Resistant starches

Current Opinion in Gastroenterology

Volumn 16, Issue 2, 2000, Pages 178-183

  Jenkins, David J A ^a   Kendall, Cyril W C ^b  

^a ST MICHAEL'S HOSPITAL   (Canada)

^b UNIVERSITY OF TORONTO   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 0001071597     PISSN: 02671379     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001574-200003000-00014     Document Type: Article

References (38)

1. Asp NG: Resistant starch: an update on its physiological effects. Adv Exp Med Biol 1997, 427:201-210.
2. Englyst HN, Kingman SM, Cummings JH: Classification and measurement of nutritionally important starch fractions. Eur J Clin Nutr 1992, 46(suppl):33S-50S.
3. Olesen M, Gudmand-Hoyer E: Maldigestion and colonic fermentation of wheat bread in humans and the influence of dietary fat. Am J Clin Nutr 1997, 66:62-66.
4. Englyst HN, Veenstra J, Hudson GJ: Measurement of rapidly available glucose (RAG) in plant foods: a potential in vitro predictor of the glycaemic response. Br J Nutr 1996, 75:327-337.
5. Jenkins DJ: Lente carbohydrate: a newer approach to the dietary management of diabetes. Diabetes Care 1982, 5:634-641.
6. Trowell H, Southgate DA, Wolever TM, Leeds AR, Gassull MA, Jenkins DJ: Dietary fibre redefined [letter]. Lancet 1976, 1(7996):967.
7. Jenkins DJ, Wolever TM, Taylor RH, Barker HM, Fielden H: Exceptionally low blood glucose response to dried beans: comparison with other carbohydrate foods. BMJ 1980, 281:578-580.
8. Jenkins DJ, Wolever TM, Thorne MJ, Jenkins AL, Wong GS, Josse RG, et al.: The relationship between glycemic response, digestibility, and factors influencing the dietary habits of diabetics. Am J Clin Nutr 1984, 40:1175-1191.
9. Noah L, Guillon F, Bouchet B, Buleon A, Molis C, Gratas M, et al.: Digestion of carbohydrate from white beans (Phaseolus vulgaris L.) in healthy humans. J Nutr 1998, 128:977-985. Feeding white beans to healthy volunteers resulted in 17% of the ingested starch reaching the cecum, judged by intubation and ileal aspiration. Comparison with pigs with ileal fistulae suggested that this may be an underestimation.
10. Read NW, Welch IM, Austen CJ, Barnish C, Bartlett CE, Baxter AJ, et al.: Swallowing food without chewing: a simple way to reduce postprandial glycaemia. Br J Nutr 1986, 55:43-47.
11. Champ MM, Molis C, Flourie B, Bornet F, Pellier P, Colonna P, et al.: Small-intestinal digestion of partially resistant cornstarch in healthy subjects. Am J Clin Nutr 1998, 68:705-710. Starch recovery from small intestinal absorption and colonic fermentation was assessed in six healthy subjects using ileal intubation and fecal analysis after consumption of high resistant starch sources (retrograded and complexed high-amylose corn starches). Retrograded (51% of starch) and complexed (21%) starches delivered significant amounts of starch to the colon that was almost all lost to fermentation. In vitro analyses underestimated the proportion of resistant starch as assessed by ileal intubation.
12. Hoebler C, Karinthi A, Chiron H, Champ M, Barry JL: Bioavallability of starch in bread rich in amylose: metabolic responses in healthy subjects and starch structure. Eur J Clin Nutr 1999, 53:360-366. Consumption of high-amylose white bread reduced the glycemic index compared with regular bread but did not alter the hydrolysis kinetics, suggesting that the resistant starch was not acting as, for example, a viscous fiber to reduce the glycemic index by reducing the overall rate of starch absorption of the nonresistant portion of the starch.
13. Jenkins DJ, Wolever TM, Taylor RH, Griffiths C, Krzeminska K, Lawrie JA, et al.: Slow release dietary carbohydrate improves second meal tolerance. Am J Clin Nutr 1982, 35:1339-1346.
14. Liljeberg HG, Akerberg AK, Bjorck IM. Effect of the glycemic index and content of indigestible carbohydrates of cereal-based breakfast meals on glucose tolerance at lunch in healthy subjects. Am J Clin Nutr 1999, 69:647-655. This thorough study demonstrated that improved second meal tolerance was seen with slow-release, or lente-type, carbohydrate sources such as barley flakes but not with all resistant starch foods.
