To determine factors beyond obesity which contribute to diabetes and cardiovascular risk in Mexicans and Mexican Americans. To test the hypothesis that at any given level of adiposity Mexican Americans will be more insulin resistant than Anglos and that the insulin resistance in Mexican Americans is proportional to the degree of Native American ancestry.
BACKGROUND: The present study was preceded by the earlier San Antonio Heart Study 1 supported under this grant. The San Antonio Heart Study 1 was a population-based survey of diabetes and cardiovascular risk factors in Mexican American and non-Hispanic whites conducted from 1979 to 1982. Participants included all men and non-pregnant women ages 24 to 64, who resided in households randomly sampled from three socio-culturally distinct neighborhoods of San Antonio. The low-income barrio residents were almost exclusively traditional Mexican-Americans. The middle-income neighborhood was ethnically balanced with equal numbers of Mexican Americans and Anglos whereas the upper income suburb was approximately 90 percent Anglo. Risk factors measured included obesity, glucose intolerance, hypertriglyceridemia, low levels of high density lipoprotein cholesterol, and blood pressure. The total number of people who were examined medically was 2,386, divided as follows: 1,288 Mexican Americans; 929 Anglos; and 169 other Hispanics such as Cubans. The San Antonio Heart Study was designed to test the hypothesis that as Mexican Americans became progressively more affluent and acculturated to 'mainstream' United States culture, they would gradually lose their diabetic pattern of cardiovascular risk factors of obesity, diabetes, and hypertriglyceridemia. DESIGN NARRATIVE: Beginning in 1979, a random sample was conducted to select participants. Sampling was performed to match the two groups on obesity, thereby enabling an analysis of the ethnic differences in diabetes and cardiovascular risk factors independent of the confounding effects of obesity. For those selected, an interview and medical examination were conducted in a mobile clinic. The interview consisted of a personal and family history of diabetes and cardiovascular risk, knowledge of and attitudes towards cardiovascular risk factors, dietary questionnaire, Rose Angina questionnaire, intermittent claudication questionnaire, and medication history. The medical examination consisted of anthropometric measurements, plasma glucose, plasma insulin, hemoglobin, serum cholesterol, triglyceride, HDL, LDL, and VLDL, genetic markers, blood pressure, skin color and electrocardiogram. It was estimated that 400 diabetics would be available over the four years of the study to permit a Diabetic Recall Examination. The purpose of the Diabetic Recall Examination was to assess possible end-organ complications of diabetes involving the eye, kidney, peripheral and autonomic nervous systems, and the peripheral vascular system. The assessment provided baseline data on diabetics which was used for a prospective incidence study. Beginning in 1989, a prevalence survey of type II diabetes mellitus and cardiovascular risk factors was conducted in a low-income barrio in Mexico City. Information collected on this population included demographic data, socioeconomic status, level of acculturation, medical history, diet, exercise, and smoking. The physical examination included measurements of blood pressure, obesity, body fat distribution, and skin color. The laboratory examination included measurements of lipids and lipoproteins, oral glucose tolerance tests, fasting and post-glucose load insulin concentrations and genetic markers. Beginning in FY 1989, Michael Stern and associates carried out an epidemiologic study of type II diabetes mellitus and cardiovascular risk factors in a low-income barrio of Mexico City and compared results to those obtained in San Antonio. They recruited and interviewed subjects for data on demographics, socioeconomic status, level of acculturation, medical history, health habits including diet, physical exercise, and smoking. The physical examination included blood pressure, obesity, body fat distribution, skin color, the latter to estimate percent Native American genetic admixture. The laboratory examination included measurements of lipids and lipoproteins, an oral glucose tolerance test to determine the prevalence of diabetes according to the National Diabetes Data Group criteria, fasting and post-glucose load insulin concentrations, and genetic markers. The study was renewed in 1996 through August, 2001. A 3.25 year followup examination (FU1) of a cohort of 2,296 Mexican men and women, ages 35-64 years at baseline, was completed. The cohort was re-examined at 3.25-year intervals (6.5 years (FU2) and 9.75 years (FU3) after baseline). The investigators tested the hypothesis that different risk factors would prevail in the early (more than 3.25 years prior to conversion to diabetes) than in the late (3.25 years or less prior to conversion) prediabetic period. They hypothesized that in the early prediabetic period risk factors associated with the Insulin Resistance Syndrome would predominate, i.e., high "specific" insulin concentration (measured by a specific immunoassay), hypertriglyceridemia, low HDL-cholesterol, and hypertension, whereas in the late prediabetic period factors associated with insulin secretory failure, i.e., increased proinsulin and low "specific" insulin, would predominate. Michael Stern and associates assessed carotid wall thickness by ultrasonography on all subjects at FU1 and planned to repeat this at FU2. They measured advanced glycation endproduct (AGE)-modified apolipoprotein B and a panel of inflammatory risk factors (serum albumin, serum amyloid A, alpha1-acid glycoprotein, and C-reactive protein) on stored contingency specimens from baseline and FU1 in order to determine if these factors predicted accelerated thickening of carotid walls and/or the development of type II diabetes. They also quantified the extent to which carotid wall thickness and ECG documented myocardial infarction preceded clinical diabetes as predicted by the "common soil" hypothesis, i.e., the hypothesis that both type II diabetes and atherosclerosis have common genetic and environmental antecedents.
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OBSERVATIONAL
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