The effect of response bias on odds ratio results was determined based on data from a population-based cardiovascular disease survey. The study subjects consisted of 5000 adult residents of a predominantly white, upper-middle class community. Information from 60% of the 1100 non-respondents was obtained by telephone. Consistent patterns of participation associated with risk factors and diseases under study were found. A simple error term was developed to convert the odds ratio for respondents to the odds ratio for the target population using individual cell response rates. This error term demonstrates that the response patterns found tended to minimize the error in odds ratio calculations for respondents. Only by obtaining relevant information on non-respondents can investigators accurately estimate response bias and its effects on the odds ratio.

Most previous studies of hyperlipidemia in diabetics are based on patients in specialty clinics or reflect an era when diabetics consumed a high-fat, low-carbohydrate diet. In this paper, data from a defined adult population aged 20-79 years in an upper middle class community in Southern California, 1972-1974, were used to ascertain the relationship of hyperlipidemia to diabetes in a current community-based population. All (n = 358) diabetics as defined by history and/or fasting hyperglycemia (fasting plasma glucose, greater than or equal to 140 mg/dl) were compared with all (n = 4387) nondiabetics defined as euglycemic (fasting plasma glucose, less than 110 mg/dl) with no personal or family history of diabetes. In both men and women 50 years of age and older, the mean cholesterol level and the prevelance of categorical hypercholesterolemia were not significantly different in diabetics vs. nondiabetics, whereas the mean triglyceride level and the prevalence of categorical hypertriglyceridemia were significantly higher in diabetics vs. nondiabetics. Case-control comparisons of 356 diabetics matched for age and obesity with 356 nondiabetics confirmed the significantly higher triglyceride levels in diabetes. Conversely, hypertriglyceridemia was associated with diabetes in 29 per cent of nonobese men and 25 per cent of obese men, and in 10 per cent of non-obese women and 21 per cent of obese women. The biologic mechanism of hypertriglyceridemia in diabetics is discussed.

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The relationship between diabetes and hypertension in 3456 residents of Rancho Bernardo, California, aged 50-79 years, surveyed in 1972-1974, was analyzed in depth in both the univariate mode and after adjustments for the potential confounding effects of age, obesity and diuretic medication. An association between diabetes and hypertension was present in both men and women at all ages, and the association was strongest for subjects having the best evidence for diabetes, i.e., both historical diabetes and fasting hyperglycemia. Adjustment for obesity reduced the association considerably, but a consistent association remained. diabetes and hypertension are linked only partially by obesity. Some of the excess risk of coronary heart disease in diabetes is probably due to hypertension.

Nutrient intake and alcohol consumption were studied in a 15% random sample of a predominantly white upper-middle class suburban community in Southern California. Based on 24-h dietary recall, 51% of the 691 men and women aged 30 to 90 yr in the study population had consumed an average of 30 g alcohol during the preceding 24 h. In general, alcohol-derived calories were added to the diet, and did not replace calories derived from other nutrients. Consequently, alcohol consumers had a significantly higher total caloric intake than did nondrinkers. Dietary differences were greatest in moderate drinkers, who tended to consume fewer nonalcohol-derived calories, and less of most specific nutrients. Although dietary differences in moderate drinkers were similar in men and women, statistically significant differences in women were limited to carbohydrate consumption. Moderate drinking men consumed significantly less protein, fat, carbohydrate, and cholesterol. These dietary differences suggest one mechanism whereby moderate alcohol consumption might reduce the risk of coronary heart disease. Although alcohol intake resulted in an increase in total calories consumed, alcohol drinkers were not more obese than nondrinkers. Since similar proportions of drinkers and nondrinkers exercised regularly, these data may suggest that alcohol calories are not fully utilized.