15. Giacco R, Clemente G, Brighenti F, Mancini M, D'Avanzo A, Coppola S, et al.: Metabolic effects of resistant starch in patients with type 2 diabetes. Diab Nutr Metab 1998, 11:330-335. In 10 type 2 diabetic subjects, breakfasts containing resistant starch produced a lower blood glucose response but did not result in improved glycemic response at lunch.
16. Jenkins DJ, Vuksan V, Kendall CW, Wursch P, Jeffcoat R, Waring S, et al.: Physiological effects of resistant starches as colonically available forms of lente carbohydrate. J Am Coll Nutr 1998, 17:609-616. Twenty-four healthy subjects took approximately 30 g daily RS2 and RS3 resistant starch for 2-week periods and had increases in fecal output and fecal butyrate concentration compared with a control phase, but no effect on blood lipids was observed. The presence of resistant starch did not alter the glycemic index of the breakfast cereal and muffin supplements used in the study.
17. Cummings JH, Beatty ER, Kingman SM, Bingham SA, Englyst HN: Digestion and physiological properties of resistant starch in the human large bowel. Br J Nutr 1996, 75:733-747.
18. Jenkins DJ, Vuksan V, Rao AV, Vidgen E, Kendall CW, Tariq N, et al.: Colonic bacterial activity and serum lipid risk factors for cardiovascular disease. Metabolism 1999, 48:264-268. This was a further analysis of data in reference 16. It demonstrated that in healthy subjects fecal starch output while consuming resistant starch diets relates to pretreatment serum lipids - that is, the more fecal starch, the lower the serum cholesterol. The data suggest that factors such as fecal microflora, which influence the degree that resistant starch is metabolized in the colon, also affect serum lipids.
19. Alles MS, Katan MB, Salemans JM, Van Laere KM, Gerichhausen MJ, Rozendaal MJ, et al.: Bacterial fermentation of fructo-oligosaccharides and resistant starch in patients with an ileal pouch-anal anastomosis. Am J Clin Nutr 1997, 66:1286-1292.
20. Birkett AM, Jones GP, de Silva AM, Young GP, Muir JG: Dietary intake and faecal excretion of carbohydrate by Australians: importance of achieving stool weights greater than 150 g to improve faecal markers relevant to colon cancer risk. Eur J Clin Nutr 1997, 51:625-632.
21. Langkilde AM, Ekwall H, Bjorck I, Asp NG, Andersson H: Retrograded high-amylose corn starch reduces cholic acid excretion from the small bowel in ileostomy subjects. Eur J Clin Nutr 1998, 52:790-795. Seven healthy patients who had undergone ileostomy were given diets for 2 days with either 5 or 39 g of resistant starch (retrograded high-amylose starch) and observed in a metabolic ward. The high-resistant starch diet caused a 42% decrease in cholic acid excretion, a 42% increase in mean wet weight concentration of bile acids, and a 70% increase in total dry weight. The data suggest that, by reducing colonic bile acid concentrations, resistant starch may reduce a possibly important risk factor for the development of colon cancer.
22. Silvester KR, Bingham SA, Pollock JR, Cummings JH, O'Neill IK: Effect of meat and resistant starch on fecal excretion of apparent N-nitroso compounds and ammonia from the human large bowel. Nutr Cancer 1997, 29:13-23.
23. 2, fecal weight, and fecal starch increased compared with control, but no differences were seen in short-chain fatty acid concentrations, pH, bile acid concentrations, or cytotoxicity of fecal water. Thus, apart from increased fecal weight, in this study, RS2 and RS3 did not reduce risk factors associated with colon cancer.
24. 2-induced cell damage after addition of short-chain fatty acids to the medium at concentrations that would be predicted to result from colonic fermentation of pectin or resistant starches.
25. 3 and phenol concentrations compared with the higher fiber - lower resistant starch Australian diet. The results raise the question of whether high levels of resistant starch associated with rice consumption produce less favorable effects than fruit, vegetable, and cereal fiber in a Western diet.
