 2003b).
Worldwide, dietary intakes of RS are believed to vary
considerably. It is estimated that intakes of RS in devel-
oping countries with high starch consumption rates
range from approximately 30 to 40 g/day (Baghurst
et al. 2001). Dietary intakes in India and China were
recently estimated at 10 and 18 g/day (Platel &
Shurpalekar 1994; Muir et al. 1998). Intakes in the EU
are thought to lie between 3 and 6 g/day (Dyssler &
Hoffmann, 1994). Dietary intakes of RS in the UK are
estimated at 2.76 g/day (Tomlin & Read 1990) and are
believed to range from 5 to 7 g/day in Australia
(Baghurst et al. 2001). In the study of Baghurst et al.
(2001) the authors analysed population dietary intakes
of RS using Australian National Dietary Survey data for
the years 1988 and 1993 and a foods database which
they constructed using analytical data from published
findings and data presented at a scientific (EURESTA)
meeting. The main sources of RS for this cohort were
cereals (42%), vegetables (26%) and fruit and fruit juice
(22%). There was little evidence of any age- or occupa-
tion-related trends in the density of RS in the diet. How-
ever, this data must be viewed with caution as it
represents only a small amount of data, a number of
techniques were used to ascertain the amount of RS in
foods, the authors reported inconsistencies in the data-
32 A. Nugent

base and the data refers to Australian dietary intakes. As Short chain fatty acids
mentioned earlier, intakes of RS in Australia are likely to
be greater than in Europe due to the commercial avail- Short chain fatty acids (SCFA) are the metabolic prod-
ability of top-selling breads and cakes that are enriched ucts of anaerobic bacterial fermentation of polysac-
with RS. charides, oligosaccharides, protein, peptide and
glycoprotein precursors in the large intestine, including
those derived from dietary fibre and RS (Andoh et al.
Physiological effects of resistant starch
2003). The principal SCFA are butyrate, propionate and
A number of physiological effects have been ascribed to acetate, although other SCFA are also produced in lesser
RS and are listed in Table 4 and will be described below. amounts (MacFarlane & MacFarlane 2003). SCFA are
RS, by escaping digestion in the small intestine, has few the preferred respiratory fuel of the cells lining the colon
interactions with other components of the upper gas- (colonocytes). They increase colonic blood flow, lower
trointestinal tract. It is fermented in the large intestine luminal pH and help prevent the development of abnor-
resulting in the production of such fermentation prod- mal colonic cell populations (Topping & Clifton 2001).
ucts as carbon dioxide, methane, hydrogen, organic SCFA are mainly found in the proximal colon where fer-
acids (e.g. lactic acid) and SCFA. However, RS is mentation is greatest, and the amount present mirrors
believed to result in only a modest production of these supply of carbohydrate in the diet (Topping et al. 2003).
gases compared with other non-digestible oligosaccha- Levels of SCFA fall during the passage of digesta
rides, fructo-oligosaccharides and lactulose (Christl through the colon; this is due to uptake and utilisation
et al. 1992). SCFA produced include butyrate, acetate by the colonocytes and bacteria. In humans, the abun-
and propionate, and it is thought that these SCFA in dance of SCFA is normally acetate > propionate >
particular mediate the effects of RS, rather than RS butyrate. Depending on diet, total SCFA concentrations
exerting a physical bulking effect (Topping et al. 2003). are usually between 70 and 140 mM in the proximal
SCFA will be discussed briefly below; other mechanisms colon and 20–70 mM in the distal colon; therefore,
by which RS may influence physiological behaviour will SCFA are found in much lower amounts in the distal
be discussed later in this review. colon (the site of many colonic diseases and most human
colon cancers). Butryate is the favoured fuel of colono-
cytes (Schwiertz et al. 2002). In vitro, butyrate can
Table 4 Physiological effects of resistant starch
reverse neoplastic changes (Ferguson et al. 2000) and it
Conditions where there may exerts trophic effects on the colonic epithelium in vivo
Potential physiological effects be a protective effect (Mentschel & Claus 2003). In addition, it can affect
gene expression and may induce cell cycle arrest or even
Improve glycaemic and insulinaemic Diabetes, impaired glucose apoptosis (naturally programmed cell death which
responses and insulin responses, the removes DNA damaged, unwanted or old cells) of
metabolic syndrome
colonocytes (Mentschel & Claus 2003). Therefore,
Improved bowel health Colorectal cancer, ulcerative
colitis, inflammatory bowel dietary interventions that increase the amount of SCFA
disease, diverticulitis, in the colon are thought to be beneficial to gut health,
constipation and SCFA are commonly used as markers of fermenta-
Improved blood lipid profile Cardiovascular disease, lipid tion and colonic health. Length of transit time and diet
metabolism, the metabolic are two variables known to influence the concentration
syndrome and types of SCFA found in the colon. A long transit
Prebiotic and culture protagonist Colonic health
time results in protein breakdown and an increased con-
Increased satiety and reduced Obesity
energy intake
tribution by amino acid fermentation to SCFA pools
Increased micronutrient absorption Enhanced mineral absorption, (MacFarlane & MacFarlane 2003), while dietary fibre
osteoporosis (including RS) can modify large bowel and faecal SCFA
Adjunct to oral rehydration Treatment of cholera, chronic levels (Bird et al. 2000a).
therapies diarrhoea However, there are several problems with using SCFA
Synergistic interactions with other Improved metabolic control as markers of (human) fermentation and colonic health.
dietary components, e.g. dietary and enhanced bowel health
As approximately 95% of SCFA are produced and
fibres, proteins, lipids
absorbed in the colon, the accuracy of faecal measure-
Thermogenesis Obesity, diabetes
ments is limited (Cummings et al. 1987). SCFA are also
Source: Adapted from Brown (2004) and Champ (2004). absorbed and transported via the portal vein to the liver,

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54


with the fraction not absorbed being distributed to other
body organs and tissues for metabolism. Therefore,
while concentrations of human peripheral blood SCFA
are sometimes measured as a surrogate marker of SCFA
fermentation, these are not representative of levels
found in the portal circulation. Similarly, hydrogen
breath tests are only general indicators of fermentation
(Topping & Clifton 2001). The gold standard method is
isotopic dilution (Sakata et al. 2003) but in practice
most human studies rely on the above indirect measures
of fermentation and many researchers choose to study
animal models, which may have slightly different distri-
butions of SCFA along the colon (Sakata et al. 2003).
For all faecal measurements, it is recommended that the
molar ratios of SCFA are measured rather than the con-
centration or the total output (Cummings et al. 1987).
Finally, it is noteworthy that the bacteria responsible for
butyrate production are largely unknown and therefore
it remains difficult to devise a dietary intervention (e.g.
using RS) to stimulate increased numbers and/or activity
of the bacteria that produce butyrate.
The effects of resistant starch on short chain
fatty acid production
Resistant starch can increase the production of SCFA
and therefore may help improve colonic health. Animal
studies in pigs and rats have reported that feeding RS
increased the caecal and faecal production of total SCFA
and also the individual concentrations of propionate,
butyrate and acetate (Ferguson et al. 2000; Hennings-
son et al. 2003). In most human studies, increased faecal
excretion and/or faecal concentrations of SCFA were
reported following supplementation with RS (Phillips
et al. 1995; Silvester et al. 1995; Cumming et al. 1996;
Birkett et al. 2000; Muir et al. 2004). However, discrep-
ancies have been observed with respect to effects on the
individual SCFA and indeed no effect was observed in
the study of Hylla et al. (1998). These differences are
most likely due to the experimental method used, the
source, type and amount of RS, interindividual varia-
tions in length of transit time and on the duration of
feeding. In particular, RS2 (from raw potato starch) is
reported to increase the concentration of butyrate in
humans and rats (Cummings et al. 1996; Ferguson et al.
2000; Martin et al. 2000; Henningsson et al. 2003),
while RS3 (retrograded starch) is reported to increase
the concentration of acetate in pigs (Martin et al. 2000),
but not in humans (Cummings et al. 1996). It has also
been reported that sufficient time for microbial adapta-
tion is necessary before changes in SCFA will be
observed (Topping & Clifton 2001).
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 33
Resistant starch and colonic function
(colorectal cancer, inflammatory bowel
disease, constipation and diverticulitis)
Dietary fibre, starch, resistant starch and colon cancer
A number of epidemiological studies have investigated
the potential benefits of dietary fibre and starch in pro-
tecting against the development of colon cancer;
however, less information is available regarding RS.
Increasing evidence points to a protective effect of
dietary fibre on colorectal cancers: in the European pro-
spective Investigation into Cancer and Nutrition (EPIC),
Bingham et al. (2003) showed that in populations with
a low to average intake of dietary fibre (measured as
non-starch polysaccharides), doubling of fibre intake
could reduce the risk of colorectal cancer by up to 40%
(Bingham et al. 2003). Cassidy et al. (1994), in an inter-
national correlative study, found a strong inverse rela-
tionship between starch intake and colon and rectal
cancer, even after adjusting for fat and protein intake.
Non-starch polysaccharides were only significantly cor-
related when combined with starch. In this study, the
authors assumed that 5% of all starch consumed was
resistant and that this RS contributed to the protective
effect of starch. However, this estimate represents a sub-
stantial amount of RS reaching the colon as dietary
intakes of starch are approximately 8–10 times higher
than intakes of non-starch polysaccharides (Cassidy
et al. 1994). In addition, no attempt was made to
account for between-country variation in dietary
sources of starch and amounts of starch eaten (Young &
Le Leu 2004). At present, epidemiological studies
addressing the relationship between colorectal cancers
and RS have not been reported.
One cohort and two case–control studies have inves-
tigated the relationship between dietary starch and col-
orectal cancer. A high intake of dietary starch was found
to be protective in the cohort study (Health Profession-
als Follow-Up Study; Giovannucci et al. 1992), but not
in two case–control studies (Haenszel et al. 1980;
Macquart-Moulin et al. 1986). More data is needed
regarding the potential protective effects of RS. How-
ever, such research is hampered by a lack of standard-
ised quantitative information relating to dietary intakes
and levels of RS in common dietary foodstuffs.
Two studies of note that are currently under-way are
the Concerted Action Polyp Prevention (CAPP) studies,
which aim to test the efficacy of RS on colorectal can-
cer prevention. CAPP-1, is a randomised double-blind
factorial design controlled trial investigating the effects
of one of four treatments in suppressing colorectal
34 A. Nugent
adenoma formation in young subjects with an inher-
ited disposition to developing colon cancer (Familial
Adenomatous Polyposis): (1) double placebo; (2) aspi-
rin (600 mg/day); (3) RS [30 g raw potato starch –
HYLON VII (1 + 1 w/w)/day]; and (4) aspirin and RS.
CAPP-2 is also a randomised double-blind factorial
design controlled trial and is using aspirin (600 mg/
day) and a different form of RS [30 g NOVELOSE
260 – NOVELOSE 330 (1 + 1 w/w)/day] in gene carri-
ers or affected family members with another hereditary
form of colorectal cancer (Hereditary Nonpolyposis
Colorectal Cancer) (Mathers et al. 2003). Although
results will not be available for several years, they
ought to provide valuable information regarding the
potential protective effects of RS on the development
of colorectal cancer.
Experimental measures used in studies of resistant
starch and colonic function
In the interim, a large number of animal and human
studies have attempted to investigate the effects of RS on
colonic function. In general, these studies have tended to
look at two main areas: outcomes of colorectal neopla-
sia and markers of colonic function and colorectal
cancer.
Commonly measured outcomes of colorectal neopla-
sia include:
• tumour formation;
• tumour size and incidence;
• cell proliferation;
• formation of DNA adducts;
• the presence of abberant crypt foci;
• apoptosis.
Aberrant crypt foci (ACF) are precursor lesions of col-
orectal cancer, which can be identified under a micro-
scope and have been found to correlate with colon
cancer risk, and adenoma size and number in humans.
DNA adducts are complexes formed from the reaction
of toxic chemicals or their metabolites with cellular
DNA. The presence of DNA adducts reflects exposure
to toxic chemicals and their bioaccumulation through-
out life: in the colonic mucosa increased levels are
thought to result in increased cancer risk (Young & Le
Leu 2004). However, concerns have been raised con-
cerning the sensitivity and specificity of the analytical
techniques for detecting these DNA adducts. Mainte-
nance of epithelial mass is important for regulation of
normal colonic function and hyperproliferation (cell
overgrowth) may result in an increased risk of colon
cancer development. Epithelial cell proliferative activity
is thought to be an intermediate risk marker for colorec-
tal cancer (Van Gorkom et al. 2002) but its exact use-
fulness as a marker of colonic cell function is unclear
and results are often difficult to interpret.
Other measured markers of colorectal cancer and
colonic function are:
• SCFA production (particularly butyrate);
• faecal pH;
• ammonia and phenol concentrations;
• faecal weight and output;
• secondary bile acid excretion;
• cytotoxicity of faecal water;
• transit time;
• activity of bacterial enzymes and microbial
populations.
In general, improved colonic function is associated with
increased SCFA production, lower pH, lower produc-
tion of ammonia and phenol, decreased secondary bile
acid excretion, reduced cytotoxicity of faecal water,
reduced transit time and altered bacterial activity. The
benefits imparted by SCFA have already been discussed.
A lower pH is thought to depress the conversion rate of
primary to secondary bile acids and lower their carci-
nogenic potential. Furthermore, a low (acid) pH in
combination with high concentrations of SCFA is
thought to prevent the overgrowth of pH-sensitive
pathogenic bacteria (Topping & Clifton 2001). Phenol
and ammonia are products of protein fermentation and
reduced concentrations indicate a decreased reliance on
protein for colonic fermentation and possibly a short-
ened transit time (Young & Le Leu 2004). Reduced
activity of certain bacterial enzymes (e.g. b-glucu-
ronidase) depresses the formation of toxic and carcino-
genic metabolites from dietary and endogenous
compounds (Young & Le Leu 2004). The effect of RS
on the activity of microbial populations will be dis-
cussed later (prebiotics).
Animal studies of resistant starch and colonic function
Studies examining the effect of RS on colonic func-
tion and colon cancer development in animals have
generally focused on pigs, mice and rats, and have
used experimentally induced colon cancer (usually
using dimethylhydrazine, azoxymethane) or colitis
(using dextran sodium sulphate) or genetic models of
intestinal tumours (e.g. Min mice). Rats and mice are
more frequently used in studies of colon function than
pigs. However, caution must be observed with regard
to the use of genetically susceptible mouse models of
colon cancer (e.g. Min model) as the cancer sites are
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

