Postprandial glucose and insulin responses to various snacks of equivalent carbohydrate content in normal subjects.

To evaluate glucose and insulin responses after ingestion of snacks, we gave healthy, nondiabetic male subjects carbohydrate equivalent (25 g) snacks or isocaloric (265 kcal) snack meals in a random crossover design. Individual snacks composed of either a milk chocolate bar, granola bar, chocolate milk, peanut butter cups, yogurt, or potato chips produced similar glucose response curves. Plasma glucose concentrations were lower (p less than or equal to 0.05) at 30 and 60 min postprandially than after a corresponding oral glucose challenge. In contrast, insulin responses to the snacks exhibited a two-fold variation in peak values. Isocaloric snack meals of cereal-milk, cheese sandwich-milk, and peanut butter sandwich-chocolate milk produced glucose and insulin responses similar to individual snacks. Although glucose concentrations at 60 min fell somewhat below baseline values after each snack, clinical hypoglycemia was not evident. These data clearly indicate a similarity in glycemic response among normal individuals consuming a variety of common snacks.

Patterns of chocolate consumption.

Although consumed in some form since at least 460 AD, cacao (Theobroma cacao) was not used in confectionery until the 19th century when the cocoa press was invented. Per capita consumption of chocolate confectionery in the United States is moderate (approximately 4.6-4.8 kg/y) compared with that of many northern European countries (approximately 7-10 kg/y). Eleven percent of the US population reported consuming chocolate candy on > or = 1 of the 3 d of recorded food intake in the US Department of Agriculture Nationwide Food Consumption Survey 1987-1988; < 1.0% consumed chocolate every day. The Western region of the United States contained the highest proportion of chocolate consumers. More whites than other racial groups were consumers. Chocolate was consumed by more people in the winter than in other seasons and more was consumed at snacks than at meals. The mean amount of chocolate consumed was approximately 30-90 g/d, depending on sex and age group. Chocolate candy was only a minor contributor (0.7-3.4%) to the overall dietary intake of total energy, fat, saturated fatty acids, and stearic acid.

Digestibility of cocoa butter and corn oil in human subjects: a preliminary study.

The comparative absorption of cocoa butter (25.5% C16:0, 34.4% C18:0, 34.4% C18:1, 3.4% C18:2) and corn oil (11.4% C16:0, 2.0% C18:0, 26.4% C18:1, 60.0% C18:2) was assessed in six healthy male subjects. During 3-d experimental diet periods, free-living subjects consumed either cocoa butter or corn oil as virtually the sole source of dietary fat, provided at 40% of the total energy intake in the form of specially formulated cookies. Fat absorption was determined by quantifying total fecal lipid excretion over the 3-d period. Total fecal lipid and fecal fatty acids were determined. The percentage of fat excreted was significantly higher (p less than or equal to 0.001) when subjects consumed the cocoa butter (10.8 +/- 3.2%) vs the corn oil (3.5 +/- 1.0%) diet. These results indicate that the digestibility of cocoa butter is significantly less than corn oil and may explain, in part, previous reports of a neutral effect of dietary cocoa butter on plasma cholesterol concentrations.

Three-generation reproductive study of cocoa powder in rats.

Male and female Sprague-Dawley rats were continuously exposed to dietary cocoa powder at levels of 0.0, 1.5, 3.5 or 5.0% for three generations. During the initial 12-wk growth periods for the F0-, F1b- and F2b-generation rats, mean methylxanthine exposures (mg/kg/day) for males/females were 30/36, 72/86 and 104/126 for the 1.5, 3.5 and 5.0% cocoa powder groups, respectively. No consistent dose-related effects on any of the monitored reproductive indices (mating, fertility, conception, gestation, viability or lactation) were noted over three generations. Minor reductions in mean body weight relative to controls at wk 12 were observed in male rats exposed to 3.5 or 5.0% cocoa powder and female rats exposed to 5.0% cocoa powder in the F1b and F2b generations. Renal tubular mineralization in the F0-generation male rats in the 5.0% cocoa powder group was the only statistically elevated histomorphological lesion observed. Plasma cholesterol concentrations in F1b-generation rats were elevated, but cocoa powder did not affect this parameter consistently across multiple generations. Thus, continuous cocoa powder consumption by rats at levels as high as 5.0% of the diet was without effect on reproductive capacity under the conditions of a standard three-generation evaluation.

Chronic toxicity/carcinogenicity studies of cocoa powder in rats.

Cocoa powder (CP) was fed at levels of 0.0 (control), 1.5, 3.5 and 5.0% for 104 wk to male and female Sprague-Dawley rats derived from the F3b generation of a multigeneration study using the same CP diets. Initial methylxanthine intake was high in all treatment groups, but steadily declined until wk 26. The high dose level provided a mean methylxanthine intake of approximately 57 mg/kg body weight/day for males and 74 mg/kg body weight/day for females from wk 26 to wk 104 of the study. Compared with controls, the historical trend of methylxanthine-associated growth stimulation was evident in rats consuming diets containing 1.5% CP, while body weight was reduced in rats consuming diets containing 3.5 and 5.0% CP. Survival rates were similar in control and CP-fed rats. No evidence of treatment-related clinical disease or ocular effects was noted. An increased incidence of bilateral testicular atrophy and aspermatogenesis was present in males consuming diets containing 5.0% CP. Non-suppurative myocarditis and interstitial fibrosis of the heart were also increased in incidence in both sexes receiving diets containing 5.0% CP. The overall incidences of both pelvic dilatation and renal pelvic microcalculi were increased in most treatment groups. Although there was no difference in the incidence of benign mammary gland fibroadenomas in female rats between the control group and any CP-fed group, a marginally significant (P = 0.04) trend test was apparent. The significance of this finding is doubtful, since the incidence of this lesion in the highest dose group was well within the historical control range for this strain of rats. No evidence of carcinogenicity from dietary CP was found in either sex.

Digestibility of cocoa butter and corn oil and their influence on fatty acid distribution in rats.

The comparative bioavailability of cocoa butter (a predominantly saturated fat) and corn oil (a predominantly unsaturated fat) was determined in male Sprague-Dawley rats by analysis of total fecal lipids following ad libitum feeding of purified diets containing 5, 10 and 20% cocoa butter or corn oil for 2 wk. Fecal lipid elimination was significantly increased (P less than 0.05) in each cocoa butter group when compared with the corresponding corn oil group, resulting in lower digestibility coefficients for cocoa butter (59-72%) than for corn oil (93-97%). Body weight gain and food intake data were similar among all treatment groups. Fecal fatty acid profiles in rats fed corn oil diets consisted primarily of 27-34% palmitic acid (16:0), 22-32% stearic acid (18:0) and 25-37% oleic acid (18:1). Palmitic, oleic and linoleic acids were also the primary fatty acids stored in epididymal fat tissue from corn oil-fed rats. In contrast, fecal fatty acids in animals fed cocoa butter diets consisted of 31-37% palmitic acid and 58-64% stearic acid; oleic acid was the major fatty acid stored in epididymal fat tissue. These results indicate that the decreased digestibility of cocoa butter is largely a result of its fatty acid composition. This reduced bioavailability of cocoa butter may be at least partially responsible for its previously described neutral effect on serum cholesterol.