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Response bias in epidemiologic studies can occur if affected individuals are more (or less) likely to participate in a survey than their unaffected counterparts. To examine the effect of response bias in the context of a family study, we conducted segregation and linkage analysis in all 1,000 individuals in the Problem 2 data set, and in two different 65% samples: one sample consisting of 648 randomly selected individuals, and the other sample nonrandomly constructed so that individuals with high levels of Q1 were oversampled. In this simulation the ability to detect major genes for Q1-Q4 in segregation analysis and to link these putative major genes to genetic markers in linkage analysis was not markedly different between the 65% random and the 65% enriched samples.

Increased adiposity has repeatedly been identified as a major risk factor for a variety of chronic diseases. However, the question still remains whether the amount of adipose tissue itself is genetically mediated. To address this question, a segregation analysis, using maximum likelihood techniques as implemented in the computer program Pedigree Analysis Package (PAP), was performed on fat mass (kilograms of body fat) in a large sample of extended Mexican American families residing in San Antonio, TX. The only model not rejected was a Mendelian mixed model for fat mass, incorporating genotype x sex interaction. In males the major gene accounted for 37% of the total variance compared with 43% in females. In both sexes homozygous recessive individuals have a fat mass more than double that of individuals of the other two genotypes. It was possible to reject linkage of the anonymous major gene for fat mass with several candidate loci for obesity. However, tentative evidence of linkage was detected with markers on both chromosomes 2 and 11, thereby providing hypotheses for future testing.

A bivariate genetic analysis, utilizing variance decomposition techniques based on maximum likelihood methods, was undertaken to examine the genetic and environmental correlations among eight skinfolds in a large pedigreed sample of Mexican Americans from San Antonio, Texas. The resulting correlation coefficients reveal significant values for both the genetic and environmental components among the traits examined. The genetic correlation coefficients showed the highest values between skinfolds from the same region (i.e., triceps, biceps, and forearm), while the environmental correlation remained fairly constant between all traits. These findings are further supported by a principal component analysis of the phenotypic, genetic, and environmental correlation matrices. This represents the first study to partition the phenotypic correlation between these traits into their genetic and environmental components. An examination of the graphical representations of the eigenvectors of these correlation matrices reveals that the patterns of central versus peripheral fat distribution seen in the phenotypic correlation matrix are largely a function of the genetic correlation structure. All these findings are interpreted as evidence of a global pleiotropic effect in the genetic expression of these traits, with what might be secondary regional pleiotropic effects among specific subsets of the skinfolds. In addition it appears that these pleiotropic effects exist against a background of a relatively constant shared environmental effect. It is concluded that these traits are not independent with respect to either shared genetic or environmental influences.

To study demographic, anthropometric and metabolic determinants of weight change, we divided a random sample of 1493 Mexican Americans and non-Hispanic whites into two groups: weight gainers and weight losers. This classification was based on the weight change during the eight-year follow-up of participants of the San Antonio Heart Study, a population-based longitudinal study of diabetes and cardiovascular disease. Men gained significantly less weight and lost more weight than women. The average gains for weight gainers were 6.1 kg and 6.8 kg for men and women respectively; and the average losses for weight losers were 4.4 and 3.4 kg for men and women respectively. There was no ethnic difference in either category of weight change. Weight gainers were significantly younger and leaner than weight losers. Fasting insulin was the only independent metabolic predictor of weight change and only among the most obese tertile of the population: the higher the baseline levels of fasting insulin, the less the likelihood of gaining and the greater the likelihood of losing weight. Our results support the hypothesis that insulin resistance is part of a negative feedback mechanism that attenuates further weight gain among the obese.

Epidemiologic studies have revealed that Mexican Americans experience an excess of non-insulin-dependent diabetes mellitus, gallbladder disease, and obesity relative to non-Hispanic whites. It has been hypothesized that the greater susceptibility of Mexican Americans to these disorders may be related to their greater degree of Amerindian genetic admixture. We evaluate the comparability of three different methods of assessing individual genetic admixture in Mexican Americans. Subjects were enrolled as part of the San Antonio Heart Study and were examined between 1979 and 1988 (n = 3301). Three different methods were used to assess Amerindian admixture: we queried subjects about their ancestors' ethnic origin, we measured subjects' skin color, and we estimated genetic admixture directly by analysis of polymorphic blood markers. These measures were generally poorly correlated with each other, with the highest correlations observed between skin color and proportion of Mexican-origin grandparents. In men, none of these three measures of genetic admixture was associated with the prevalence of diabetes, gallbladder disease, or obesity. In women, consistent positive associations were observed between admixture and all three diseases, regardless of the admixture measure used (ie, disease prevalence was higher among women with more Amerindian admixture). In both sexes, height was negatively correlated with all three measures of admixture, and admixture was also significantly correlated with body mass index and central adiposity in women. These data suggest that the three measures considered may assess different dimensions of admixture, but that for epidemiologic research, no one may be claimed to be superior to the others.