predominately in the small intestine, rather than in the
large intestine – the site where RS is fermented and
thought to confer maximal benefits (Young & Le Leu
2004).
As presented in Table 5, a protective effect of RS on
the formation of ACF has been observed in two animal
studies (Thorup et al. 1995; Cassand et al. 1997) but
not in the study of Young et al. (1996) where raw potato
starch (RS2) at a level of 20% carbohydrate content
(14.4 g/100 g diet) increased the density of ACF. Inter-
estingly, this effect was lost when RS was fed in combi-
nation with wheat bran (Young et al. 1996). Various
forms of RS (chiefly RS2 and RS3) appear to consis-
tently increase faecal output and weight (Cassand et al.
1997; Ebihara et al. 1998; Maziere et al. 1998; Bird
et al. 2000b; Ferguson et al. 2000), reduce faecal and/or
caecal pH (Caderni et al. 1996; Cassand et al. 1997;
Maziere et al. 1998; Le Leu et al. 2003), decrease levels
of ammonia (Silvi et al. 1999) and favourably modulate
the activity of bacterial enzymes (Maziere et al. 1998;
Silvi et al. 1999). However, results with respect to
tumour incidence and size, cell proliferation and DNA
damage/adduct formation are less clear. Feeding RS had
no effect on tumour incidence in four animal studies
(Sakamoto et al. 1996; Young et al. 1996; Pierre et al.
1997; Maziere et al. 1998) but had a negative effect on
tumour frequency in the study of Williamson et al.
(1999) and resulted in increased tumour size in that of
Young et al. (1996). Increased cellular proliferation was
reported by Young et al. (1996) but not in the study of
Silvi et al. (1999).
Interestingly it would appear that feeding RS at high
levels, in combination with other dietary macronutrients
may also directly affect outcomes. Conlon & Bird
(2003) reported a protective effect against DNA damage
when male Sprague Dawley rats were fed RS (Hi-maize
or NOVELOSE) with 10% sunflower oil rather than
when fed the RS with 10% fish oil for 8 weeks. The
opposite was seen when rats were fed 10% fish oil or
sunflower oil and 10% fibre (as cellulose or wheat
bran). Similarly, Toden et al. (2003) showed that when
male Sprague Dawley rats were fed a high protein diet
(15 or 25% casein) with RS (48% Hi-maize), the RS diet
attenuated colonic damage and thinning of colonic
mucous observed with the high protein diet alone. The
need for further research investigating the effect of RS is
highlighted by the study by Ferguson et al. (2003) who
reported an increased bioavailability of a food carcino-
gen (2-amino-3-methylimidazo[4,5-f]quinoline; IQ)
after feeding rats RS.
In conclusion, animal studies would suggest that RS
appears to have a protective effect on markers of colonic
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 35
function (e.g. SCFA concentrations, pH, etc.). Results
are less clear with respect to tumour formation, size, cel-
lular proliferation and DNA damage. Differences in
results may be in part due to the animal models and
types of carcinogens used, the different types of RS (RS
used was mainly RS2 or RS3) or even the different feed-
ing regimens. Further research is needed using different
types and mixes of RS, and examining any potential
interactions between RS and other macronutrients com-
monly found in the diet (e.g. protein and fat).
Human studies of resistant starch and
colonic function
A limited number of studies have investigated the
effects of different types of RS and colonic function in
humans; summaries of the major studies are presented
in Table 6. Positive effects of supplementation with RS
have been observed in most studies examining transit
time (Hylla et al. 1998; Muir et al. 2004) and faecal
output and/or bulk (Van Munster et al. 1994; Phillips
et al. 1995; Cummings et al. 1996; Heijnen et al. 1998;
Hylla et al. 1998; Jenkins et al. 1998; Muir et al. 2004).
In addition, most authors reported a stool-softening
effect.
While a lack of effect of RS on SCFA production/con-
centration was reported by three authors (Heijnen et al.
1998; Hylla et al. 1998; Grubben et al. 2001), six other
reports would suggest that RS does confer beneficial
effects on SCFA and in particular butyrate (van Munster
et al. 1994; Phillips et al. 1995; Cummings et al. 1996;
Noakes et al. 1996; Jenkins et al. 1998; Muir et al.
2004). Further evidence that RS supplementation may
enhance fermentation of starch in the large intestine is a
decrease in faecal pH (Phillips et al. 1995; Birkett et al.
1996; Noakes et al. 1996; Van Gorkom et al. 2002;
Muir et al. 2004) and a reduction in the concentrations
of products of protein fermentation in the faeces, i.e.
decreased levels of ammonia and phenol and an
increased excretion of nitrogen (Birkett et al. 1996;
Heijnen et al. 1997; Muir et al. 2004). Indeed in the
short communication by Heijnen et al. (1997), the
authors reported that a decrease in faecal ammonia was
only observed after supplementation with the RS2
source, HYLON VII, and not with RS3 (extruded, ret-
rograded HYLON VII). However, inconsistencies also
exist in human studies: supplementation with RS had no
effect on pH in three studies (Heijnen et al. 1998;
Jenkins et al. 1998; Grubben et al. 2001) and while RS
was found to decrease the concentration of soluble bile
acids in faecal water (Van Munster et al. 1994; Noakes
et al. 1996; Grubben et al. 2001), it had no effect in the
 36

Table 5 Animal intervention studies examining the effects of resistant starch on colonic function
A. Nugent

Author Animal model Intervention Parameters measured Outcome

Thorup et al. (1995)
Wistar rats Carbohydrate content of diet replaced by: sucrose, ACF RPSØ total and larger ACF
(azoxymethane) cornstarch or RPS (RS2; 67 g/100 g)
Caderni et al. (1996) Sprague Dawley rats Sucrose, glucose, fructose, cornstarch or Cell proliferation NSD
(Dimethylhydrazine) HYLON VII (RS2) Caecal pH Ø
Caecal concentrations SCFA Ø
Sakamoto et al. (1996) Sprague Dawley rats 3 or 10 g/100 g cellulose or Tumour incidence NSD
(Dimethylhydrazine) 3 or 10 g/100 g RS3 (high amylose maize SCFA and butyrate production ≠
starch hydrolysed with pancreatin) Faecal output ≠
Young et al. (1996) Sprague Dawley rats Low RS, low fibre diet or Tumour incidence NSD
(Dimethylhydrazine) 14.4 g/100 g diet RPS (RS2) or Tumour size and multiplicity ≠
14.4 g/100 g RPS and 14.4 g/100 g wheat bran ACF ≠ density
Cell proliferation ≠
Faecal output ≠
Pierre et al. (1997) C57BL/6 J min mice RS-free diet (2% cellulose, no RS) or Tumour incidence NSD
Wheat bran (18.8 g/100 g) or
RS3 (high amylose cornstarch; 18.8 g/100 g)
Maziere et al. (1998) Sprague Dawley rats RS-free diet (2% cellulose) or ACF Ø
(Dimethylhydrazine) 25 g/100 g RS3 (high-amylose maize starch) Caecal pH Ø
Faecal weight and output ≠
Bacterial enzyme activity ≠ b-glucuronidase activity
Cassand et al. (1997) Sprague Dawley rats Retrograded high-amylose cornstarch (RS3) ACF Ø
Faecal output ≠
Faecal pH Ø
SCFA ≠ total and butyrate
Kleeson et al. (1997) Wistar rats RPS, or retrograded potato starch (RS2) SCFA ≠SCFA
10 g/100 g ≠ butyrate, RS2
Eibhara et al. (1998) Wistar rats Potato starch or Faecal output ≠
CMS Caecal SCFA Ø butyrate with CMS
Caecal bile acids ≠ with CMS
Silvi et al. (1999) Fisher rats RS- and cellulose-free diet (2.1%) or Caecal SCFA ≠ butyrate
Retrograded amylose starch (15 g/100 g) Bacterial enzyme activity Ø b-glucuronidase activity
Ammonia production Ø
Cell proliferation NSD
Williamson et al. (1999) Min mouse RS- and NSP-free diet or Tumour incidence ≠ with RS diet
1:1 RPS (RS2) and high-amylose maize diet (RS3)

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

 Author Animal model Intervention Parameters measured Outcome
Bird et al. (2000b) Pigs Brown rice or SCFA excretion ≠
white rice and bran Large bowel digesta mass ≠
Ferguson et al. (2000) Wistar rats RS- and NSP-free diet or Faecal output ≠
Potato starch or SCFA ≠ including butyrate
High amylose maize starch or Transit time ^ by potato starch and
a-amylase treated Hi-maize (35 g/100 g) a-amylase treated
Hi-maize

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

Wang et al. (2002) Balb/C mice Amylomaize starch SCFA ≠ butyrate in faeces
Modified amylomaize starch (40 g/100 g diet)
Ferguson et al. (2003) Wistar rats RS- and NSP-free diet Faecal output ≠
Potato starch and high amylose maize starch (35 g/100 g) Excretion of the food carcinogen, IQ ≠ carcinogen bioavailbility
Le Leu et al. (2003) Sprague Dawley rats High amylose maize starch pH Ø
Conlon & Bird (2003) Sprague Dawley rats 10 g/100 g fish oil or sunflower oil Colonic DNA damage ≠ DNA damage with RS
And and fish oil vs. RS and
10 g/100 g dietary fibre (wheat bran or cellulose) sunflower oil
Or Reverse with dietary fibre.
10 g/100 g RS (Hi-maize or NOVELOSE)
Toden et al. (2003) Sprague Dawley rats 15 or 25 g/100 g casein with or without 48% Hi-maize DNA damage Ø with RS diet
Thining of mucosal layer Ø with RS diet
Kestell et al. (2004) Wistar rats RS- and fibre-free diet Metabolism and disposal of the food carcinogen, IQ RS≠ number of intact IQ and
Potato starch Hi-maize Ø level of metabolites
Apple pectin
Wheat straw

ACF, aberrant crypt foci; CMS, chemically modified starch; IQ, 2-amino-3-methylimidazo[4,5-f]quinoline; NSD, non-significant difference; RS, resistant starch; RPS, raw potato starch; SCFA; short chain fatty acid.
Some of the data contained in this table was reprinted with kind permission from Young & Le Leu (2004) In: Journal of AOAC International 87: 779–84. Copyright (2004) AOAC INTERNATIONAL.
Health properties of RS
37
 38

Table 6 Human intervention studies examining the effects of resistant starch on colonic function

Author Sample size and study length Intervention Parameters measured Outcome
A. Nugent

Tomlin & Read (1990) 8 subjects 6 large bowls Cornflakes (10.33 g RS) Breath hydrogen ≠
or
6 large bowls Rice Krispies (0.86 g RS)
Van Munster et al. (1994) 14 healthy subjects fed the diets for 45 g HYLON VII (32%) RS Cell proliferation Ø
3 weeks or Faecal output ≠
low RS, 20 g natural fibre pH NSD
Faecal SCFA ≠ total SCFA and butyrate
Breath hydrogen ≠
Bile acid excretion Ø secondary bile acids and concentrations
Cytotoxicity of soluble bile acids
Ø
Phillips et al. (1995) 11 healthy subjects in a crossover High RS (Hi-maize or cooked or uncooked Faecal output ≠
study for 3 weeks green banana flour; 26–50 g RS/day) or Faecal pH Ø
low RS diet (3–8 g RS/day) SCFA ≠ butyrate and acetate
Excretion of starch ≠
pH Ø by 0.6 units
Birkett et al. (1996) 11 subjects in randomised controlled High RS (39 g/day, RS1, RS2, RS3 mix) or Faecal nitrogen excretion ≠
cross-over for 3 weeks low RS (5 g/day) Faecal ammonia Ø
Faecal phenols Ø
Faecal pH Ø
Cummings et al. (1996) 12 healthy subjects fed each diet for RS2 – potato and banana starch Faecal weight ≠
15-day periods RS3 – maize and wheat starch SCFA ≠
RS-free diet (wheat starch) NSP breakdown Ø breakdown and ≠ faecal NSP
RS diets contained 17–30 g RS
Noakes et al. (1996) 23 hypertriglycerimd emics High amylose maize starch (17–25 g RS/day) or Bile acids Ø secondary bile acids in faecal water
for 4 weeks Oat bran pH Ø
SCFA ≠ faecal total SCFA and faecal butyrate
Heijnen et al. (1998) 24 healthy volunteers fed each diet Uncooked HYLON VII (32 g RS2/day) Faecal output ≠
for 1-week periods Retrograded high amylose cornstarch pH NSD
(32 g RS2/day) SCFA NSD
Glucose syrup Bile acids NSD
Cytotoxicity NSD
Hylla et al. (1998) 12 healthy volunteers for 4 weeks High RS – high amylose maize (55.2 g RS/day) Faecal weight ≠
Low RS – corn starch (7.7 g RS/day) SCFA NSD
Bile acids Ø total and secondary concentrations
Transit time ≠
Bacterial enzymes Ø b-glucosidase activity
Sterols Ø faecal total sterols

