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To study genetic and environmental determinants of non-insulin-dependent (type II) diabetes, we compared a random sample of 35- to 64-yr-old Mexican-American men and women living in several low-income barrio neighborhoods of San Antonio to similarly aged Mexicans living in a low-income colonia of Mexico City (Colonia Liberales). A total of 1138 Mexican Americans, representing 64.3% of the original sample, and 646 Mexicans, representing 69.2% of the original sample, participated in the survey. Diabetes was diagnosed using World Health Organization criteria. Genetic susceptibility to type II diabetes was inferred from the percentage of Native American genetic admixture as estimated from skin reflectance measurements. The prevalence of diabetes was 36% higher among San Antonio Mexican Americans than among Mexicans in Mexico City; this difference was highly statistically significant (age- and sex-adjusted prevalence ratio 1.36, P = 0.006). This excess was observed despite the fact that genetic susceptibility, as inferred from the admixture estimates, was similar in the two cities. On the other hand, Mexicans were somewhat leaner as measured by body mass index and skin folds. Mexican women consumed fewer total calories than Mexican-American women, but there was no difference in the caloric intake of men. Mexico City residents ate less fat (18–19% of total calories vs. 31–32% in San Antonio, P 0.001), more carbohydrate (64–65 vs. 49%, P 0.001), and performed more physical activity than San Antonio Mexican Americans. Mexicans appeared to consume more refined sugar than Mexican Americans. Mexicans had lower total cholesterol but higher triglyceride and fasting insulin concentrations than Mexican Americans (all P 0.002). The latter two observations are compatible with the hypothesis that the high-carbohydrate diet in Mexico City stimulated carbohydrate-induced hypertriglyceridemia, which was not offset by the greater degree of physical activity and leanness of Mexicans compared with Mexican Americans. The results of this study suggest that environmental factors can override genetic susceptibility in the expression of the type II diabetes trait.
Stern et al. (Wed,) studied this question.