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Keywords:

  •  colonic health;
  • fibre;
  • glucose metabolism;
  • resistant starch

Abstract

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 content 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 investigation 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 definition 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.


What is starch?

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Starches are one of the main forms of dietary carbohydrates (the others being sugars). Starchy foods are derived from plant sources such as potatoes and cereal products (e.g. breads), and are staple items in the British diet (BNF 1994). In plants, starch occurs as granules that provide an economical means of storing carbohydrate in an insoluble and tightly packed manner (Imberty et al. 1991). The size and shape of these granules varies among plant species and also cultivars of the same species (Baghurst et al. 1996).

Chemically, starches are polysaccharides, i.e. they are composed of a number of monosaccharides or sugar (glucose) molecules linked together with α1–4 and/or α1–6 linkages. Two main structural types of starch exist: amylose which is a linear α1–4 molecule and typically constitutes 15–20% of starch, and amylopectin which is a larger branched molecule with α1–4 and α1–6 linkages and is a major component of starch (BNF 1990). Two crystalline structures of starch have been identified (an ‘A’ and ‘B’ type), which contain differing proportions of amylopectin. A type starches are found in cereals, while B type starches are found in tubers and amylose-rich starches. A third type called ‘C type’ appears to be a mixture of both A and B forms and is found in legumes (Topping & Clifton 2001). In general, digestible starches are broken down (hydrolysed) by the enzymes α-amylases, glucoamylase and sucrase-isomaltase in the small intestine to yield free glucose that is then absorbed.

What is resistant starch?

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

In 1982, while developing an in vitro assay for non-starch polysaccharides (a type of dietary fibre), Englyst and coworkers found that some starch remained after enzymic hydrolysis. Follow-up studies with healthy ileostomy subjects confirmed the presence of similar starches, which resisted digestion in the stomach and small intestine. Further analysis revealed that these starches could be fermented in the large intestine in vivo. The term ‘resistant starch’ (RS) was coined and used to describe these starches (Englyst et al. 1982). Although the term ‘resistant starch’ is not defined by any government agency (Goldring 2004), a group of scientists funded by the European Union (EU) in a concerted action known as EURESTA (FLAIR Concerted Action no. 11 Physiological Implications of the Consumption of Resistant Starch in Man) defined RS as the ‘total amount of starch, and the products of starch degradation that resists digestion in the small intestine of healthy people’ (Asp 1992). RS that reaches the large intestine can act as a substrate for microbial fermentation, the end-products being hydrogen, carbon dioxide, methane and short chain fatty acids (SCFA) (Englyst et al. 1996). However, as the EURESTA definition describes RS in terms of its physiological functionality, rather than its physical or chemical characteristics, scientists have defined a number of categories of RS to describe how the starches may escape digestion in upper gastrointestinal tract.

Structure of resistant starch

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

The resistance of starch to digestion is influenced by the nature of the association between starch polymers, with higher amylose levels in the starch being associated with slower digestibility rates. Both B and C type starches appear to be more resistant to digestion with high-amylose maize producing RS which has been particularly useful in the preparation of foods (Brown 2004).

Retrograded starches refer to certain structural forms of RS. Retrogradation occurs when starch is cooked in water beyond its gelatinisation temperature and then cooled. Amylose is found in the amphorous parts of the starch crystal, while amylopectin gives starch its crystalline structure. Upon heating with excess water and at sufficiently high temperatures, the starch crystalline regions ‘melt’. The starch granules gelatinise and the starch is subsequently more easily digested. However, these starch gels are unstable and upon cooling re-form crystals that are resistant to hydrolysis by amylases (i.e. are resistant to digestion). Slow cooling of the gelatinised starch favours Type A crystallisation while slow cooling in excess water favours Type B crystallisation. This process is known as retrogradation (Topping & Clifton 2001). In general, starches rich in amylose are naturally more resistant to digestion and also more susceptible to retrogradation.

Classification and food sources of resistant starch

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Resistant starch has been classified into four general subtypes called RS1–RS4 (Englyst et al. 1992; Brown et al. 1995). Table 1 outlines a summary of the different types of RS, their classification criteria and food sources. Briefly, RS1 is the term given to RS where the starch is physically inaccessible to digestion, e.g. due to the presence of intact cell walls in grains, seeds or tubers. RS2 describes native starch granules that are protected from digestion by the conformation or structure of the starch granule as in raw potatoes and green bananas. A particular type of RS2 is unique as it retains its structure and resistance even during the processing and preparation 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 analysed (Brown 2004).