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

 Author Sample size and study length Intervention Parameters measured Outcome

Jenkins et al. (1998) 24 healthy subjects fed each diet for RS2 (21.5 g RS/day) Faecal bulk ≠
2 weeks with a 2-week washout RS3 (27.9 g RS/day) SCFA ≠ butyrate: SCFA ratio
period Wheat bran (1.5 g RS/day)
Low fibre diet (2.3 g RS/day)
Grubben et al. (2001) 23 patients with recently removed 45 g amylomaize (28 g RS/day as a capsule) or Cell proliferation NSD

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

colonic adenomas for 4 weeks 45 g maltodextrin Faecal weight NSD
pH NSD
SCFA excretion ≠ faecal butyrate
Bile acids ≠ primary and secondary bile acids in faecal
water
Van Gorkom et al. (2002) 111 sporadic adenoma patients High RS: 30 g HYLON VII (19 g RS) or Cell proliferation NSD
Controlled placebo
Wacker et al. (2002) 12 healthy subjects for 4 weeks High RS: HYLON VII (50.7–59.7 g/day) or Cell proliferation NSD
(only 8 volunteers for DNA data) Low RS: cornstarch DNA adducts ≠ adduct levels in colonic mucosa
Muir et al. (2004) 20 volunteers for 3 weeks Wheat bran (12 g fibre) Faecal output ≠
RS and Wheat bran (22 g RS and 12 g fibre/day) Transit time ≠
Faecal pH Ø
SCFA ≠ faecal concentration
Phenol Ø
Ammonia Ø

NSD, non-significant difference; RS, resistant starch; SCFA, short chain fatty acid.
Some of the data contained in this table was reprinted with kind permission from Young & Le Leu (2004) In: Journal of AOAC International 87: 779–84. Copyright (2004) AOAC INTERNATIONAL.
Health properties of RS
39
40 A. Nugent
trial of Heijnen et al. (1998). It is thought that the con-
centrations of soluble bile acids in the faeces are a better
indicator of potential colonic mucosal damage than
total faecal bile acids as it is the soluble acids that are
available for contact with the mucosa (Rafter et al.
1986).
A limited number of studies have examined the effect
of RS on cellular proliferation and DNA damage. Only
Van Munster et al. 1994) reported a small decrease in
cellular proliferation, while three other studies have
showed no effect (Grubben et al. 2001; Van Gorkom
et al. 2002; Wacker et al. 2002). The only study at
present to examine the effect of RS on DNA adduct for-
mation in humans (Wacker et al. 2002) found increased
levels of adducts in volunteers following a high-RS diet.
Clearly, there still remains a need for further research
into the effects of RS on human colonic function and
markers of colon cancer risk. It is difficult to explain
the discrepancies between the studies, however, there
were large variations in study sample size, duration,
dose of RS and even form of RS. For example, in the
study of Grubben et al. (2001), the authors reported no
effect of RS supplementation on a variety of parame-
ters including faecal output, pH, SCFA production and
cell proliferation. However, RS in this study was given
in the form of a capsule rather than in a natural food
form. Similarly, the study of Heijnen et al. (1998) was
only a week in length and may not have allowed a suit-
able adaptation time. Finally, human studies have
included healthy volunteers and patients with hyper-
triglyceridemia, or patients with sporadic or recently
removed adenomas, which makes direct comparisons
regarding colonic function difficult. In conclusion, it
would appear that RS can improve certain markers of
colonic function in humans (e.g. increase faecal output,
faecal bulk and transit time and decrease pH and
ammonia levels, increase SCFA and decrease bile salts
in faecal water). More research is needed to elucid-
ate the exact effects of RS on cellular and molecular
functions before a direct protective effect can be
determined.
Resistant starch and inflammatory bowel disease,
diverticulitis and constipation
A limited number of studies have examined the potential
benefits of RS in ameliorating the symptoms of inflam-
matory bowel diseases such as ulcerative colitis. Ulcer-
ative colitis refers to a chronic, often recurrent
ulceration of the mucosa and submucosa of the colon
(Mahon & Arlin 1992). SCFA enemas can be used to
treat ulcerative colitis in human patients therefore in
principle, if RS increases SCFA production it may prove
a useful adjunct to traditional treatment regimens.
Based on this hypothesis, RS has been studied (and is
sometimes used) as a treatment for ulcerative colitis.
This relies on the in vivo generation of SCFA and
butyrate to treat the ulcerations.
In the study of Jacobasach et al. (1999) Sprague Daw-
ley rats with chemically induced colitis were then fed
diets rich in RS2 (granular pea starch at a level of
15.38 g/100 g) for 21 days. RS-fed rats showed earlier
improvements in histological markers of inflammation
and normalisation of cell functions such as activation of
colonic cell proliferation, restoration of apoptotic
responses and uptake of SCFA. In addition, RS also
enhanced the growth of intestinal bacteria presumed to
promote health (Jacobasach et al. 1999). Similarly,
Moreau et al. (2003) examined the potential healing
properties of feeding RS3 (11.5 g/100 g) for 14 days to
Sprague Dawley rats in which colitis had been induced
by dextran sodium sulphate. The RS-rich diet improved
caecal and distal macroscopic and histological observa-
tions and increased caecal levels of butyrate compared
with a fructo-oligosaccharide-rich diet and the control
diet (RS and fructo-oligosaccharide-free) (Moreau et al.
2003). Therefore, it would appear that RS can confer
some healing properties in the management of inflam-
matory bowel disease, at least in rats, however, data in
humans are lacking.
There is a lack of studies testing the potential benefits
of RS in the management of diverticulitis and constipa-
tion, however, due to the beneficial effects of RS supple-
mentation on stool bulk, stool consistency and transit
time for example, it is possible that increasing dietary
intakes of RS may help ameliorate these conditions.
Indeed a number of over the counter products for bowel
health are now available.
It is possible that by combining RS with other forms
of dietary fibre, it may have more favourable effects on
bowel health than consuming RS or dietary fibre alone.
A number of studies are currently investigating this
hypothesis. A recent study by Muir et al. (2004) in 20
volunteers with a family history of colorectal cancer
showed that wheat bran (12 g/day) when given in com-
bination with RS (22 g/day) had more benefits on bowel
health over 3 weeks than wheat bran alone. The wheat
bran–RS combination successfully reduced transit time
and faecal pH, increased faecal output and excretion of
SCFA (e.g. butyrate) and lowered total phenol concen-
trations. This study suggests that the health benefits of
RS can be maximised when given in conjunction with
different types of dietary fibres.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

Resistant starch and colonic microflora: prebiotics
and probiotics
Gibson & Roberfroid (1995) defined prebiotics as
‘growth substrates directly specifically towards poten-
tially beneficial bacteria already resident in the colon’.
Prebiotics are non-digestible food ingredients that stim-
ulate the growth and/or activity of bacteria in the colon,
thereby improving host health. Probiotics refer to cul-
tures of live micro-organisms which when applied to
man or animal may beneficially improve the properties
of indigenous flora. Synbiotics refer to a mixture of pre-
and probiotics where there is a synergistic interaction
between the specific probiotic and a particular prebiotic
(Topping et al. 2003).
RS appears to function as a prebiotic and symbiotic
(Brown et al. 1997; Wang et al. 1999). Studies in
humans and pigs have revealed that consumption of
high-RS diets result in a time-dependent shift in faecal
and large-bowel SCFA profiles, suggesting a change in
the autochthonous (local) microbial population and that
RS could interact with gut bacteria (Topping et al.
2003). It is also worth noting that RS appears to func-
tion differently than more well known prebiotics (e.g.
fructo-oligosaccharides); when the RS and fructo-
oligosaccharides were fed together, the increase in faecal
bacteria was greater than the individual increases
observed when these two ingredients were fed separately
(Brown et al. 1998).
It is thought that RS may act as a feeding substrate for
Bifidobacteria in vitro (Wang et al. 1999) and that it
may provide protection to these bacteria in vivo as they
travel through the upper gastrointestinal tract (Wang
et al. 1999). In vitro studies have also shown that sev-
eral categories of RS (including RS2 and RS4) may phys-
ically associate with several Bifidobacteria species
(Brown et al. 1998) protecting them from attack during
food preparation and storage (Brown et al. 1997), as
well as during transit through the gastrointestinal tract
(Wang et al. 1999). Because of these protective effects,
RS may be described as a ‘culture protagonist’ (Conway
2001) and RS has been combined with Bifidobacteria in
yoghurt (Crittenden et al. 2001). However, there is a
lack of data relating to the efficacies of the individual
types of RS.
There are shortcomings with using probiotics to pro-
mote gut health: only a small proportion of ingested
organisms reach the colon intact and once probiotic
consumption decreases the organisms are washed out of
the gastrointestinal tract (Topping et al. 2003). RS may
safeguard against these losses by providing physical pro-
tection and by slowing the rate at which the bacteria are
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 41
lost once probiotic consumption ceases. Initial data
show that when RS is fed in combination with fructo-
oligosaccharides, no decline in faecal numbers of bacte-
ria was observed (Brown et al. 1998). Based on this
data, Topping et al. (2003) suggested that probiotics
may not need to be consumed as often if combined with
foods rich in RS or fructo-oligosaccharides. However,
more research in humans is needed, particularly with
respect to the doses of RS needed and the differences in
efficacy between the different types of RS.
In addition to these prebiotic effects, RS also appears
to exert other health-promoting actions on gut health.
RS (high amylose starch) supplementation, in associa-
tion with oral hydration therapy, is reported to reduce
fluid loss and halve recovery time when fed to people
with cholera-induced diarrhoea (Ramakrishna et al.
2000). Similar benefits have been found after feeding
green bananas to children with other forms of infectious
diarrhoea (Rabbani et al. 2001) and after feeding
cooked rice to pigs infected with the pathogen Brachys-
pira hydodysenteriae (Hampson et al. 2000). It is
thought that RS may confer these benefits through
increased fluid absorption as a result of greater SCFA
production (Topping et al. 2003). SCFA stimulate water
and cation (sodium, potassium, calcium) uptake in the
proximal colon and, through their action on muscular
activity and blood flow in the colon, may directly reduce
the severity of diarrhoea. One hypothesis is that RS may
affect the viability of the cholera organism in the gut
whereby the cholera bacteria adhere to the RS, in a sim-
ilar manner to Bifidobacteria, and are removed from the
infection site (Topping et al. 2003). However, more
research is needed to clarify the exact role of RS in the
treatment of diarrhoea and its mechanisms of action.
Furthermore, the efficacy of the various types of RS
needs to be established.
Resistant starch and metabolic responses
Consumption of soluble fibre can confer benefits to
heart health, influencing both lipid and glucose metab-
olism. RS shares some common properties with soluble
dietary fibres insofar as it is poorly digested in the small
intestine and largely digested and metabolised (fer-
mented) in the colon releasing SCFA. However, unlike
soluble fibre, the fraction of RS arriving at the colon is
not viscous, it can easily be incorporated into most
starchy foods in the diet and is considered more palat-
able (Demigné et al. 2001). A significant number of
studies have examined whether RS affects lipid and glu-
cose metabolism (including glycaemic index), energy
expenditure and macronutrient oxidation.
42 A. Nugent

Resistant starch and lipid metabolism
As is evident in Table 7, RS appears to particularly
affect lipid metabolism based on studies in rats where
reductions in a number of measures of lipid metabolism
have been observed. These include total lipids, total cho-
lesterol, low density lipoproteins (LDL), high density
lipoproteins (HDL), very low density lipoproteins
(VLDL), intermediate density lipoproteins (IDL), trig-
lycerides, triglyceride-rich lipoproteins. In these studies,
reductions of up to 22–32% in plasma cholesterol levels
and 29–42% in plasma triglyceride levels were noted. In
the study of Younes et al. (1995), RS was more effective
than the drug cholestyramine (a bile sequestrant) in low-
ering plasma cholesterol and triglyceride levels. RS has
also been shown to be effective in lowering plasma cho-
lesterol levels in genetically obese and lean rats (Mathé
et al. 1993) and in diabetic rats (Kim et al. 2003).
Some earlier studies in humans reported a beneficial
effect of feeding RS on fasting plasma triglyceride and
cholesterol levels (Behall et al. 1989; Reiser et al. 1989;
Noakes et al. 1996), however, it would appear that RS
does not affect total lipids (Behall & Howe 1995;
Heijnen et al. 1996; Noakes et al. 1996; Jenkins et al.
1998), triglycerides (Van Amelsvoort & Westrate 1992;
Raben et al. 1994, 1997; Behall & Howe 1995; Heijnen
et al. 1996; Jenkins et al. 1998); HDL or LDL (Heijnen
et al. 1996; Noakes et al. 1996; Jenkins et al. 1998) or
VLDL levels in humans (Behall & Howe 1995; Noakes
et al. 1996). Therefore, on balance RS does not appear
to influence these markers of lipid metabolism in
humans.

