Resistant starch (RS) is starch and products of its small intestinal digestion that enter the large bowel. It occurs for various reasons including chemical structure, cooking of food, chemical modification, and food mastication. Human colonic bacteria ferment RS and nonstarch polysaccharides (NSP; major components of dietary fiber) to short-chain fatty acids (SCFA), mainly acetate, propionate, and butyrate. SCFA stimulate colonic blood flow and fluid and electrolyte uptake. Butyrate is a preferred substrate for colonocytes and appears to promote a normal phenotype in these cells. Fermentation of some RS types favors butyrate production. Measurement of colonic fermentation in humans is difficult, and indirect measures (e.g., fecal samples) or animal models have been used. Of the latter, rodents appear to be of limited value, and pigs or dogs are preferable. RS is less effective than NSP in stool bulking, but epidemiological data suggest that it is more protective against colorectal cancer, possibly via butyrate. RS is a prebiotic, but knowledge of its other interactions with the microflora is limited. The contribution of RS to fermentation and colonic physiology seems to be greater than that of NSP. However, the lack of a generally accepted analytical procedure that accommodates the major influences on RS means this is yet to be established.

Background: It is currently unclear whether altering the carbohydrate-to-protein ratio of low-fat, energy-restricted diets augments weight loss and cardiometabolic risk markers.

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Colorectal cancer is a major cause of cancer mortality and is considered to be largely attributable to inappropriate lifestyle and behavior patterns. The purpose of this review was to undertake a comparison of the strength of the associations between known and putative risk factors for colorectal cancer by conducting 10 independent meta‐analyses of prospective cohort studies. Studies published between 1966 and January 2008 were identified through EMBASE and MEDLINE, using a combined text word and MESH heading search strategy. Studies were eligible if they reported estimates of the relative risk for colorectal cancer with any of the following: alcohol, smoking, diabetes, physical activity, meat, fish, poultry, fruits and vegetables. Studies were excluded if the estimates were not adjusted at least for age. Overall, data from 103 cohort studies were included. The risk of colorectal cancer was significantly associated with alcohol: individuals consuming the most alcohol had 60% greater risk of colorectal cancer compared with non‐ or light drinkers (relative risk 1.56, 95% CI 1.42–1.70). Smoking, diabetes, obesity and high meat intakes were each associated with a significant 20% increased risk of colorectal cancer (compared with individuals in the lowest categories for each) with little evidence of between‐study heterogeneity or publication bias. Physical activity was protective against colorectal cancer. Public‐health strategies that promote modest alcohol consumption, smoking cessation, weight loss, increased physical activity and moderate consumption of red and processed meat are likely to have significant benefits at the population level for reducing the incidence of colorectal cancer. © 2009 UICC

Growing evidence from animal studies supports the anti-diabetic properties of some dietary polyphenols, suggesting that dietary polyphenols could be one dietary therapy for the prevention and management of Type 2 diabetes. This review aims to address the potential mechanisms of action of dietary polyphenols in the regulation of glucose homeostasis and insulin sensitivity based on in vitro and in vivo studies, and to provide a comprehensive overview of the anti-diabetic effects of commonly consumed dietary polyphenols including polyphenol-rich mixed diets, tea and coffee, chocolate and cocoa, cinnamon, grape, pomegranate, red wine, berries and olive oil, with a focus on human clinical trials. Dietary polyphenols may inhibit α-amylase and α-glucosidase, inhibit glucose absorption in the intestine by sodium-dependent glucose transporter 1 (SGLT1), stimulate insulin secretion and reduce hepatic glucose output. Polyphenols may also enhance insulin-dependent glucose uptake, activate 5′ adenosine monophosphate-activated protein kinase (AMPK), modify the microbiome and have anti-inflammatory effects. However, human epidemiological and intervention studies have shown inconsistent results. Further intervention studies are essential to clarify the conflicting findings and confirm or refute the anti-diabetic effects of dietary polyphenols.

Overweight women with polycystic ovary syndrome (PCOS) were randomized to a high protein (HP; 40% carbohydrate and 30% protein; n = 14) or a low protein (LP; 55% carbohydrate and 15% protein) diet (n = 14). The intervention consisted of 12 wk of energy restriction (∼6000 kJ/d), followed by 4 wk of weight maintenance. Pregnancies (two HP and one LP); improvements in menstrual cyclicity, lipid profile, and insulin resistance (as measured by the homeostasis model); and decreases in weight (7.5%) and abdominal fat (12.5%) occurred independently of diet composition. Improvements in menstrual cyclicity were associated with greater decreases in insulin resistance and fasting insulin (P = 0.011). On the LP diet, high density lipoprotein cholesterol decreased 10% during energy restriction (P = 0.008), and the free androgen index increased 44% in weight maintenance stages (P = 0.027). Weight loss leads to improvements in cardiovascular and reproductive parameters potentially mediated by improvements in surrogate measures of insulin resistance. An HP weight loss diet may result in minor differential endocrine and metabolic improvements.