Table 1.  Classification of types of resistant starch, food sources and factors affecting their resistance to digestion in the colon
Type of RSDescriptionFood sourcesResistance reduced by
  1. RS, resistant starch.

RS1Physically protectedWhole- or partly milled grains and seeds, legumes, pastaMilling, chewing
RS2Ungelatinised resistant granules with B-type crystallinity and are hydrolysed slowly by α-amylasesRaw potatoes, green bananas, some legumes, high amlyose starchesFood processing and cooking
RS3Retrograded starch (i.e. non-granular starch-derived materials)Cooked and cooled potatoes, bread, cornflakes, food products with prolonged and/or repeated moist heat treatmentProcessing conditions
RS4Chemically modified starches due to cross-bonding with chemical reagents, ethers, esters, etc.Some fibre-drinks, foods in which modified starches have been used (e.g. certain breads and cakes)Less susceptible to digestibility in vitro

Although RS is found naturally in all starch-containing 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 processing 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 structure of starch can influence the amount of RS present, other factors intrinsic to starchy foods can affect α-amylase activity and therefore starch breakdown. These include the formation of amylose-lipid complexes, the presence of native α-amylase inhibitors and also non-starch polysaccharides, all of which can directly affect α-amylase activity (Englyst et al. 1992). Extrinsic additives may also bind to starch making it more or less susceptible 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 definitions of dietary fibre have been suggested whereby dietary fibre may be defined as part of a plant, as chemical substances, according to indigestibility in the small intestine and/or by its beneficial digestive and physiological 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 substances. 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, 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 Academies 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 definition 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 composition tables are still based on the Englyst method (see labelling section).

Measurement of resistant starch

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 α-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 materials, but it has not been shown to analyse all RS as defined (Champ et al. 2003b). It is based on the principle 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 followed 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).

Table 2.  Resistant starch contents of a number of sample foods and commercially manufactured sources of resistant starch
Food sampleRS content (as assessed using AOAC 2002.02)
  1. Source: Reprinted with kind permission from McCleary & Rossiter (2004). Copyright (2004) AOAC INTERNATIONAL.

Wheat bran 0.42
Rye crispbread 1.2
Kidney beans 5.3
Corn flakes 2.8
Native potato starch78.1
Cooked and cooled potato starch 3.8
HYLON VII53.7
Hi-maize 104345.7
NOVELOSE 24046.9
ActiStar58.0
CrystaLean40.9

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 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

In addition to the natural food sources of RS, some commercially 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 categorised as RS2, is now sold throughout the world by National Starch and Chemical Co. and is used in products 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 tapioca starch (Crosby 2003). NOVELOSE 330® (National Starch and Chemical Limited) and CrystaLean (Opta Food Ingredients, Inc.) are also examples of commercially developed RS3 which is derived from high amylose maize (Yue & Waring 1998). Research is intensifying regarding RS4 chemically modified starches; RS4 which have been created using difunctional 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 commercially 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 commercial 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 marketed for those following low-carbohydrate dieting regimens. 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

Calorific value and dietary intakes of resistant starch

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Experimentally, the energy value of RS has been calculated as approximately 8 kJ/g (2 kcal/g). This is considerably 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 developing 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 occupation-related trends in the density of RS in the diet. However, 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 database and the data refers to Australian dietary intakes. As mentioned earlier, intakes of RS in Australia are likely to be greater than in Europe due to the commercial availability of top-selling breads and cakes that are enriched with RS.

Physiological effects of resistant starch

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

A number of physiological effects have been ascribed to RS and are listed in Table 4 and will be described below. RS, by escaping digestion in the small intestine, has few interactions with other components of the upper gastrointestinal tract. It is fermented in the large intestine resulting in the production of such fermentation products as carbon dioxide, methane, hydrogen, organic acids (e.g. lactic acid) and SCFA. However, RS is believed to result in only a modest production of these gases compared with other non-digestible oligosaccharides, fructo-oligosaccharides and lactulose (Christl et al. 1992). SCFA produced include butyrate, acetate and propionate, and it is thought that these SCFA in particular mediate the effects of RS, rather than RS exerting a physical bulking effect (Topping et al. 2003). SCFA will be discussed briefly below; other mechanisms by which RS may influence physiological behaviour will be discussed later in this review.