Table 7 Summary of the effects of resistant starch (RS) on markers of lipid metabolism in animals (A) and humans (H)*

Parameter RS exerted a positive effect RS had no effect

Triglycerides De Deckere et al. (1993), 1995) (A) Van Ameslvoort & Westrate (1992) (H)
Verbeek et al. (1995) (A) Kim et al. (2003) (A)
Younes et al. (1995) (A) Raben et al. (1994) (H)
Cheng & Lai (2000) (A) Behall & Howe (1995) (H)
Lopez et al. (2001) (A) Heijnen et al. (1996) (H)
Kishida et al. (2001) (A) Raben et al. (1997) (H)
Han et al. (2003a, 2003b) (A) Jenkins et al. (1998) (H)
Behall et al. (1989) (H)
Reiser et al. (1989) (H)
Noakes et al. (1996) (H)
Total cholesterol (total lipids) Mathe et al. (1993) (A) De Deckere et al. (1995) (A)
De Deckere et al. (1993) (A) Kishida et al. (2001) (A)
Verbeek et al. (1995) (A) Behall & Howe (1995) (H)
Younes et al. (1995) (A) Noakes et al. (1996) (H)
Cheng & Lai (2000) (A) Heijnen et al. (1996) (H)
Kim et al. (2003) (A) Jenkins et al. (1998) (H)
Kishida et al. (2001) (A)
Lopez et al. (2001) (A)
Kim et al. (2003) (A)
Han et al. (2003a, 2003b) (A)
Reiser et al. (1989) (H)
Behall et al. (1989) (H)
High density lipoproteins Han et al. (2003a, 2003b) (A) Cheng & Lai (2000) (A)
Younes et al. (1995) (A) Lopez et al. (2001) (A)
Kishida et al. (2001) (A) Kim et al. (2003) (A)
Noakes et al. (1996) (H)
Heijnen et al. (1996) (H)
Jenkins et al. (1998) (H)
Low density lipoproteins Han et al. (2003a, 2003b) (A)
Younes et al. (1995) (A)
Kishida et al. (2001) (A)
Intermediate density and/or very low density lipoproteins Han et al. (2003a, 2003b) (A)
Triglyceride-rich lipoproteins Kishida et al. (2001) (A)
Younes et al. (1995) (A)
Lopez et al. (2001) (A)

*A positive effect refers to an increase in the concentrations of high density lipoproteins but a decrease in the concentrations of all other parameters.

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

 Health properties of RS 43

Resistant starch and insulin and
glucose metabolism
Insulin is a hormone that enables glucose uptake by
muscle and adipose cells, thereby lowering blood glu-
cose levels. It also inhibits the use of stored body fat and
together with an array of other physiological signals can
modulate appetite and satiety signals. RS-rich foods
release glucose slowly and therefore one would expect
this to result in a lowered insulin response, greater
access to and use of stored fat and, potentially, a muted
generation of hunger signals. Not only would these con-
ditions help in the management of clinical conditions,
such as diabetes and impaired glucose tolerance, but
also possibly in the treatment of obesity and in weight
management.
There have been a number of studies examining the
effects of various forms and doses of RS on glucose (gly-
caemic) and insulin (insulinaemic) responses. Most stud-
ies in humans have focused on postprandial glycaemic
and/or insulinaemic responses and have varied in qual-
ity (see below). There is a lack of consensus regarding
the precise effects of RS on insulin and glucose
responses: 15 studies have reported an improvement in
these measures following the consumption of a RS-rich
test-meal, while 10 have showed no, or a physiologically
irrelevant effect. It is noteworthy that, to date, there are
no reports of RS worsening insulin and glucose
responses. In general, positive effects were usually
observed shortly (i.e. within the first 2–8 h) after the
high RS-meal (Higgins 2004). It would also appear that
RS consumption may confer a small decrease in post-
prandial glycaemia, but is associated with more physi-
ologically significant reductions in postprandial
insulinaemia. From these studies it was concluded that
RS must contribute at least 14% of total starch intake in
order to confer any benefits to glycaemic or insulinaemic
responses (Behall & Hallfrisch 2002; Brown et al. 2003;
Higgins 2004). Table 8 lists the studies analysed.
Difficulties arise when trying to compare these studies
as the composition of the test and control meals often
vary in terms of amount of digestible starch, total
dietary fibre and macronutrients present. Most food
sources contain digestible starch as well as RS, yet often
the content of digestible starch is overlooked (Champ
2004). In addition, some of the test foods/meals

Table 8 Summary of studies examining the effects of resistant starch (RS) on glucose and insulin responses in humans

Resistant starch decreased Resistant starch had no effect on

Glucose responses Insulin responses Glucose responses Insulin responses

Krezowski et al. (1987)*‡
NSD
Holm & Bjorck (1992)*
Liljeberg et al. (1994)*
Raben et al. (1994)*
Byrnes et al. (1995)*
Granfeldt et al. (1995)*
Lintas et al. (1995)†
— De Roos et al. (1995)*§
Achour et al. (1997)*
Raben et al. (1997)*
Hoebler et al. (1999)*
Vonk et al. (2000)*
Skrabanja et al. (2001)*
Behall & Hallfrisch (2002)*‡
Anderson et al. (2002)*
Robertson et al. (2003)*
NSD Goddard et al. (1984)*† Goddard et al. (1984)*†
Behall et al. (1988)* Reiser et al. (1989)*‡¶ Reiser et al. (1989)*‡¶
Holm & Bjorck (1992)* Van Amelsvoort & Westrate (1992)* Van Amelsvoort & Westrate (1992)*
Liljeberg et al. (1994)* Westrate & van Amelsvoort (1993)* Westrate & van Amelsvoort (1993)*
Raben et al. (1994)* Ranganathan et al. (1994)* Ranganathan et al. (1994)*
Byrnes et al. (1995)* Heijnen et al. (1995)* Heijnen et al. (1995)*
Granfeldt et al. (1995)* Noakes et al. (1996)* Noakes et al. (1996)*
— Jenkins et al. (1998)* Jenkins et al. (1998)*
Nestel et al. (2004)* Nestel et al. (2004)*
Achour et al. (1997)*
Raben et al. (1997)*
Hoebler et al. (1999)*
—
Skrabanja et al. (2001)*
Behall & Hallfrisch (2002)*‡
—

*Indicates a postprandial measurement.

†Small decreases in glucose and insulin were observed at early time-points, but overall there were no significant differences in glucose or insulin levels.
‡indicates that the study group were overweight (body mass index > 25), hyperinsulinemic or diabetic
§Insulin response was measured using a urinary markers of insulin secretion only. RS3 had an effect, whereas RS2 did not.
¶
measured as glycaemic index only.
— indicates parameter not measured or results not presented.
NSD; non-significant difference.

© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

44 A. Nugent
contained extremely low (i.e. <5%) or no dietary fat
(Goddard et al. 1984; Krezowski et al. 1987; Liljeberg
1994; Raben et al. 1994; Ranganathan et al. 1994; de
Roos et al. 1995; Granfeldt et al. 1995; Heijnen et al.
1995; Larsen et al. 1996; Noakes et al. 1996; Raben
et al. 1997; Hoebler et al. 1999; Vonk et al. 2000;
Anderson et al. 2002). Two of these studies did not
match the test meals for fat content (Krezowski et al.
1987; Granfeldt et al. 1995). This is important as the fat
content of a meal lowers the glycaemic response by three
possible mechanisms: (1) by slowing the gastric empty-
ing rate; (2) by increasing the secretion of gastric inhib-
itory polypeptide (GIP) a secretagogue that stimulates
the release of insulin; and (3) by forming fat complexes
that cause conformational changes in starch/lipid com-
plexes and slow the rate and extent of their digestion
(Heijnen et al. 1995).
Problems also arise when studies fail to match the test
meals for total dietary fibre content. A good example of
a study which matched two test meals with high and low
levels of RS for total dietary fibre content is that of Van
Amelsvoort & Westrate (1992). In this study, plasma
glucose concentrations were initially decreased at
1 hour post-test meal, but at 6 h no effects on plasma
glucose and insulin levels were observed (Van Amels-
voort & Westrate 1992). In other instances, the choice
of control meal may have influenced outcomes. Reiser
et al. (1989) compared the effects of a high amylose
cornstarch with a high-fructose diet, despite the fact that
fructose itself can modulate postprandial glycaemia and
insulinaemia in rats (Lee & Wolever 1998) and in
humans (Elliott et al. 2002).
The physico-chemical properties of foods can directly
affect the amount of RS present and can also affect
blood glucose and insulin responses. The influence of
the physico-chemical properties of starchy foods on
metabolic responses is clearly indicated in the study of
Heijnen et al. (1995). In this study, RS (Ultraset; a com-
mercially manufactured high amylose starch) when pro-
vided in a drink or pudding resulted in a lowered
immediate postprandial glucose response. Only the
drink attenuated early insulin responses. The RS-
enriched pudding did not affect insulin responses and
the same RS when incorporated in a bread roll did not
affect insulin or glucose responses.
Less information is available regarding the effects of
eating diets rich in RS on long-term glucose responses
and insulin sensitivity in animals or humans; at present
available studies in humans have not lasted longer than
16 weeks and studies in animals no longer than
52 weeks (Higgins et al. 1996). Studies with rats indi-
cate that compared with feeding RS, digestible starch
causes insulin resistance (as assessed using an intrave-
nous glucose tolerance test) at 16 weeks of feeding
(Byrnes et al. 1995; Higgins et al. 1996; Wiseman et al.
1996). Long-term studies in humans are also lacking.
Behall & Howe 1995) compared the effects of high and
low RS (amylose) diets in normal and hyperinsulin-
maeic subjects for 14 weeks. Compared with a low
amylose (cornstarch) diet, the RS-rich diet caused a
decrease in the plasma insulin response as assessed by a
starch-tolerance test. However, no effect on glucose
responses was seen and the insulin data are difficult to
compare as different test-meals were used after the low
and high RS-feeding periods (Higgins 2004). In a simi-
lar study with normo-glycaemic subjects, Behall et al.
(1989) reported no significant effect on glucose
responses or insulin sensitivity (as assessed by a glucose
tolerance test) following 5 weeks of feeding a high RS-
diet. More research is needed to examine the effects of
RS on insulin sensitivity using validated methods such
as the hyperinsulinaemic-euglycaemic clamp (gold stan-
dard) method. These studies should ideally be longer in
length than 5 weeks.
More studies are also needed examining the effects of
RS on insulin and glucose responses in animals and indi-
viduals with impaired glucose responses. To date, the
majority of studies have been in healthy animals or
humans. Kim et al. (2003) showed no improvement in
blood glucose or insulin concentrations in streptozocin-
induced diabetic rats fed a RS-rich diet. Conversely,
Lintas et al. (1995a, 1995b) reported an improved glu-
cose response in volunteers with type 2 diabetes follow-
ing the consumption of diets rich in natural RS (from
durum wheat spaghetti, pearled barley or unripened
bananas), and a worsened glycaemic response following
the consumption of ripened bananas.
There is also a lack of information available regarding
the influence of chemically modified RS on insulin and
glucose metabolism. Raben et al. (1997) investigated the
effect of feeding a test-meal containing native potato
starch, 1–2% acetylated potato starch or potato starch
enriched with 2% b-cyclodextrin on a number of met-
abolic factors. The b-cyclodextrin-starch resulted in a
lower initial glucose peak that was associated with
attenuated plasma insulin and GIP. Plasma concentra-
tions of glucagon-like peptide-1 (GLP-1; a stimulator of
insulin secretion in the distal small intestine) were not
affected. The authors concluded from this study that
perhaps the b-cyclodextrin enriched starch may have
been absorbed more distally or may have resulted in
delayed gastric emptying (Raben et al. 1997); however,
in general there is a lack of information regarding the
effects of chemically modified starches.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