26. Williamson SL, Kartheuser A, Coaker J, Kooshkghazi MD, Fodde R, Burn J, et al.: Intestinal tumorigenesis in the Apc1638N mouse treated with aspirin and resistant starch for up to 5 months. Carcinogenesis 1999, 20:805-810. A mouse model with a mutant allele in the adenomatous polyposis (Apc) gene, in which spontaneous small intestinal tumors develop, showed development of more tumors when fed resistant starch from potato or high-amylose maize. The effect was reduced with aspirin. This finding is disturbing if the mouse model is relevant to humans. It may be that only those with mutations in the Apc gene are at risk.
27. Giovannucci E, Rimm EB, Stampfer MJ, Colditz GA, Ascherio A, Willett WC: Aspirin use and the risk for colorectal cancer and adenoma in male health professionals. Ann Intern Med 1994, 121:241-246.
28. Giovannucci E, Egan KM, Hunter DJ, Stampfer MJ, Colditz GA, Willett WC, et al.: Aspirin and the risk of colorectal cancer in women. N Engl J Med 1995, 333;609-614.
29. Brighenti F, Casiraghi MC, Baggio C: Resistant starch in the Italian diet. Br J Nutr 1998, 80:333-341.
30. Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC: Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA 1997, 277:472-477.
31. Salmeron J, Ascherio A, Rimm EB, et al.: Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care 1997, 20:545-550.
32. Liu S, Stampfer M, Manson JE, et al.: A prospective study of dietary glycemic load, carbohydrate and risk of coronary heart disease in US women [abstract]. FASEB J 1998, 12:A260. This analysis of data from the Nurses' Health Study demonstrated that, in approximately 80,000 nurses observed for 10 years, the higher the glycemic index of the diet the greater the relative risk of cardiovascular disease.
33. Frost G, Leeds A, Doré C, Madeiros S, Brading S, Dornhorst A: Glycaemic index as a determinant of serum HDL-cholesterol concentration. Lancet 1999, 353:1045-1048. A study of more than 2,000 British adults showed that the higher the HDL cholesterol level, the lower the diet glycemic index, indicating that the HDL effect may explain the reduced risk of coronary heart disease.
34. Ford E, Liu S: Glycemic index, glycemic load, and serum high-density lipoprotein (HDL) cholesterol concentrations among United States adults [abstract]. Circulation 1999, in press. This assessment of the National Health and Nutrition Examination Survey (NHANES) III data (in more than 30,000 American adults) demonstrated that the higher the glycemic index of the diet, the lower the HDL cholesterol level. This study also provides a reason for the protective effect of low glycemic index diets related to coronary heart disease risk according to one study (Reference 32).
35. Hill MJ: Cereals, cereal fibre and colorectal cancer risk: a review of the epidemiological literature. Eur J Cancer Prev 1997, 6:219-225.
36. Fuchs CS, Giovannucci EL, Colditz GA, Hunter DJ, Stampfer MJ, Rosner B, et al.: Dietary fiber and the risk of colorectal cancer and adenoma in women. N Engl J Med 1999, 340:169-176. This study, also from the Nurses' Health Study, was disappointing in not showing a protective role of fiber for colorectal cancer, even in the highest quintile of fiber consumption. Nevertheless, women in the highest quintile of intake consumed only an average of slightly more than 24 g of fiber daily, less than the 25 to 30 g advocated. An effect of different types of fiber at levels eaten in some vegetarian diets or in high-fiber diets eaten in parts of the world such as sub-Saharan Africa cannot be ruled out.
37. McKeown-Eyssen G: Epidemiology of colorectal cancer revisited: are serum triglycerides and/or plasma glucose associated with risk? Cancer Epidemiol Biomarkers Prev 1994, 3:687-695.
38. Hu FB, Manson JE, Liu S, Hunter D, Colditz GA, Michels KB, et al.: Prospective study of adult onset diabetes mellitus (type 2) and risk of colorectal cancer in women. J Natl Cancer Inst 1999, 91:542-547. In the follow-up of the Nurses' Health Study (118,403 women), 892 new cases of colorectal cancer were observed. Compared with nondiabetic nurses, those with diabetes had an increased adjusted relative risk for colon cancer (RR = 1.49; P = 0.01), rectal cancer (RR = 1.11; P = 0.76), advanced colorectal cancer (RR = 1.56; P=0.02), and fatal colorectal cancer (RR = 2.39; P = 0.0005). If high glycemic index diets result in diabetes and diabetes relates to colorectal cancer, then these diets support the link between glycemic index of slowly absorbed starch and reduction in colorectal cancer risk.