Table 4.  Physiological effects of resistant starch
Potential physiological effectsConditions where there may be a protective effect
  1. Source: Adapted from Brown (2004) and Champ (2004).

Improve glycaemic and insulinaemic responsesDiabetes, impaired glucose and insulin responses, the metabolic syndrome
Improved bowel healthColorectal cancer, ulcerative colitis, inflammatory bowel disease, diverticulitis, constipation
Improved blood lipid profileCardiovascular disease, lipid metabolism, the metabolic syndrome
Prebiotic and culture protagonistColonic health
Increased satiety and reduced energy intakeObesity
Increased micronutrient absorptionEnhanced mineral absorption, osteoporosis
Adjunct to oral rehydration therapiesTreatment of cholera, chronic diarrhoea
Synergistic interactions with other dietary components, e.g. dietary fibres, proteins, lipidsImproved metabolic control and enhanced bowel health
ThermogenesisObesity, diabetes

Short chain fatty acids

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Short chain fatty acids (SCFA) are the metabolic products of anaerobic bacterial fermentation of polysaccharides, oligosaccharides, protein, peptide and glycoprotein precursors in the large intestine, including those derived from dietary fibre and RS (Andoh et al. 2003). The principal SCFA are butyrate, propionate and acetate, although other SCFA are also produced in lesser amounts (MacFarlane & MacFarlane 2003). SCFA are the preferred respiratory fuel of the cells lining the colon (colonocytes). They increase colonic blood flow, lower luminal pH and help prevent the development of abnormal colonic cell populations (Topping & Clifton 2001). SCFA are mainly found in the proximal colon where fermentation is greatest, and the amount present mirrors supply of carbohydrate in the diet (Topping et al. 2003). Levels of SCFA fall during the passage of digesta through the colon; this is due to uptake and utilisation by the colonocytes and bacteria. In humans, the abundance of SCFA is normally acetate > propionate > butyrate. Depending on diet, total SCFA concentrations are usually between 70 and 140 m m in the proximal colon and 20–70 mM in the distal colon; therefore, SCFA are found in much lower amounts in the distal colon (the site of many colonic diseases and most human colon cancers). Butryate is the favoured fuel of colonocytes (Schwiertz et al. 2002). In vitro, butyrate can reverse neoplastic changes (Ferguson et al. 2000) and it exerts trophic effects on the colonic epithelium in vivo (Mentschel & Claus 2003). In addition, it can affect gene expression and may induce cell cycle arrest or even apoptosis (naturally programmed cell death which removes DNA damaged, unwanted or old cells) of colonocytes (Mentschel & Claus 2003). Therefore, dietary interventions that increase the amount of SCFA in the colon are thought to be beneficial to gut health, and SCFA are commonly used as markers of fermentation and colonic health. Length of transit time and diet are two variables known to influence the concentration and types of SCFA found in the colon. A long transit time results in protein breakdown and an increased contribution by amino acid fermentation to SCFA pools (MacFarlane & MacFarlane 2003), while dietary fibre (including RS) can modify large bowel and faecal SCFA levels (Bird et al. 2000a).

However, there are several problems with using SCFA as markers of (human) fermentation and colonic health. As approximately 95% of SCFA are produced and absorbed in the colon, the accuracy of faecal measurements is limited (Cummings et al. 1987). SCFA are also absorbed and transported via the portal vein to the liver, 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 distributions 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 concentration 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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; Henningsson 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, discrepancies 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 variations 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 adaptation is necessary before changes in SCFA will be observed (Topping & Clifton 2001).

Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Dietary fibre, starch, resistant starch and colon cancer

A number of epidemiological studies have investigated the potential benefits of dietary fibre and starch in protecting 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 prospective 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 international correlative study, found a strong inverse relationship between starch intake and colon and rectal cancer, even after adjusting for fat and protein intake. Non-starch polysaccharides were only significantly correlated 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 substantial 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 investigated the relationship between dietary starch and colorectal cancer. A high intake of dietary starch was found to be protective in the cohort study (Health Professionals 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. However, such research is hampered by a lack of standardised 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 cancer prevention. CAPP-1, is a randomised double-blind factorial design controlled trial investigating the effects of one of four treatments in suppressing colorectal adenoma formation in young subjects with an inherited disposition to developing colon cancer (Familial Adenomatous Polyposis): (1) double placebo; (2) aspirin (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 carriers 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 neoplasia and markers of colonic function and colorectal cancer.

Commonly measured outcomes of colorectal neoplasia 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 colorectal cancer, which can be identified under a microscope 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 throughout life: in the colonic mucosa increased levels are thought to result in increased cancer risk (Young & Le Leu 2004). However, concerns have been raised concerning the sensitivity and specificity of the analytical techniques for detecting these DNA adducts. Maintenance 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 colorectal cancer (Van Gorkom et al. 2002) but its exact usefulness 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 production 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 carcinogenic 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 shortened transit time (Young & Le Leu 2004). Reduced activity of certain bacterial enzymes (e.g.β-glucuronidase) depresses the formation of toxic and carcinogenic metabolites from dietary and endogenous compounds (Young & Le Leu 2004). The effect of RS on the activity of microbial populations will be discussed later (prebiotics).

Animal studies of resistant starch and colonic function

Studies examining the effect of RS on colonic function 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 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. Interestingly, this effect was lost when RS was fed in combination with wheat bran (Young et al. 1996). Various forms of RS (chiefly RS2 and RS3) appear to consistently 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).

Table 5.  Animal intervention studies examining the effects of resistant starch on colonic function
AuthorAnimal modelInterventionParameters measuredOutcome
  1. 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.

  2. Some of the data contained in this table was reprinted with kind permission from Young & Le Leu (2004) In: Journal of AOAC International87: 779–84. Copyright (2004) AOAC INTERNATIONAL.