Resistant starch and macronutrient
oxidation, satiety and weight loss
A number of authors have examined the potential of RS
to alter macronutrient and in particular fat oxidation. It
is proposed that eating a diet rich in RS may potentially
increase the mobilisation and use of fat stores as a direct
result of any reduction in insulin secretion (Tapsell
2004). Experimentally, this is indicated by a reduced
respiratory quotient (RQ). RQ is a relative measure of
oxygen uptake and is indicative of the use of fat/carbo-
hydrate as fuel whereby a high RQ is reflective of high
carbohydrate oxidation. Studies to date in humans
would indicate that diets rich in RS do not affect total
energy expenditure, carbohydrate oxidation or fat oxi-
dation (Ranganathan et al. 1994; Tagliabue et al. 1995;
Howe et al. 1996; Raben et al. 1997). Although in the
study of Tagliabue et al. (1995) the authors found that a
RS-rich meal resulted in a short-term reduction in glu-
cose oxidation and diet-induced thermogenesis and an
increase in fat oxidation, these effects were lost after
adjusting for total carbohydrate intake (Tagliabue et al.
1995). In addition, oxidation effects were only observed
for a relatively short time period (5 h) and the test-meal
used contained no fat (Higgins 2004). Achour et al.
(1997) examined the effect of RS on RQ during a post-
absorptive period (i.e. 27 h after an initial RS-rich
mixed meal and 10 h after a second identical RS-rich
mixed meal). In this study, the authors unexpectantly
noted a significantly increased RQ (i.e. indicating
increased carbohydrate oxidation), which they attrib-
uted to increased bacterial fermentation in the colon.
Clearly, more studies are needed to examine whether RS
can influence macronutrient oxidation in humans. These
studies should be longer in duration (i.e. reflect the sev-
eral hours needed for normal transit time in humans)
and ideally should use more accurate measures of RQ
(i.e. direct calorimetry, rather than indirect calorimetry
used in the above studies).
Animal studies indicate that feeding high doses of RS
may decrease adipocyte cell size (De Deckere et al.
1993; Lerer-Metzger et al. 1996; Kabir et al. 1998;
Kishida et al. 2001) and lower fat pad weight (De Deck-
ere et al. 1993). RS was also shown to reduce the activ-
ity of lipogenic enzymes such as fatty acid synthase (the
rate limiting enzyme in fat synthesis, Younes et al. 1995)
and the expression of the protein responsible for insulin-
stimulated glucose uptake (GLUT-4; Kabir et al. 1998)
in these animals. As hypothesised by Higgins (2004) this
may imply that (at least in rats) a high-RS diet may
reduce the initial increase in plasma glucose and non-
esterified fatty acids levels, naturally observed after eat-
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 45
ing a food, and as a result attenuate glucose uptake and
lipogenesis in the adipocytes. In other words, RS may
result in a smaller fat pad size and/or mass due to
reduced glucose uptake and lipogenesis by the fat cells.
However, no information exists regarding RS and adi-
pocyte size and function in humans, and more animal
studies are needed.
Any food/food ingredient that can increase satiety
may play a vital role in weight-loss diets. Some studies
have examined the potential of RS as a satiety agent.
These appear to show a weak or no association
between RS and satiety over the course of several hours
or an entire day. de Roos et al. (1995) reported that
long-term consumption of RS was more satiating than
glucose, but the effect was small and did not affect daily
caloric intake. Anderson et al. (2002) reported that
high-RS meals caused less satiety than low-RS meals at
1 hour post-ingestion, while in the study of Skrabanja
et al. (2001) human volunteers reported that breads
rich in RS (sourced from buckwheat groats) imparted
greater satiety than white bread, but only between 70
and 120 min post-meal. RS did not affect satiety in the
studies of Holm & Bjorck (1992), Westrate & van
Amelsvoort (1993) or Mèance et al. (1999), but
resulted in satiety in those of van Amelsvoort &
Westrate (1992), Raben et al. (1994), Skrabanja et al.
(2001). It is noteworthy that these studies also showed
a decrease in blood glucose levels following the con-
sumption of a high-RS meal; therefore, it would appear
that satiety is closely linked to blood glucose levels
(Higgins 2004).
Future studies need to objectively measure satiety and
account for changes in blood glucose levels using stan-
dardised test meals matched for macronutrients and
fibre content but containing different levels of RS.
Glycaemic index, glycaemic response and
glycaemic load
The glycaemic index (GI) is a physiological concept used
to classify carbohydrate containing foods. It is closely
tied in with the term ‘glycaemic response’. Both refer to
the ability of a particular food to elevate postprandial
blood glucose concentrations. GI is measured as the
incremental area under the blood glucose curve after
consumption of 50 g of available carbohydrate from a
test food, divided by the area under the curve after eat-
ing a similar amount of available carbohydrate in a con-
trol food (generally white bread or glucose) (Ludwig &
Eckel 2002). Foods with a high GI value release glucose
rapidly into the blood stream (i.e. elicit a rapid glycae-
mic response), while foods with a low GI value release
46 A. Nugent
glucose more slowly into the bloodstream and result in
improved glycaemic and insulinaemic responses. They
may also modulate macronutrient (fat) oxidation.
Recently, there has been a flurry of public and commer-
cial interest in the GI concept and its possible inclusion
on food labels, both as an aid for the management of
diabetes and to indicate potential foods that may aid
weight loss and management (McKevith 2004). It is
known that dietary fibre may contribute to an improved
(i.e. slower more controlled) glycaemic response and, in
general, high-fibre foods are assigned a lower GI value.
Interest is now increasing in assigning GI values to RS-
rich foods. However, it must be remembered that for
foods enriched with truly resistant starches, a reduced
glycaemic response may simply result from a lack of
available digestible starch, rather than any specific phys-
iological effects per se and that any readily digestible
starch present in the food would be absorbed as normal
(Hoebler et al. 1999; Jenkins et al. 2002). Nonetheless
there will be a physiological effect as a result of lowering
the content of digestible starch by replacing it with RS.
Glycaemic index refers to the nature of carbohydrate
in a food. However, people eat meals (mixes of foods)
and generally carbohydrate-containing foods are eaten
alongside foods containing protein and/or fat. In addi-
tion, the total carbohydrate content (quantity) varies
between foods. To account for this, the concept of gly-
caemic load (GL) was developed which considers both
the carbohydrate content per serving of a food and its
GI value, i.e. the quantity and nature of carbohydrate
present. Using GL, it is easier to account for a range of
foodstuffs and also portion size. It is possible to lower
GL by replacing the carbohydrate content with protein,
fat or other lower GI carbohydrates. As RS has a low
glycaemic response, adding it as an ingredient to foods
will help lower the overall GL value of the food (par-
ticularly if it is replacing existing readily absorbed forms
of carbohydrate). Since the concept of GI and GL is
becoming more popular in the public domain, RS is
likely to become an increasingly attractive ingredient to
many food manufacturers (particularly those of breads
and cakes or similar products which traditionally may
have had higher GI value).
Other health benefits associated with
resistant starch
Resistant starch is reported to enhance the ileal absorp-
tion of a number of minerals in rats and humans. Lopez
et al. (2001) and Younes et al. (1995) reported an
increased absorption of calcium, magnesium, zinc, iron
and copper in rats fed RS-rich diets, in contrast Kishida
et al. (2001) reported no effect. In humans, these effects
appear to be limited to calcium (Trinidad et al. 1996;
Coudray et al. 1997). RS may therefore improve the
ileal absorption of a number of dietary minerals but any
effect in humans is likely to be small.
More recently RS has been reported to influence
immune function, particularly the production of a num-
ber of pro-inflammatory cytokines (e.g. tumour necrosis
factor alpha) and the expression of a number of recep-
tors on T- and B-lymphocytes and macrophages that are
required for the initiation of immune responses [cluster
of definition 3 (CD3), CD4, CD8, lymphocyte function-
associated antigen-1 (LFA-1), intercellular adhesion
molecule-1 (ICAM-1), Mac-1] (Segain et al. 2000; Sot-
nikova et al. 2002). If RS can beneficially modulate
immune function it could impart real benefits to patients
with inflammatory bowel disease. Therefore, the
immuno-modulatory potential of RS, particularly on
gut-associated immune cells, warrants further research.
Putative mechanisms of action of
resistant starch
With respect to gut health, RS may impart some benefits
by decreasing transit time and increasing faecal output.
Prebiotics effects associated with the consumption of
RS, such as the growth of beneficial microbial popula-
tions and a lowered activity of certain bacterial enzymes
(e.g. b-glucuronidase), would be expected to have ben-
eficial impacts on colonic bacterial activity (Young & Le
Leu 2004).
However, it is likely that RS mediates some or a large
proportion of its effects through the actions of SCFA.
As mentioned earlier, SCFA are important fuels for
maintaining normal colonic function; they can regulate
colonocyte gene expression, cell cycle and apoptosis
and can also exert trophic effects on the colonic epithe-
lium (Mentschel & Claus 2003). Recently it has been
reported that butyrate can directly inhibit inflamma-
tory responses by down-regulating the activity of the
transcription factor Nuclear Factor kappa B (NF-kB).
NF-kB is a central regulator of many immune and
inflammatory responses and increased activity of NF-
kB has been observed in patients with inflammatory
bowel disease (Segain et al. 2000). Therefore, it is pos-
sible that RS may mediate some of its beneficial effects
on colonic function (particularly in inflammatory
bowel disease) by increasing the production of
butyrate, which may in turn influence NF-kB expres-
sion and activity.
Increasing SCFA production also lowers colonic pH
and increases the excretion of bile acids. A lowered pH
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

is thought to be protective against colorectal cancer and
inhibits the transformation of primary to secondary bile
acids. Secondary bile acids are cytotoxic to colonic cells
and are thought to be tumour promoters (Young & Le
Leu 2004). Therefore, RS may also confer benefits to gut
health via the actions of SCFA on pH and a reduced pro-
duction of secondary bile acids.
One of the SCFA acetate can inhibit cholesterolgene-
sis and is lipolytic in rats: in humans it can decrease the
availability of free fatty acids (high concentrations of
free fatty acids are deleterious for human health as they
are associated with decreased insulin sensitivity and
impaired glucose uptake). Propionate is an effective
inhibitor of fatty acid and cholesterol synthesis in vitro
(Beynen et al. 1982; Berggren et al. 1996). In the study
of Cheng & Lai (2000), the authors hypothesised that
the decrease in serum total cholesterol observed was
linked to an increased production of propionate,
another SCFA. However, it is unlikely that propionate is
responsible for these reductions in cholesterol as RS was
found to reduce plasma cholesterol levels in germ-free
mice (i.e. mice lacking the microbial population neces-
sary to produce propionate) (Sacquet et al. 1983).
Therefore, RS may exert its effects on metabolic factors
through these SCFA, but any effect on lipid metabolism
in humans is unlikely to be mediated by propionate
alone and is likely to be much less than that reported
in vitro or in animal studies.
With respect to lipid and glucose metabolism and
insulin sensitivity, there are a number of other mecha-
nisms by which RS could exert its effects. RS is reported
to increase the activity of the enzyme HMG-CoA
(3-hydroxy-3-methylglutaryl-co A; the rate limiting
enzyme in cholesterol synthesis) and to decrease the
expression of fatty acid synthase (FAS; the enzyme
responsible for the rate limiting step in fat synthesis) and
GLUT4 (the protein responsible for insulin-stimulated
glucose uptake) (Younes et al. 1995; Kabir et al. 1998),
but it had no effect on the activity of the enzyme lipo-
protein lipase in rats (De Deckere et al. 1993). RS is also
reported to decrease total cholesterol absorption (Lopez
et al. 2001), to alter the balance of secretion of the hor-
mones glucagon and insulin (Champ 2004), to increase
the expression of the hepatic LDL receptor in rats
(Fukushima et al. 2001) and to enhance bile acid secre-
tion (Mathe et al. 1993; Kishida et al. 2001). All of
these effects would directly affect lipid and glucose
metabolism. However, critically and unlike soluble
dietary fibre, RS arriving in the colon is not viscous and
has no ion exchange properties; therefore this mecha-
nism is unlikely to be responsible for any lipid-lowering
effects following the consumption of RS.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 47
With respect to all of the above mentioned physiolog-
ical effects, it is noteworthy that the different forms of
RS should not be assumed to be physiologically equiv-
alent. As mentioned earlier, large intra-individual differ-
ences exist between the amount of RS reaching the
colon. Indeed in one human study (Cummings et al.
1996), fermentation of RS was impaired in 26% of
cases. In addition, as it is impossible to quantify the
amount of RS reaching the human colon, researchers
must rely on the use of in vitro or indirect methods of
assessment. It is likely that physiological responses will
be affected by type and dose of RS used, whether the RS
was used as an individual food or included as a whole
meal, the level at which other macronutrients are
included and what cooking conditions were used. It is
important to stress that a lot of the studies analysed in
this review have used foods or drinks enriched with
uncooked commercially available starches, generally at
doses much higher than that consumed as part of a nor-
mal diet. As part of normal dietary intakes, humans
usually obtain RS from cooked foods, e.g. corn-flakes,
cooked breads and pastas, and cooked and chilled pota-
toes, and the influence of RS from these foodstuffs also
merits attention. Furthermore, the majority of studies
have used animal models. Pigs are often used as a model
for human because they will eat similar foods to
humans and their digestive system performs in a man-
ner closer to humans than many other animal models
but chemical agents commonly used to induce colon
cancer in experimental animals cannot be used in pigs
as they result in hepatic necrosis without intestinal can-
cer. In addition, no genetically predisposed porcine
model of colon cancer exists, resulting in rodents and
mice being commonly used despite the fact that they
practice coprophagy. Coprophagy is the process
whereby food passes through their digestive system
twice and is likely to influence SCFA production
(Topping & Clifton 2001).
Safety of resistant starch
Resistant starch appears to have no adverse impact on
gastrointestinal function in well-nourished people and
may even promote health in children with diarrhoeal
disease (Topping & Clifton 2001). In addition, it
appears to be more readily acceptable than other
forms of dietary fibre (e.g. wheat bran) at high levels
in the human diet (Ferguson et al. 2003). It has been
reported that it is not feasible for humans to consume
more than 30 g/day of RS due to problems with flatu-
lence, belching, bloating, mild laxative effects and
stomach aches (Heijnen et al. 1996); however, it is
48 A. Nugent
unlikely that humans would consume such high levels
of RS without aggressive supplementation and in some
instances RS was supplemented in association with
other forms of dietary fibre. No cases of allergic reac-
tions have been reported following supplementation
with more traditional forms of RS, such as those made
from high amylose maize (Goldring 2004). At present,
other new sources of starch being used which are
based on other types of starch including tapioca,
potato and wheat. At present, there is little informa-
tion regarding their effects, or those of RS4, in
humans; more comprehensive information and studies
are needed in vivo.
Labelling and legislation of fibre and
resistant starch
At present, there is no legal definition for RS and with
respect to labelling, RS falls under the remit of dietary
fibre. Several countries including the USA, UK, Austra-
lia, Canada, Denmark, Finland, Italy, Sweden and Japan
use the AOAC method 985.29 (Prosky et al. 1985) for
measuring and labelling the dietary fibre content of
foods. As this method accounts for some of the RS
present within foods, part of the published value for
fibre will include RS, if present. The UK has tradition-
ally used the Englyst method (Englyst et al. 1992) for
determining dietary fibre; this method does not measure
RS present in foods. Although, the Food Standards
Agency (UK) now recommends that industry use the
AOAC method (which does measure some RS), prob-
lems arise as the UK government recommendations for
population dietary fibre intakes are still based on the
Englyst method. In addition, the existing UK food com-
position tables list dietary fibre values as measured by
the Englyst method. These food composition tables are
used by health professionals, some food manufacturers
and catering outlets to determine the fibre content of
foods and diets eaten.
The agreed energy value for carbohydrates is 4 kcal/g.
In Europe, the Nutrition Labelling Directive does not
specify an energy value to be used for fibre, and the
value is therefore considered to be zero (BNF 2002). In
Australia and Japan, dietary fibres have been assigned
higher energy values (of 1.8 kcal/g and 2 kcal/g), respec-
tively. In the USA, labelling of total dietary fibre is
mandatory. The labelling of soluble and insoluble
dietary fibre is optional and a labelling scheme has been
defined whereby the energy value assigned to insoluble
fibre is 0 kcal/g and the energy value for soluble fibre is
4 kcal/g.
Currently, non-modified resistant starches are consid-
ered safe under existing food classifications and legisla-
tions in the US and in Europe. In Europe and the EU,
chemically modified starches are regulated as modified
starches under the European Parliament and Council
Directive 95/2/EC in Europe and under 21 CFR
172.892 in the US. Canada has a distinct legislative pro-
cess for all novel dietary fibres, however, as yet resistant
starches have not been evaluated in Canada and cannot
be claimed on the product label.
Globally, there is increasing interest amongst manu-
facturers of commercial sources of RS in labelling foods
rich in RS. This is mainly due to the desirable properties
associated with foods rich in RS: their potential health
benefits and lowered food energy value in foods where
RS replaces digestible starch. Both are of interest to food
manufacturers who wish to include RS as an ingredient
in low-energy and low-carbohydrate foodstuffs and
slimming/‘diet’ products. The US allows manufacturers
to label foods with terms such as ‘resistant’ or ‘indigest-
ible’, but they must clearly label the legally approved
name of the corresponding starches. The US also allows
self-declared ‘structure-function’ claims without restric-
tion (e.g. fibre maintains bowel regularity), but restric-
tions exist regarding ‘health’ claims linking food
substances with diseases (e.g. antioxidants may reduce
the risk of cancer).These claims must be supported by
scientific factual evidence. In contrast in the EU, no dis-
tinction between structure-function and health claims is
made, and under current regulations, no preventative,
curative or disease treatment properties can be assigned
to particular foods (BNF 2002). Proposed EU legislation
would allow nutrition and health claims, but only for
certain categories. With respect to label claims on RS-
rich foods in Europe, much will depend on the final
details of these new regulations.
For food labelling purposes, producers and regulators
first need an agreed definition and method of analysis
for both dietary fibre and RS. The use of different meth-
ods of analysis of dietary fibre makes comparisons of the
fibre content of foodstuffs difficult between countries.
With respect to RS, an agreed method is needed that is
robust, reproducible, repeatable and simple to complete.
Consensus on such an agreed method is likely to be
hotly debate as the amount of RS in foods will continue
to be affected by external influences such as degree of
ripeness, transit time, extent of chewing.
Conclusion
Resistant starch, the portion of starch and starch prod-
ucts that resist digestion, appears to confer several
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

