Cocoa powder increases postprandial insulinemia in lean young adults.

We hypothesized that chocolate products elicit higher insulin responses than matched products with alternate flavoring. To test this, we used a within-subject, repeated-measures comparison of six pairs of foods, one flavored with chocolate (cocoa powder) and the other not. Healthy subjects (n = 10, 4 men, 6 women) tested each pair of foods. Postprandial glucose and insulin levels were determined at intervals over 2 h using standardized glycemic index (GI) methodology. The product categories were chocolate bars, cakes, breakfast cereals, ice creams, flavored milks and puddings. Although the GI did not differ within each pair, the insulin index (II) of the chocolate product was always higher, by a mean of 28%, than the alternate flavored product (P < 0.001). The greatest difference occurred within the flavored milk category in which the chocolate version elicited 45% greater insulinemia than the strawberry flavored milk (P = 0.021). Macronutrient composition (fat, protein, sugar, fiber or energy density) accounted for nearly all of the variation in GI among the foods, but did not explain differences in insulinemia. The presence of cocoa powder in foods leads to greater postprandial insulin secretion than alternate flavorings. Specific insulinogenic amino acids or greater cephalic phase insulin release may explain the findings.

The degree of fat saturation does not alter glycemic, insulinemic or satiety responses to a starchy staple in healthy men.

Inclusion of fat reduces the glycemic response to a carbohydate meal, although the effect of different types of fat on glycemic, insulinemic and satiety responses is unclear. Ten healthy men received 50-g carbohydrate portions of mashed potato with isoenergetic amounts of butter (saturated fatty acid), Sunola oil (monounsaturated fatty acid) or sunflower oil (PUFA) and two 50-g glucose loads on separate days. Capillary blood was collected at regular intervals for 2 h. Satiety ratings were assessed by use of a rating scale. The glycemic index (GI), insulin index (II) and satiety index (SI) scores were calculated. Energy intakes from a meal consumed ad libitum at 2 h and for the remainder of the day were quantified. The GI values ranged from 68 +/- 8 to 74 +/- 10 and the II values ranged from 113 +/- 10 to 122 +/- 17, but there was no effect of fat type. SI scores and subsequent energy intake did not differ among the test meals. Substitution of unsaturated fats for saturated fatty acids had no acute benefits on postprandial glycemia, insulin demand or short-term satiety in young men.

International table of glycemic index and glycemic load values: 2002.

Reliable tables of glycemic index (GI) compiled from the scientific literature are instrumental in improving the quality of research examining the relation between GI, glycemic load, and health. The GI has proven to be a more useful nutritional concept than is the chemical classification of carbohydrate (as simple or complex, as sugars or starches, or as available or unavailable), permitting new insights into the relation between the physiologic effects of carbohydrate-rich foods and health. Several prospective observational studies have shown that the chronic consumption of a diet with a high glycemic load (GI x dietary carbohydrate content) is independently associated with an increased risk of developing type 2 diabetes, cardiovascular disease, and certain cancers. This revised table contains almost 3 times the number of foods listed in the original table (first published in this Journal in 1995) and contains nearly 1300 data entries derived from published and unpublished verified sources, representing > 750 different types of foods tested with the use of standard methods. The revised table also lists the glycemic load associated with the consumption of specified serving sizes of different foods.

Glycemic index and obesity.

Although weight loss can be achieved by any means of energy restriction, current dietary guidelines have not prevented weight regain or population-level increases in obesity and overweight. Many high-carbohydrate, low-fat diets may be counterproductive to weight control because they markedly increase postprandial hyperglycemia and hyperinsulinemia. Many high-carbohydrate foods common to Western diets produce a high glycemic response [high-glycemic-index (GI) foods], promoting postprandial carbohydrate oxidation at the expense of fat oxidation, thus altering fuel partitioning in a way that may be conducive to body fat gain. In contrast, diets based on low-fat foods that produce a low glycemic response (low-GI foods) may enhance weight control because they promote satiety, minimize postprandial insulin secretion, and maintain insulin sensitivity. This hypothesis is supported by several intervention studies in humans in which energy-restricted diets based on low-GI foods produced greater weight loss than did equivalent diets based on high-GI foods. Long-term studies in animal models have also shown that diets based on high-GI starches promote weight gain, visceral adiposity, and higher concentrations of lipogenic enzymes than do isoenergetic, macronutrientcontrolled, low-GI-starch diets. In a study of healthy pregnant women, a high-GI diet was associated with greater weight at term than was a nutrient-balanced, low-GI diet. In a study of diet and complications of type 1 diabetes, the GI of the overall diet was an independent predictor of waist circumference in men. These findings provide the scientific rationale to justify randomized, controlled, multicenter intervention studies comparing the effects of conventional and low-GI diets on weight control.