Thorup et al. (1995)Wistar rats (azoxymethane)Carbohydrate content of diet replaced by: sucrose, cornstarch or RPS (RS2; 67 g/100 g)ACFRPS[DOWNWARDS ARROW] total and larger ACF
Caderni et al. (1996)Sprague Dawley rats (Dimethylhydrazine)Sucrose, glucose, fructose, cornstarch or HYLON VII (RS2)Cell proliferationNSD
Caecal pH[DOWNWARDS ARROW]
Caecal concentrations SCFA[DOWNWARDS ARROW]
Sakamoto et al. (1996)Sprague Dawley rats (Dimethylhydrazine)3 or 10 g/100 g cellulose or 3 or 10 g/100 g RS3 (high amylose maize starch hydrolysed with pancreatin)Tumour incidenceNSD
SCFA and butyrate production[UPWARDS ARROW]
Faecal output[UPWARDS ARROW]
Young et al. (1996)Sprague Dawley rats (Dimethylhydrazine)Low RS, low fibre diet or 14.4 g/100 g diet RPS (RS2) or 14.4 g/100 g RPS and 14.4 g/100 g wheat branTumour incidenceNSD
Tumour size and multiplicity[UPWARDS ARROW]
ACF[UPWARDS ARROW] density
Cell proliferation[UPWARDS ARROW]
Faecal output[UPWARDS ARROW]
Pierre et al. (1997)C57BL/6 J min miceRS-free diet (2% cellulose, no RS) or Wheat bran (18.8 g/100 g) or RS3 (high amylose cornstarch; 18.8 g/100 g)Tumour incidenceNSD
Maziere et al. (1998)Sprague Dawley rats (Dimethylhydrazine)RS-free diet (2% cellulose) or 25 g/100 g RS3 (high-amylose maize starch)ACF[DOWNWARDS ARROW]
Caecal pH[DOWNWARDS ARROW]
Faecal weight and output[UPWARDS ARROW]
Bacterial enzyme activity[UPWARDS ARROW]β-glucuronidase activity
Cassand et al. (1997)Sprague Dawley ratsRetrograded high-amylose cornstarch (RS3)ACF[DOWNWARDS ARROW]
Faecal output[UPWARDS ARROW]
Faecal pH[DOWNWARDS ARROW]
SCFA[UPWARDS ARROW] total and butyrate
Kleeson et al. (1997)Wistar ratsRPS, or retrograded potato starch (RS2) 10 g/100 gSCFA[UPWARDS ARROW]SCFA
 [UPWARDS ARROW] butyrate, RS2
Eibhara et al. (1998)Wistar ratsPotato starch or CMSFaecal output[UPWARDS ARROW]
Caecal SCFA[DOWNWARDS ARROW] butyrate with CMS
Caecal bile acids[UPWARDS ARROW] with CMS
Silvi et al. (1999)Fisher ratsRS- and cellulose-free diet (2.1%) or Retrograded amylose starch (15 g/100 g)Caecal SCFA[UPWARDS ARROW] butyrate
Bacterial enzyme activity[DOWNWARDS ARROW]β-glucuronidase activity
Ammonia production[DOWNWARDS ARROW]
Cell proliferationNSD
Williamson et al. (1999)Min mouseRS- and NSP-free diet or 1:1 RPS (RS2) and high-amylose maize diet (RS3)Tumour incidence[UPWARDS ARROW] with RS diet
Bird et al. (2000b)PigsBrown rice or white rice and branSCFA excretion[UPWARDS ARROW]
Large bowel digesta mass[UPWARDS ARROW]
Ferguson et al. (2000)Wistar ratsRS- and NSP-free diet or Potato starch or High amylose maize starch or a-amylase treated Hi-maize (35 g/100 g)Faecal output[UPWARDS ARROW]
SCFA[UPWARDS ARROW] including butyrate
Transit time^ by potato starch and α-amylase treated
 Hi-maize
Wang et al. (2002)Balb/C miceAmylomaize starch Modified amylomaize starch (40 g/100 g diet)SCFA[UPWARDS ARROW] butyrate in faeces
Ferguson et al. (2003)Wistar ratsRS- and NSP-free diet Potato starch and high amylose maize starch (35 g/100 g)Faecal output[UPWARDS ARROW]
Excretion of the food carcinogen, IQ[UPWARDS ARROW] carcinogen bioavailbility
Le Leu et al. (2003)Sprague Dawley ratsHigh amylose maize starchpH[DOWNWARDS ARROW]
Conlon & Bird (2003)Sprague Dawley rats10 g/100 g fish oil or sunflower oil And 10 g/100 g dietary fibre (wheat bran or cellulose) Or 10 g/100 g RS (Hi-maize or NOVELOSE)Colonic DNA damage[UPWARDS ARROW] DNA damage with RS and fish oil vs. RS and sunflower oil
 Reverse with dietary fibre.
Toden et al. (2003)Sprague Dawley rats15 or 25 g/100 g casein with or without 48% Hi-maizeDNA damage[DOWNWARDS ARROW] with RS diet
Thining of mucosal layer[DOWNWARDS ARROW] with RS diet
Kestell et al. (2004)Wistar ratsRS- and fibre-free diet Potato starch Hi-maize Apple pectin Wheat strawMetabolism and disposal of the food carcinogen, IQRS[UPWARDS ARROW] number of intact IQ and [DOWNWARDS ARROW] level of metabolites

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 carcinogen (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 function (e.g. SCFA concentrations, pH, etc.). Results are less clear with respect to tumour formation, size, cellular 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 feeding regimens. Further research is needed using different types and mixes of RS, and examining any potential interactions between RS and other macronutrients commonly 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.

Table 6.  Human intervention studies examining the effects of resistant starch on colonic function
AuthorSample size and study lengthInterventionParameters measuredOutcome
  1. NSD, non-significant difference; RS, resistant starch; SCFA, short chain fatty acid.

  2. Some of the data contained in this table was reprinted with kind permission from Young & Le Leu (2004) In: Journal of AOAC International87: 779–84. Copyright (2004) AOAC INTERNATIONAL.