health benefits. It may confer considerable benefits to
human colonic health, but appears to have less of an
impact on markers of lipid and glucose metabolism.
Comparisons between studies are hampered by poor
experimental design and differences in the type and dose
of RS used. It is likely that RS mediates some or all of its
effects through the action of SCFA but interest is
increasing regarding its prebiotic effects. At present, RS
is included under the umbrella of the Institute of Med-
icine of the National Academies and the AACC defini-
tions of dietary fibre and it is measured under the remit
of the AOAC method for analysis of dietary fibre and
labelled accordingly. In the UK, the AOAC method is
recommended by the Food Standards Agency as the
method of choice for measuring dietary fibre. However,
confusion arises as the government recommendations
for population dietary intakes of fibre, and existing food
composition tables, are based on the Englyst method
(which does not account for RS). Pressure to agree a
legal definition and universal method for the analysis of
both RS and dietary fibre is likely to increase, due to the
potential of RS to enhance colonic health and to act as
a vehicle to increase the total dietary fibre content of
foodstuffs, particularly those which are low in energy
and in total carbohydrate content. Future research pri-
orities include a more in-depth exploration of the effects
of RS on colonic function and inflammatory bowel dis-
ease. There is also a need for properly designed, con-
trolled studies to determine the exact effects of RS on
human lipid and glucose metabolism, particularly over
longer time periods and, in individuals with impaired
glucose responses. The potential of RS as an agent in
weight loss and maintenance regimens will undoubtedly
be explored as part of attempts to curb the global
increasing incidence of obesity. An analysis of the cost/
benefit ratio of such an intervention in comparison with
other dietary manipulations and pharmacological treat-
ments would be useful. As yet, the exact mechanisms of
action by RS remain unknown and more studies are
needed to confirm whether these effects are mediated via
SCFA and/or prebiotic effects. However, there is a real
need to determine the molecular mechanisms of action
of RS. It has been reported that butyrate (a product of
RS fermentation) can influence the transcription factor
NF-kB, but more information is needed regarding its
potential effects on other molecular pathways.
Acknowledgements
The author wishes to thank National Starch and Chem-
ical Limited for financial support in the publication of
the finished report.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 49
References
Achour L, Flourie B, Briet F et al. (1997) Metabolic effects of digest-
ible and partially indigestible cornstarch: a study in the absorptive
and postabsorptive periods in healthy humans. American Journal of
Clinical Nutrition 66: 1151–9.
Anderson GH, Catherine NL, Woodend DM et al. (2002) Inverse
association between the effect of carbohydrates on blood glucose
and subsequent short-term food intake in young men. American
Journal of Clinical Nutrition 76: 1023–30.
Andoh A, Tsujikawa T & Fujiyama Y (2003) Role of dietary fibre and
short-chain fatty acids in the colon. Current Pharmaceutical Design
9 (4): 347–58.
Anon (2000) AACC Board holds midyear meeting. Cereal Foods
World 45: 325.
Asp NG (1992) Resistant Starch-Proceedings from the second plenary
meeting of EURESTA: European FLAIR Concerted Action, 11 on
physiological implications of the consumption of resistant starch in
man. Preface. European Journal of Clinical Nutrition 46: S1.
Baghurst PA, Baghurst KI & Record SJ (1996) Dietary fibre, non-
starch polysaccharides and resistant starch – a review. Supplement
to Food Australia 48 (3): S3–S35.
Baghurst K, Baghurst PA & Record SJ (2001) Dietary fibre, non-
starch polysaccharide and resistant starch intakes in Australia. In:
CRC Handbook of Dietary Fibre in Human Health, (GA Spiller
ed.), pp. 583–91. CRC Press LLC, Boca Raton, FL, USA.
Behall KM & Hallfrisch J (2002) Plasma glucose and insulin reduc-
tion after consumption of breads varying in amylose content. Euro-
pean Journal of Clinical Nutrition 56: 913–20.
Behall KM & Howe JC (1995) Effect of long-term consumption of
amylose vs amylopectin starch on metabolic variables in human
subjects. American Journal of Clinical Nutrition 61: 334–40.
Behall KM, Scholfield DJ & Canary J (1988) Effect of starch structure
on glucose and insulin responses in adults. American Journal of
Clinical Nutrition 47: 429–32.
Behall KM, Scholfield DJ, Yuhaniak I et al. (1989) Diets containing
high amylose vs amylopectin starch: effects on metabolic variables
in human subjects. American Journal of Clinical Nutrition 49: 337–
44.
Berggren AM, Nyman MGL & Lundquist I (1996) Influence of orally
and rectally administered propionate on cholesterol and glucose
metabolism in obese rats. British Journal of Nutrition 76: 287–94.
Beynen AC, Buechler K & Van Der Molen AJ (1982) The effects of
lactate and acetate on fatty acid and cholesterol biosynthesis by iso-
lated rat hepatocytes. International Journal of Biochemistry 14:
165–9.
Bingham SA, Day NE, Luben R et al. (2003) Dietary fibre in food and
protection against colorectal cancer in the European Prospective
Investigation into Cancer and Nutrition (EPIC): an observational
study. Lancet 362 (9388): 1000.
Bird AR, Brown IL & Topping DL (2000a) Starches, resistant
starches, the gut microflora and human health. Current Issues in
Intestinal Microbiology 1 (1): 25–37.
Bird AR, Hayakawa T, Marsono Y et al. (2000b) Coarse brown rice
increases faecal and large bowel short-chain fatty acids and starch
but lowers calcium in the large bowel in pigs. Journal of Nutrition
130: 1780–7.
Birkett AM, Mathers JC, Jones GP et al. (2000) Changes to the quan-
tity and processing of starchy foods in a Western diet can increase
50 A. Nugent
polysaccharides escaping digestion and improve in vitro fermenta-
tion variables. British Journal of Nutrition 84: 63–72.
Birkett A, Muir J, Phillips J et al. (1996) Resistant starch lowers fecal
concentrations of ammonia and phenols in humans. American Jour-
nal of Clinical Nutrition 63: 766–72.
BNF (1990) Complex Carbohydrates in Foods: the Report of The
British Nutrition Foundation’s Task Force. Chapman & Hall, Lon-
don.
BNF (1994) Briefing Paper: Starchy Foods in the Diet. BNF, London.
BNF (2002) Briefing Paper: Nutrition Labelling and Health Claims.
BNF, London.
Brown I (1996) Complex carbohydrates and resistant starch. Nutri-
tion Reviews 54 (11): S115–19.
Brown IL (2004) Applications and uses of resistant starch. Journal of
the Association of Official Analytical Chemists International 87 (3):
727–32.
Brown IL, McNaught KJ & Moloney E (1995) Hi-maize™: new
directions in starch technology and nutrition. Food Australia 47:
272–5.
Brown MA, Storlien LH, Brown IL et al. (2003) Cooking attenuates
the ability of high-amylose meals to reduce plasma insulin concen-
trations in rats. British Journal of Nutrition 90: 823–7.
Brown IL, Wang X, Topping DL et al. (1998) High amylose maize
starch as a versatile prebiotic for use with probiotic bacteria. Food
Australia 47: 272–5.
Brown I, Warhurst M, Arcot J et al. (1997) Fecal numbers of Bifido-
bacteria are higher in pigs fed Bifidobacterium longum with a high
amylose cornstarch than with a low amylose cornstarch. Journal of
Nutrition 127: 1822–7.
Byrnes SE, Miller JC & Denyer GS (1995) Amylopectin starch pro-
motes the development of insulin resistance in rats. Journal of
Nutrition 125: 1430–7.
Caderni G, Luceri C, Lancioni L et al. (1996) Dietary sucrose, glucose,
fructose, and starches affect colonic function in rats. Nutrition and
Cancer 25 (2): 179–86.
Cassand P, Maziere S, Champ M et al. (1997) Effects of resistant
starch-and vitamin A-supplemented diets on the promotion of pre-
cursor lesions of colon cancer in rats. Nutrition and Cancer 27: 53–
9.
Cassidy A, Bingham SA & Cummings JH (1994) Starch intake and
colorectal cancer risk: an international comparison. British Journal
of Cancer 69: 937–42.
Champ MJ (2004) Physiological aspects of resistant starch and in vivo
measurements. Journal of the Association of Official Analytical
Chemists International 87 (3): 749–55.
Champ M, Langkilde AM, Brouns F et al. (2003a) Advances in
dietary fibre characterisation. 1. Definition of dietary fibre, physio-
logical relevance, health benefits and analytical benefits. Nutrition
Research Reviews 16: 71–82.
Champ M, Langkilde AM, Brouns F et al. (2003b) Advances in
dietary fibre characterization. 2. Consumption, chemistry, physiol-
ogy and measurement of resistant starch; implications for health
and food labelling. Nutrition Research Reviews 16: 143–61.
Cheng HH & Lai MH (2000) Fermentation of resistant rice starch
produces propionate reducing serum and hepatic cholesterol in rats.
Journal of Nutrition 130: 1991–5.
Christl SU, Murgatroyd PR, Gibson GR et al. (1992) Production,
metabolism, and excretion of hydrogen in the large intestine. Gas-
troenterology 102: 1269–77.
Conlon MA & Bird AR (2003) Interactions of dietary fibre and resis-
tant starch with oil on genetic damage in the rat colon. Asia Pacific
Journal of Clinical Nutrition 12: S54.
Conway PL (2001) Prebiotics and human health: the state-of-the-art
and future perspectives. Scandinavian Journal of Nutrition 45: 13–
21.
Coudray C, Bellanger J, Castiglia-Delavaud C et al. (1997) Effect of
soluble or partly soluble dietary fibres supplementation on absorp-
tion and balance of calcium, magnesium, iron and zinc in healthy
young men. European Journal of Clinical Nutrition 51: 375–80.
Crittenden RG, Morris LF, Harvey ML et al. (2001) Selection of a
Bifidobacterium strain to complement resistant starch in a synbiotic
yoghurt. Journal of Applied Microbiology 90: 268–78.
Crosby GA (2003) Resistant starch makes better carbs. Functional
Foods and Nutraceuticals 6: 34–6.
Cummings JH, Beatty ER, Kingman SM et al. (1996) Digestion and
physiological properties of resistant starch in the human large
bowel. British Journal of Nutrition 75: 733–47.
Cummings JH, Pomare EW, Branch WJ et al. (1987) Short chain fatty
acids in human large intestine, portal, hepatic and venous blood.
Gut 28: 1221–7.
De Deckere EAM, Kloots WJ & van Amelsvoort JMM (1993) Resis-
tant starch decreases serum total cholesterol and triacylglycerol
concentrations in rats. Journal of Nutrition 123: 2142–51.
De Deckere EAM, Kloots WJ & van Amelsvoort JMM (1995) Both
raw and retrograded starch decrease serum triacylglycerol concen-
tration and fat accretion in the rat. British Journal of Nutrition 73:
287–98.
De Vries JW (2003) Defining dietary fibre. Proceedings of the Nutri-
tion Society 61 (1): 37–43.
De Vries JW (2004) Dietary fibre: the influence of definition on anal-
ysis and regulation. Journal of the Association of Official Analytical
Chemists International 87 (3): 682–706.
Demigné C, Rémésy C & Morand C (2001) Resistant Starches and
lipid metabolism. In: Handbook of Dietary Fibre, (SS Cho & M
Kreher eds), pp. 159–68. Marcel Dekker Inc., New York, USA.
DH (1991) Report on Health and Social Subjects, No 41. Dietary
Reference Values for Food Energy and Nutrients for the United
Kingdom. HMSO: London.
Dyssler P & Hoffmann D (1994) Estimation of resistant starch intake
in Europe. In: Proceedings of the Concluding Plenary Meeting of
EURESTA, (N-G Asp, J MM van Amelsvoort & JGAJ Hautvast
eds), pp. 84–6. EURESTA, Wageningen, The Netherlands.
Ebihara K, Shiraishi R & Okuma K (1998) Hydroxypropyl-modified
potato starch increases fecal bile acid excretion in rats. Journal of
Nutrition 128: 848–54.
Elliott SS, Keim NL, Stern JS et al. (2002) Fructose, weight gain, and
the insulin resistance syndrome. American Journal of Clinical
Nutrition 76 (5): 911–22.
Englyst HN, Kingman SM & Cummings JH (1992) Classification and
measurement of nutritionally important starch fractions. European
Journal of Clinical Nutrition 46 (2): S33–50.
Englyst HN, Kingman SM, Judson GJ et al. (1996) Measurement of
resistant starch in vitro and in vivo. British Journal of Nutrition 75:
749–55.
Englyst H, Wiggins HS & Cummings JH (1982) Determination of the
non-starch polysaccharides in plant foods by gas-liquid chromatog-
raphy of constituent sugars as alditol acetates. Analyst 107: 307–
18.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

