Recent recommendations for the dietary management of diabetes mellitus state that diet needs to be individualized so that there is improved glucose and lipid control in the patient. In a majority of individuals with diabetes, this is best done with a diet that is low in fat and high in carbohydrate, particularly that of cereal origin. However, symptoms of hyper- and hypoglycemia must be averted. Most cereal products, however, tend to have a high glycemic index Cereals such as Prowashonupana barley or fractions of oat bran are particularly high in the soluble fiber beta-glucan, which when taken with a meal increases the viscosity of the meal bolus once it has reached the small intestine, where the absorption of nutrients occurs. This high viscosity delays absorption. A 50% reduction in glycemic peak can be achieved with a concentration of 10% beta-glucan in a cereal food. A significant lowering of plasma LDL cholesterol concentrations can also be anticipated with the daily consumption of > or = 3 g of beta-glucan. Diabetic individuals can benefit from diets that are high in beta-glucan, which, as a component of oats and barley, can be incorporated into breakfast cereals and other products.

Resting metabolic rate (RMR) was measured in 154 women and 48 men before the beginning of a weight reduction program. In both sexes there were significant univariate correlations between RMR and fat-free mass, body fat, weight, fat cell weight, and fat cell number (from total body water). Women also showed significant correlations between RMR and fat cell number (from total body potassium), free triiodothyronine index, and fasting and postglucose insulin levels. Multiple regression analysis showed that both fat-free mass and fat cell weight and number were significant predictors of RMR. The contribution of fat-free mass was three to five times greater per kg than that of body fat. There was no significant contribution of thyroid hormones or insulin to the prediction of RMR. Fat cell number and fat cell weight were significant predictors of RMR, whether determined from body water, body potassium, or a formula using both water and potassium. There was no significant difference in regression coefficients between men and women. Thus the difference in RMR between the sexes is probably caused by the higher proportion of fat-free mass in men. The effect of age was small and not statistically significant.

Weight loss reduces many of the health hazards associated with obesity including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, sleep apnea, hypoxemia and hypercarbia, and osteoarthritis. Potential adverse effects of weight loss include a greater risk for gallstone formation and cholecystitis, excessive loss of lean body mass, water and electrolyte problems, mild liver dysfunction, and elevated uric acid levels. Less consequential problems such as diarrhea, constipation, hair loss, and cold intolerance may also occur. The short-term adverse effects are not severe enough to contraindicate weight loss, nor do they outweigh its short-term benefits.

To clarify the independent relationships of obesity and overweight to cardiovascular disease risk factors and sex steroid levels, three age-matched groups of men were studied: (i) 8 normal weight men, < 15% body fat, by hydrostatic weighing; (il) 16 overweight, obese men, > 25% body fat and 135-160% of ideal body weight (IBW); and (ill) 8 overweight, lean men, 135-160% IBW, but < 15% fat. Diastolic blood pressure was significantly greater for the obese (mean±SEM, 82±2 mmHg) than the normal (71±2) and overweight lean (72±2) groups, as were low density lipoprotein levels (131±9 vs. 98+11 and 98+14 mg/dl), the ratio of high density lipoprotein to total cholesterol (0.207±0.01 vs. 0.308±0.03 and 0.302±0.03), fasting plasma insulin (22±3 vs. 12±1 and 13±2 ;U/ml), and the estradiol/testosterone ratio (0.076±0.01 vs. 0.042+0.02 and 0.052±0.02); P < 0.05. Estradiol was 25% greater for the overweight lean group (40±5 pg/ml) than the obese (30±3 pg/ml) and normal groups (29±2 pg/ml), P = 0.08, whereas total testosterone was significantly lower in the obese (499±33 ng/dl) compared with the normal and overweight, lean groups (759±98 and 797±82 ng/dl). Estradiol was uncorrelated with risk factors and the estradiol/testosterone ratio appeared to be a function of the reduced testosterone levels in obesity, not independently correlated with lipid levels after adjustment for body fat content. Furthermore, no risk factors were significantly different between the normal and overweight lean groups. We conclude that (a) body composition, rather than body weight per se, is associated with increased cardiovascular disease risk factors; and (b) sex steroid alterations are related to body composition and are not an independent cardiovascular disease risk factor.

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