Tomlin & Read (1990)8 subjects6 large bowls Cornflakes (10.33 g RS) or 6 large bowls Rice Krispies (0.86 g RS)Breath hydrogen[UPWARDS ARROW]
Van Munster et al. (1994)14 healthy subjects fed the diets for 3 weeks45 g HYLON VII (32%) RS or low RS, 20 g natural fibreCell proliferation[DOWNWARDS ARROW]
Faecal output[UPWARDS ARROW]
pHNSD
Faecal SCFA[UPWARDS ARROW] total SCFA and butyrate
Breath hydrogen[UPWARDS ARROW]
Bile acid excretion[DOWNWARDS ARROW] secondary bile acids and concentrations of soluble bile acids
Cytotoxicity[DOWNWARDS ARROW]
Phillips et al. (1995)11 healthy subjects in a crossover study for 3 weeksHigh RS (Hi-maize or cooked or uncooked green banana flour; 26–50 g RS/day) or low RS diet (3–8 g RS/day)Faecal output[UPWARDS ARROW]
Faecal pH[DOWNWARDS ARROW]
SCFA[UPWARDS ARROW] butyrate and acetate
Excretion of starch[UPWARDS ARROW]
pH[DOWNWARDS ARROW] by 0.6 units
Birkett et al. (1996)11 subjects in randomised controlled cross-over for 3 weeksHigh RS (39 g/day, RS1, RS2, RS3 mix) or low RS (5 g/day)Faecal nitrogen excretion[UPWARDS ARROW]
Faecal ammonia[DOWNWARDS ARROW]
Faecal phenols[DOWNWARDS ARROW]
Faecal pH[DOWNWARDS ARROW]
Cummings et al. (1996)12 healthy subjects fed each diet for 15-day periodsRS2 – potato and banana starchRS3 – maize and wheat starchRS-free diet (wheat starch) RS diets contained 17–30 g RSFaecal weight[UPWARDS ARROW]
SCFA[UPWARDS ARROW]
NSP breakdown[DOWNWARDS ARROW] breakdown and [UPWARDS ARROW] faecal NSP
Noakes et al. (1996)23 hypertriglycerimd emics for 4 weeksHigh amylose maize starch (17–25 g RS/day) or Oat branBile acids[DOWNWARDS ARROW] secondary bile acids in faecal water
pH[DOWNWARDS ARROW]
SCFA[UPWARDS ARROW] faecal total SCFA and faecal butyrate
Heijnen et al. (1998)24 healthy volunteers fed each diet for 1-week periodsUncooked HYLON VII (32 g RS2/day) Retrograded high amylose cornstarch (32 g RS2/day) Glucose syrupFaecal output[UPWARDS ARROW]
pHNSD
SCFANSD
Bile acidsNSD
CytotoxicityNSD
Hylla et al. (1998)12 healthy volunteers for 4 weeksHigh RS – high amylose maize (55.2 g RS/day) Low RS – corn starch (7.7 g RS/day)Faecal weight[UPWARDS ARROW]
SCFANSD
Bile acids[DOWNWARDS ARROW] total and secondary concentrations
Transit time[UPWARDS ARROW]
Bacterial enzymes[DOWNWARDS ARROW]β-glucosidase activity
Sterols[DOWNWARDS ARROW] faecal total sterols
Jenkins et al. (1998)24 healthy subjects fed each diet for 2 weeks with a 2-week washout periodRS2 (21.5 g RS/day) RS3 (27.9 g RS/day) Wheat bran (1.5 g RS/day) Low fibre diet (2.3 g RS/day)Faecal bulk[UPWARDS ARROW]
SCFA[UPWARDS ARROW] butyrate: SCFA ratio
Grubben et al. (2001)23 patients with recently removed colonic adenomas for 4 weeks45 g amylomaize (28 g RS/day as a capsule) or 45 g maltodextrinCell proliferationNSD
Faecal weightNSD
pHNSD
SCFA excretion[UPWARDS ARROW] faecal butyrate
Bile acids[UPWARDS ARROW] primary and secondary bile acids in faecal water
Van Gorkom et al. (2002)111 sporadic adenoma patientsHigh RS: 30 g HYLON VII (19 g RS) or Controlled placeboCell proliferationNSD
Wacker et al. (2002)12 healthy subjects for 4 weeks (only 8 volunteers for DNA data)High RS: HYLON VII (50.7–59.7 g/day) o Low RS: cornstarchCell proliferationNSD
DNA adducts[UPWARDS ARROW] adduct levels in colonic mucosa
Muir et al. (2004)20 volunteers for 3 weeksWheat bran (12 g fibre) RS and Wheat bran (22 g RS and 12 g fibre/day)Faecal output[UPWARDS ARROW]
Transit time[UPWARDS ARROW]
Faecal pH[DOWNWARDS ARROW]
SCFA[UPWARDS ARROW] faecal concentration
Phenol[DOWNWARDS ARROW]
Ammonia[DOWNWARDS ARROW]