Ferguson LR, Tasman-Jones C, Englyst H et al. (2000) Comparative
effects of three resistant starch preparations on transit time and
short-chain fatty acid production in rats. Nutrition and Cancer 36
(2): 230–7.
Ferguson LR, Zhu S & Kestell P (2003) Contrasting effects of non-
starch polysaccharide and resistant starch-based diets on the dispo-
sition and excretion of the food carcinogen, 2-amino-3-methylimi-
dazo[4,5-f]quinoline (IQ), in a rat model. Food Chemistry and
Toxicology 41: 785–92.
Fukushima M, Ohashi T, Kojima M et al. (2001) Low density lipo-
protein receptor mRNA in rat liver is affected by resistant starch of
beans. Lipids 36: 129–34.
Gibson GR & Roberfroid MB (1995) Dietary modulation of the
human colonic microbiota: introducing the concept of prebiotics.
Journal of Nutrition 125: 1401–12.
Giovannucci E, Stampfer MJ, Colditz G et al. (1992) Relationship of
diet to risk of colorectal adenoma in men. Journal of the National
Cancer Institute 84: 91–8.
Goddard MS, Young G & Marcus R (1984) The effect of amylose
content on insulin and glucose responses to ingested rice. American
Journal of Clinical Nutrition 39: 388–92.
Goldring JM (2004) Resistant starch: safe intakes and legal status.
Journal of the Association of Official Analytical Chemists Interna-
tional 87 (3): 733–9.
Granfeldt Y, Drews A & Bjorck I (1995) Arepas made from high amy-
lose corn flour produce favorably low glucose and insulin responses
in healthy humans. Journal of Nutrition 125: 459–65.
Grubben MJ, van den Braak CC, Essenberg M et al. (2001) Effect of
resistant starch on potential biomarkers for colonic cancer risk in
patients with colonic adenomas: a controlled trial. Digestive Dis-
eases and Sciences 46 (4): 750–6.
Haenszel W, Locke FB & Segi M (1980) A case-control study of large
bowel cancer in Japan. Journal of National Cancer Institute 64: 98.
Hampson DJ, Robertson ID, La T et al. (2000) Influences of diet
and vaccination on colonization of pigs by the intestinal spirocha-
ete. Brachyspira (Serpulina) Pilosicoli Veterinary Medicine 73:
75–84.
Han KH, Fukushima M, Kato T et al. (2003a) Enzyme-resistant
fractions of beans lowered serum cholesterol and increased sterol
excretions and hepatic mRNA levels in rats. Lipids 38 (9): 919–
24.
Han KH, Fukushima M, Shimizu K et al. (2003b) Resistant
starches of beans reduce the serum cholesterol concentrations in
rats. Journal of Nutritional Science and Vitaminology (Tokyo) 49:
281–6.
Heijnen ML, Deurenberg P, van Amelsvoort JMM et al. (1997) Ret-
rograded (RS3) but not uncooked (RS2) resistant starch lowers fae-
cal ammonia concentrations in healthy men. American Journal of
Clinical Nutrition 65: 167–8.
Heijnen ML, Van Amelsvoort JMM, Deurenberg P et al. (1996) Nei-
ther raw nor retrograded resistant starch lowers fasting serum cho-
lesterol concentrations in healthy normolipidaemic subjects.
American Journal of Clinical Nutrition 64: 312–18.
Heijnen ML, van Amelsvoort JMD, Eurenberg P et al. (1998) Limited
effect of consumption of uncooked (RS2) or retrograded (RS3)
resistant starch on putative risk factors for colon cancer in healthy
men. American Journal of Clinical Nutrition 67: 322–31.
Heijnen ML, van Amelsvoort JM & Westrate JA (1995) Interaction
between physical structure and amylose: amylopectin ratio of foods
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 51
on postprandial glucose and insulin responses in healthy subjects.
European Journal of Clinical Nutrition 49: 446–57.
Henderson L, Gregory J, Irving K et al. (2003) The National Diet and
Nutrition Survey: Adults Aged 19–64 Years, Volume 2: Energy, Pro-
tein, Carbohydrate, Fat and Alcohol Intake. HMSO, London.
Henningsson AM, Margareta E, Nyman GL et al. (2003) Influences of
dietary adaptation and source of resistant starch in the hindgut of
rats. British Journal of Nutrition 89 (3): 319–28.
Higgins JA (2004) Resistant starch: metabolic effects and potential
health benefits. Journal of the Association of Official Analytical
Chemists International 87 (3): 761–8.
Higgins JA, Brand Miller JC & Denyer GS (1996) Development
of insulin resistance in the rat is dependent on the rate of glu-
cose absorption from the diet. Journal of Nutrition 126 (5):
596–602.
Hoebler C, Karinthi A, Chiron H et al. (1999) Bioavailability of starch
in bread rich in amylose: metabolic responses in healthy subjects
and starch structure. European Journal of Clinical Nutrition 53:
360–6.
Holm J & Bjorck I (1992) Bioavailability of starch in various wheat-
based bread products: evaluation of metabolic responses in healthy
subjects and rate and extent of vitro starch digestion. American
Journal of Clinical Nutrition 55: 420–9.
Howe JC, Rumpler WV & Behall KM (1996) Dietary starch compo-
sition and level of energy intake alter nutrient oxidation in ‘carbo-
hydrate-sensitive’ men. Journal of Nutrition 126: 2120–9.
Hylla S, Gostner A, Dusel G et al. (1998) Effects of resistant starch on
the colon in healthy volunteers: possible implications for cancer pre-
vention. American Journal of Clinical Nutrition 67: 136–42.
Imberty A, Buléon A, Tran V & Pérez S (1991) Recent Advances in
knowledge of starch structure. Starch 43: 375–84.
Institute of Medicine (2002) Dietary Reference Intakes: Energy, Car-
bohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino
Acids. National Academies Press, Washington, DC.
Jacobasach G, Schmiedl D, Kruschewski M et al. (1999) Dietary resis-
tant starch and chronic inflammatory bowel diseases. International
Journal of Colorectal Disease 14 (4–5): 201–11.
Jenkins DJ, Kendal CW, Augustin LS et al. (2002) High-complex car-
bohydrate or lente carbohydrate foods? American Journal of Med-
icine 113: 30S–37S.
Jenkins JA, Vuksan V, Kendall CWC et al. (1998) Physiological effects
of resistant starches on fecal bulk, short chain fatty acids, blood lip-
ids and glycaemic index. Journal of the American College of Nutri-
tion 17 (6): 609–16.
Jones (2000) Update on defining dietary fibre. Cereal Foods World 45:
219–20.
Kabir M, Rizkalla SW, Quignard-Boulange A et al. (1998) A high gly-
cemic index starch diet affects lipid storage-related enzymes in nor-
mal and to a lesser extent in diabetic rats. Journal of Nutrition 128:
35–43.
Kestell P, Zhu S, Ferguson LR (2004) Mechanisms by which resistant
starches and non starch polysaccharide sources affect the metabo-
lism and disposition of the food carcinogen, 2-amino-3-methylimi-
dazo [4,5-F] quinoline. Journal of Chromatography Analytical
Technologies in the Biomedical and Life Sciences 802: 201–10.
Kim WK, Chung MK, Kang NE et al. (2003) Effect of resistant starch
from corn or rice on glucose control, colonic events, and blood lipid
concentrations in streptozotocin-induced diabetic rats. Journal of
Nutritional Biochemistry 14: 166–72.
52 A. Nugent
Kishida T, Nogami H, Himeno S et al. (2001) Heat moisture treat-
ment of high amylose cornstarch increases its resistant starch con-
tent but not its physiologic effect in rats. Journal of Nutrition 131:
2716–21.
Kleeson B, Stoof G, Proll J et al. (1997) Feeding resistant starch affects
fecal and cecal microflora and short-chain fatty acids in rats.
Journal of Animal Science 75: 2453–62.
Krezowski PA, Nuttall FO, Gannon MC et al. (1987) Insulin and glu-
cose responses to various starch-containing foods in type II diabetic
subjects. Diabetes Care 10 (2): 205–12.
Larsen HN, Rasmussen OW, Rasmussen PH et al. (1996) Glycaemic
index of parboiled rice depends on the severity of processing: study
in type 2 diabetic subjects. European Journal of Clinical Nutrition
54: 380–5.
Le Leu RK, Brown IL, Hu Y et al. (2003) Effect of resistant starch on
genotoxin-induced apoptosis, colonic epithelium, and lumenal con-
tents in rats. Carcinogenesis 24: 1347–52.
Lee B & Wolever T (1998) Effect of glucose, sucrose and fructose on
plasma glucose and insulin responses in normal humans: compari-
son with white bread. European Journal of Clinical Nutrition 52:
924–8.
Lerer-Metzger M, Rizkalla SW, Luo J et al. (1996) Effects of long-
term low-glycaemic index starchy food on plasma glucose and lipid
concentrations and adipose tissue cellularity in normal and diabetic
rats. British Journal of Nutrition 75: 723–32.
Liljeberg H (1994) Bioavailability of starch in bread products. Post-
prandial glucose and insulin responses in healthy subjects and in
vitro resistant starch content. European Journal of Clinical Nutri-
tion 48: 151–63.
Lintas C, Cappelloni M, Adorisio S et al. (1995b) Effect of ripening on
resistant starch and total sugars in Musa paradisiacal sapientum:
glycaemic and insulinaemic responses in normal subjects and
NIDDM patients. European Journal of Clinical Nutrition 49:
S303–306.
Lintas C, Cappelloni M, Bonmassar L et al. (1995a) Dietary fibre,
resistant starch and in vitro starch digestibility of cereal meals. Gly-
caemic and insulinaemic responses in NIDDM patients. European
Journal of Clinical Nutrition 49: S264–S267.
Liversey G (1994) Energy value of resistant starch. In: Proceedings
of the Concluding Plenary Meeting of EURESTA, (N-G Asp,
JMM van Amelsvoort & JGAJ Hautvast eds), pp. 56–62. EUR-
ESTA, Wageningen, The Netherlands.
Lopez HW, Levrat-Verny MA, Coudray C et al. (2001) Class 2 resis-
tant starches lower plasma and liver lipids and improve mineral
retention in rats. Journal of Nutrition 131: 1283–9.
Ludwig DS & Eckel RH (2002) The glycaemic index at 20y. American
Journal of Clinical Nutrition 76: 264S–5S.
McCleary BV & Monaghan DA (2002) Measurement of resistant
starch. Journal of the Association of Official Analytical Chemists
International 85: 665–75.
McCleary BV & Rossiter P (2004) Measurement of novel dietary
fibres. Journal of the Association of Official Analytical Chemists
International 87 (3): 707–17.
MacFarlane S & MacFarlane GT (2003) Regulation of short-chain
fatty acid production. Proceedings of the Nutrition Society 62 (1):
67–72.
McKevith BM (2004) Nutritional aspects of cereals. Nutrition Bulle-
tin 29 (2): 111–42.
Macquart-Moulin G, Riboli E, Cornee J et al. (1986) Case-control
study on colorectal cancer and diet in Marseilles. International
Journal of Cancer 38: 183–91.
Mahon LK & Arlin MT (1992) Krause’s Food, Nutrition and Diet
Therapy. W.B. Saunders Company: Philadelphia, USA.
Martin LJM, Dumon HJW, Lecannu G et al. (2000) Potato and high-
amylose maize starches are not equivalent producers of butyrate for
the colonic mucosa. British Journal of Nutrition 84: 689–96.
Mathé D, Riottot M, Rostaqui N et al. (1993) Effect of amylomaize
starch on plasma lipoproteins of lean and obese zucker rats. Journal
of Clinical Biochemistry and Nutrition 14: 17–21.
Mathers JC, Mickleburgh I, Chapman PC et al. (2003) Can resistant
starch and/or aspirin prevent the development of colonic neoplasia?
Proceedings of the Nutrition Society 62 (1): 51–7.
Maziere S, Meflah K, Tavan E et al. (1998) Effect of resistant starch
and/or fat-soluble vitamins A and E on the initiation stage of aber-
rant crypts in rat colon. Nutrition and Cancer 31 (3): 168–77.
Mèance S, Achour L, Briend A (1999) Comparison of starch digest-
ibility of a blended food prepared with and without extrusion
cooking. European Journal of Clinical Nutrition 53: 844–49.
Mentschel J & Claus R (2003) Increased butyrate formation in the pig
colon by feeding raw potato starch leads to a reduction of colono-
cyte apoptosis and a shift to the stem cell compartment. Metabolism
52 (11): 1400–5.
Moreau NM, Martin LJ, Toquet CS et al. (2003) Restoration of the
integrity of rat caeco-colonic mucosa by resistant starch, but not by
fructo-oligosaccharides, in dextran sulfate sodium induced experi-
mental colitis. British Journal of Nutrition 90 (1): 75–85.
Muir JB, Walker KZ, Kaimakamis MA et al. (1998) Modulation of
fecal markers relevant to colon cancer risk: a high-starch Chinese
diet did not generate expected beneficial changes relative to a West-
ern-type diet. American Journal of Clinical Nutrition 68: 372–9.
Muir JG, Yeow EGW, Keogh J et al. (2004) Combining wheat bran
with resistant starch has more beneficial effects on fecal indexes
than does wheat bran alone. American Journal of Clinical Nutrition
79: 1020–8.
Nestel P, Cehun M & Chronopoulos A (2004) Effects of long-term
consumption and single meals of chickpeas on plasma glucose, insu-
lin, and triacylglycerol concentrations. American Journal of Clinical
Nutrition 79 (3): 390–5.
Niba L (2003) Processing effects on susceptibility of starch to diges-
tion in some dietary starch sources. International Journal of Food
Sciences and Nutrition 54: 97–109.
Noakes M, Clifton PM, Nestel PJ et al. (1996) Effect of high-amylose
starch and oat bran on metabolic variables and bowel function in
subjects with hypertriglyceridemia. American Journal of Clinical
Nutrition 64: 944–51.
Phillips J, Muir HG, Birkett A et al. (1995) Effect of resistant starch
on fecal bulk and fermentation dependent events in humans. Amer-
ican Journal of Clinical Nutrition 62: 121–30.
Pierre F, Perrin P, Champ M et al. (1997) Short-chain fructo-oligosac-
charides reduce the occurrence of colon tumors and develop gut-
associated lymphoid tissue in Min mice. Cancer Research 57: 225–
8.
Platel K & Shurpalekar KS (1994) Resistant starch content of Indian
foods. Plant Foods Human Nutrition 45: 91–5.
Prosky L, Asp NG, Furada I et al. (1985) Determination of total
dietary fiber in foods and food products: collaborative study. Jour-
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54

nal of the Association of Official Analytical Chemists International
68: 677–9.
Rabbani GH, Teka T, Zaman B et al. (2001) Clinical studies in per-
sistent diarrhea: dietary management with green banana or pectin in
Bangladeshi children. Gastroenterology 121: 554–60.
Raben A, Andersen K, Karberg MA et al. (1997) Acetylation of or b-
cyclodextrin addition to potato starch: beneficial effect on glucose
metabolism and appetite sensations. American Journal of Clinical
Nutrition 66: 304–14.
Raben A, Tagliabue A, Christensen NJ et al. (1994) Resistant starch:
the effect on postprandial glycaemia, hormonal response, and sati-
ety. American Journal of Clinical Nutrition 60: 544–51.
Rafter J, Eng VW, Furrer R, Medline A, Bruce WR (1986) Effects of
calcium and pH on the mucosal damage produced by deoxycholic
acid in the rat colon. Gut 27: 1320–9.
Ramakrishna BS, Venkataraman S, Srinivasan P et al. (2000) Amy-
lase-resistant starch plus oral rehydration solution for cholera. New
England Journal of Medicine 342: 308–13.
Ranganathan S, Champ M, Pechard C et al. (1994) Comparative
study of the acute effects of resistant starch and dietary fibres on
metabolic indexes in men. American Journal of Clinical Nutrition
59: 879–83.
Reiser S, Powell AS, Scholfield DJ et al. (1989) Day-long glucose, insu-
lin, and fructose responses of hyperinsulinemic and nonhyperin-
sulinemic men adapted to diets containing either fructose or high-
amylose cornstarch. American Journal of Clinical Nutrition 50:
913–20.
Robertson MD, Currie JM, Morgan LM et al. (2003) Prior short-term
consumption of resistant starch enhances postprandial insulin sen-
sitivity in healthy subjects. Diabetologia 46 (5): 659–65.
de Roos N, Heijnen ML, De Graff C et al. (1995) Resistant starch has
little effect on appetite, food intake and insulin secretion of healthy
young men. European Journal of Clinical Nutrition 49: 532–41.
Sacquet E, Leprince C & Riotott M (1983) Effect of amylomaize
starch on cholesterol and bile acid metabolisms in germfree (axenic)
and conventional (holoxenic) rats. Reproduction Nutrition Devel-
opment 23: 783–92.
Sakamoto J, Nakaji S, Sugawara K et al. (1996) Comparison of resis-
tant starch with cellulose diet on 1,2-dimethylydrazine-induced
colonic carcinogenesis in rats. Gastroenterology 110 (1): 116–20.
Sakata T, Kojima T, Fujieda M et al. (2003) Influences of probiotic
bacteria on organic acid production by pig caecal bacteria in vitro.
Proceedings of the Nutrition Society 62 (1): 73–80.
Schwiertz A, Lehmann U, Jacobasch G et al. (2002) Influence of resis-
tant starch on the SCFA production and cell counts of butyrate-pro-
ducing Eubacterium spp. in the human intestine. Journal of Applied
Microbiology 93 (1): 157–62.
Segain JP, Raingeard de la Bletiere D, Bourreille A et al. (2000)
Butyrate inhibits inflammatory responses through NFkappaB inhi-
bition: implications for Crohn’s disease. Gut 47 (3): 397–403.
Silvester KR, Englyst HN & Cummings JH (1995) Ileal recovery of
starch from whole diets containing resistant starch measured in
vitro and fermentation of ileal effluent. American Journal of Clini-
cal Nutrition 62: 403–11.
Silvi S, Rumney CJ, Cresci I et al. (1999) Resistant starch modifies gut
microflora and microbial metabolism in human flora-associated rats
inoculated with faeces from Italian and UK donors. Journal of
Applied Microbiology 86: 521–30.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54
Health properties of RS 53
Skrabanja V, Liljeberg HG, Kreft I et al. (2001) Nutritional properties
of starch in buckwheat products: studies in vitro and in vivo. Jour-
nal of Agricultural and Food Chemistry 49 (1): 490–6.
Sotnikova EV, Martynova EA & Gorbacheva EV et al. (2002) Resis-
tant starches and immune system. Voprosy Pitaniia 71 (5): 34–8.
Tagliabue A, Raben A, Heijnen ML et al. (1995) The effect of raw
potato starch on energy expenditure and substrate oxidation. Amer-
ican Journal of Clinical Nutrition 61: 1070–5.
Tapsell LC (2004) Diet and metabolic syndrome: where does resistant
starch fit in? Journal of the Association of Analytical Chemists
International 87 (3): 756–60.
Thorup I, Meyer O & Kristiansen E (1995) Effect of potato starch,
cornstarch and sucrose on aberrant crypt foci in rats exposed to
azoxymethane. Anticancer Research 15: 2101–5.
Toden S, Toden S, Bird AR et al. (2003) Resistant starch attenuates
colonic DNA damage induced by a high protein diet in rats. Asia
Pacific Journal of Clinical Nutrition 12: S13.
Tomlin J & Read NW (1990) The effect of resistant starch on colon
function in humans. British Journal of Nutrition 64: 589–95.
Topping DL & Clifton PM (2001) Short-chain fatty acids and human
colonic function: roles of resistant starch and nonstarch polysac-
charides. Physiological Reviews 81 (3): 1031–64.
Topping DL, Fukushima M & Bird AR (2003) Resistant starch as a
prebiotic and symbiotic: state of the art. Proceedings of the Nutri-
tion Society 62: 171–6.
Trinidad TP, Wolever TMS & Thompson LU (1996) Effect of acetate
and propionate on calcium absorption from the rectum and distal
colon of humans. American Journal of Clinical Nutrition 63: 574–
8.
Van Amelsvoort JM & Westrate JA (1992) Amylose-amylopectin
ratio in a meal affects postprandial variables in male volunteers.
American Journal of Clinical Nutrition 55: 712–18.
Van Gorkom BA, Karrenbeld A, Van Der Sluis T et al. (2002) Calcium
or resistant starch does not affect colonic epithelial cell proliferation
throughout the colon in adenoma patients: a randomized controlled
trial. Nutrition and Cancer 43 (1): 31–8.
Van Munster IP, Tangerman A & Nagengast FM (1994) Effect of
resistant starch on colonic ermentation, bile acid metabolism,
mucosal proliferation. Digestive Diseases and Sciences 39 (4): 834–
42.
Verbeek MF, DeDeckere EM, Tijburg LBM et al. (1995) Influence of
dietary retrograded starch on the metabolism of neutral steroids
and bile acids in rats. British Journal of Nutrition 74: 807–20.
Vonk RJ, Haegedoorn RE, de Graff R et al. (2000) Digestion of so-
called resistant starch sources in the human small intestine. Amer-
ican Journal of Clinical Nutrition 72: 432–8.
Wacker M, Wanek P, Eder E et al. (2002) Effect of enzyme-resistant
starch on formation of 1,N2-propanodeoxyguanosine adducts of
trans-4-Hydroxy-2-nonenal and cell proliferation in the colonic
mucosa of healthy volunteers. Cancer Epidemiology, Biomarkers
and Prevention 11: 915–20.
Wang X, Conway PL, Brown IL et al. (1999) In vitro utilization of
amylopectin and high-amylose maize (Amylomaize) starch granules
by human colonic bacteria. Journal of Applied Microbiology 87:
631–9.
Westrate JA & Van Amelsvoort JM (1993) Effects of the amylose con-
tent of breakfast and lunch on postprandial variables in male vol-
unteers. American Journal of Clinical Nutrition 58: 180–6.
54 A. Nugent
Williamson SL, Kartheuser A, Coaker J et al. (1999) Intestinal
tumorigenesis in the Apc1638N mouse treated with aspirin
and resistant starch for up to 5 months. Carcinogenesis 20:
805–10.
Wiseman CE, Higgins JA, Denyer GS et al. (1996) Amylopectin starch
induces non-reversible insulin resistance in rats. Journal of Nutri-
tion 126: 410–15.
Wong X, Brown IL, Khaled D et al. (2002) Manipulation of colonic
bacteria and volatile fatty acid production by dietary high amylose
maize (amylomaize) starch granules. Journal of Applied Microbiol-
ogy 93: 390–7.
Younes H, Levrat MA, Demige C et al. (1995) Resistant starch is more
effective than cholestyramine as a lipid-lowering agent in the rat.
Lipids 30: 847–53.
Young GP & Le Leu RK (2004) Resistant starch and colorectal neo-
plasia. Journal of the Association of Official Analytical Chemists
International 87 (3): 775–86.
Young GP, McIntyre A, Albert V et al. (1996) Wheat bran suppresses
potato starch-potentiated colorectal tumorigenesis at the aberrant
crypt stage in a rat model. Gastroenterology 110: 508–14.
Yue P & Waring S (1998) Resistant starch in food applications. Cereal
Foods World 43 (9): 690–5.
© 2005 British Nutrition Foundation Nutrition Bulletin, 30, 27–54