While a lack of effect of RS on SCFA production/concentration 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, retrograded 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 trial of Heijnen et al. (1998). It is thought that the concentrations 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 formation 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 parameters 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 suitable adaptation time. Finally, human studies have included healthy volunteers and patients with hypertriglyceridemia, 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 inflammatory bowel diseases such as ulcerative colitis. Ulcerative 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 Dawley 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 observations 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 inflammatory 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 constipation, however, due to the beneficial effects of RS supplementation 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 combination 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 concentrations. This study suggests that the health benefits of RS can be maximised when given in conjunction with different types of dietary fibres.

Resistant starch and colonic microflora: prebiotics and probiotics

Gibson & Roberfroid (1995) defined prebiotics as ‘growth substrates directly specifically towards potentially beneficial bacteria already resident in the colon’. Prebiotics are non-digestible food ingredients that stimulate the growth and/or activity of bacteria in the colon, thereby improving host health. Probiotics refer to cultures 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 function 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 several categories of RS (including RS2 and RS4) may physically 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 promote 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 protection and by slowing the rate at which the bacteria are lost once probiotic consumption ceases. Initial data show that when RS is fed in combination with fructo-oligosaccharides, no decline in faecal numbers of bacteria 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 association 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 Brachyspira 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 similar 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Consumption of soluble fibre can confer benefits to heart health, influencing both lipid and glucose metabolism. RS shares some common properties with soluble dietary fibres insofar as it is poorly digested in the small intestine and largely digested and metabolised (fermented) 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 palatable (Demignéet al. 2001). A significant number of studies have examined whether RS affects lipid and glucose metabolism (including glycaemic index), energy expenditure and macronutrient oxidation.

Resistant starch and lipid metabolism

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 cholesterol, low density lipoproteins (LDL), high density lipoproteins (HDL), very low density lipoproteins (VLDL), intermediate density lipoproteins (IDL), triglycerides, 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 lowering plasma cholesterol and triglyceride levels. RS has also been shown to be effective in lowering plasma cholesterol levels in genetically obese and lean rats (Mathéet al. 1993) and in diabetic rats (Kim et al. 2003).

Table 7.  Summary of the effects of resistant starch (RS) on markers of lipid metabolism in animals (A) and humans (H)*
ParameterRS exerted a positive effectRS had no effect
  • *

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

TriglyceridesDe 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 lipoproteinsHan 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 lipoproteinsHan et al. (2003a, 2003b) (A) 
Younes et al. (1995) (A) 
Kishida et al. (2001) (A) 
Intermediate density and/or very low density lipoproteinsHan et al. (2003a, 2003b) (A) 
Triglyceride-rich lipoproteinsKishida et al. (2001) (A) 
Younes et al. (1995) (A) 
Lopez et al. (2001) (A) 

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.

Resistant starch and insulin and glucose metabolism

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Insulin is a hormone that enables glucose uptake by muscle and adipose cells, thereby lowering blood glucose 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 conditions 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 (glycaemic) and insulin (insulinaemic) responses. Most studies in humans have focused on postprandial glycaemic and/or insulinaemic responses and have varied in quality (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 postprandial glycaemia, but is associated with more physiologically 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.

Table 8.  Summary of studies examining the effects of resistant starch (RS) on glucose and insulin responses in humans
Resistant starch decreasedResistant starch had no effect on
Glucose responsesInsulin responsesGlucose responsesInsulin responses
  • *

    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.

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

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 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 emptying rate; (2) by increasing the secretion of gastric inhibitory polypeptide (GIP) a secretagogue that stimulates the release of insulin; and (3) by forming fat complexes that cause conformational changes in starch/lipid complexes 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 Amelsvoort & 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 commercially manufactured high amylose starch) when provided 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 indicate that compared with feeding RS, digestible starch causes insulin resistance (as assessed using an intravenous 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 hyperinsulinmaeic 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 similar 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 standard) 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 individuals 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 glucose response in volunteers with type 2 diabetes following 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%β-cyclodextrin on a number of metabolic factors. The β-cyclodextrin-starch resulted in a lower initial glucose peak that was associated with attenuated plasma insulin and GIP. Plasma concentrations 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 β-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.

Resistant starch and macronutrient oxidation, satiety and weight loss

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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/carbohydrate 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 oxidation (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 glucose 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 attributed 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 several 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 Deckere et al. 1993). RS was also shown to reduce the activity 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 eating 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 adipocyte 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 consumption 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 standardised test meals matched for macronutrients and fibre content but containing different levels of RS.

Glycaemic index, glycaemic response and glycaemic load

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 eating a similar amount of available carbohydrate in a control 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 glycaemic response), while foods with a low GI value release 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 commercial 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 physiological 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 addition, the total carbohydrate content (quantity) varies between foods. To account for this, the concept of glycaemic 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 (particularly 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Resistant starch is reported to enhance the ileal absorption 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 number of pro-inflammatory cytokines (e.g. tumour necrosis factor alpha) and the expression of a number of receptors 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; Sotnikova 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 populations and a lowered activity of certain bacterial enzymes (e.g.β-glucuronidase), would be expected to have beneficial 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 epithelium (Mentschel & Claus 2003). Recently it has been reported that butyrate can directly inhibit inflammatory responses by down-regulating the activity of the transcription factor Nuclear Factor κappa B (NF-κB). NF-κB is a central regulator of many immune and inflammatory responses and increased activity of NF-κB has been observed in patients with inflammatory bowel disease (Segain et al. 2000). Therefore, it is possible 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-κB expression and activity.

Increasing SCFA production also lowers colonic pH and increases the excretion of bile acids. A lowered pH 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 production of secondary bile acids.

One of the SCFA acetate can inhibit cholesterolgenesis 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 necessary 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 mechanisms 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 lipoprotein 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 hormones 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 secretion (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 mechanism is unlikely to be responsible for any lipid-lowering effects following the consumption of RS.

With respect to all of the above mentioned physiological effects, it is noteworthy that the different forms of RS should not be assumed to be physiologically equivalent. As mentioned earlier, large intra-individual differences 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 normal 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 potatoes, 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 manner 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 cancer. 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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 flatulence, belching, bloating, mild laxative effects and stomach aches (Heijnen et al. 1996); however, it is 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 reactions 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 information 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

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, Australia, 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 traditionally 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), problems arise as the UK government recommendations for population dietary fibre intakes are still based on the Englyst method. In addition, the existing UK food composition 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), respectively. 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 considered safe under existing food classifications and legislations 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 process 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 manufacturers 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 ‘indigestible’, but they must clearly label the legally approved name of the corresponding starches. The US also allows self-declared ‘structure-function’ claims without restriction (e.g. fibre maintains bowel regularity), but restrictions 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 distinction 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 methods 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

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References

Resistant starch, the portion of starch and starch products that resist digestion, appears to confer several 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 Medicine of the National Academies and the AACC definitions 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 priorities include a more in-depth exploration of the effects of RS on colonic function and inflammatory bowel disease. There is also a need for properly designed, controlled 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 treatments 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-κB, but more information is needed regarding its potential effects on other molecular pathways.

References

  1. Top of page
  2. Abstract
  3. What is starch?
  4. What is resistant starch?
  5. Structure of resistant starch
  6. Classification and food sources of resistant starch
  7. Resistant starch as a component of dietary fibre
  8. Measurement of resistant starch
  9. Commercially manufactured sources of resistant starch
  10. Calorific value and dietary intakes of resistant starch
  11. Physiological effects of resistant starch
  12. Short chain fatty acids
  13. The effects of resistant starch on short chain fatty acid production
  14. Resistant starch and colonic function (colorectal cancer, inflammatory bowel disease, constipation and diverticulitis)
  15. Resistant starch and metabolic responses
  16. Resistant starch and lipid metabolism
  17. Resistant starch and insulin and glucose metabolism
  18. Resistant starch and macronutrient oxidation, satiety and weight loss
  19. Glycaemic index, glycaemic response and glycaemic load
  20. Other health benefits associated with resistant starch
  21. Putative mechanisms of action of resistant starch
  22. Safety of resistant starch
  23. Labelling and legislation of fibre and resistant starch
  24. Conclusion
  25. Acknowledgements
  26. References
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