Objective: To examine the long-term stability of the World Health Organization criteria for diabetes in the 8-yr follow-up of the San Antonio Heart Study. A problem with older criteria for diagnosing diabetes was that many individuals classified as having borderline or chemical diabetes reverted to nondiabetic status on follow-up. Few studies have addressed this issue among diabetic patients who meet the more stringent, modern National Diabetes Data Group or World Health Organization criteria., Research Design and Methods: We studied 98 Mexican-American and 44 non-Hispanic white type II diabetic patients 8 yr after they were diagnosed according to World Health Organization criteria in a population-based epidemiological survey. Patients were classified as follows: whether they were on pharmacological treatment for diabetes at baseline, or, if not, whether they had a prior diagnosis of diabetes at the time of their baseline survey visit or were newly diagnosed., Results: Of the 142 patients who met the study criteria for type II diabetes at baseline and whose status at follow-up was known, 20 (14.1%; 95% confidence interval 9.0-20.5%) no longer met criteria at follow-up 8 yr later. All but 2 of those who reverted to nondiabetic status were from the newly diagnosed group. Two of 20 had lost more than 5.0 kg over the 8 yr and an additional 5 had lost 2.5-5.0 kg. The 20 patients who reverted to nondiabetic status lacked many of the associated anthropometric, physiological, and metabolic findings of diabetes such as obesity, unfavorable body fat distribution, and dyslipidemia. Moreover, only one had proteinuria, and none had any grade of diabetic retinopathy at baseline., Conclusions: Epidemiological surveys that rely on a single oral glucose tolerance test to determine the prevalence of type II diabetes may overestimate prevalence by as much as 16% (95% confidence interval 10.5-23.6%) (142/122 = 1.16). The actual overestimate could well be less because some patients who truly have diabetes at baseline may be in remission at follow-up as a result of significant weight loss. Despite these difficulties, the modern National Diabetes Data Group and World Health Organization criteria are more stable than earlier criteria.

International dietary comparisons present a number of methodologic difficulties. We developed two semiquantitative food frequency questionnaires for use in Mexico City and San Antonio, Texas. The Mexico City questionnaire contained 85 food items and the San Antonio questionnaire contained 108. Thirty-six items were common to both questionnaires. The questionnaires were administered to 128 Mexican Americans, 35 to 64 years old, residing in a low-income barrio neighborhood of San Antonio and to 644 similarly aged Mexicans residing in a low-income "colonia" of Mexico City. Major differences in fat and carbohydrate intake as a percent of total kilocalories were observed between the two study groups, with Mexico City residents consuming approximately 18 to 21% of calories from fat and 68 to 72% from carbohydrate compared to 29 to 33% from fat and 48 to 52% from carbohydrate for Mexican Americans from San Antonio. Both of these differences were highly statistically significant (P < 0.001). A number of arguments support the validity of these findings. First, the distribution of high- and low-fat foods was similar on both questionnaires. Also, of the top-ten foods (as contributors to total kilocalorie intake) in San Antonio, seven were high in fat (> 30% of kilocalories), whereas this was true of only three of the top-ten foods in Mexico City.

We developed predictive models for type II diabetes using stepwise multiple logistic regression analyses of a cohort of 844 Mexican Americans and 641 non-Hispanic whites who were nondiabetic at baseline and who were then followed for 8 yr. Models were developed for the overall population and separately for each sex and ethnic group. For optimal models, the multiple logistic regression program selected potential risk factors from a panel of 5 categorical and 14 continuous demographic, anthropometric, metabolic, and hemodynamic variables. For reduced models, the list of candidate variables was restricted to those commonly used in ordinary clinical practice, i.e., skinfolds, and serum insulin and postural glucose load variables were excluded. For all models, the stepwise process selected a mixture of anthropometric, glucose, lipid, and hemodynamic variables. The top 15% of the risk continuum for each model was defined as high risk to compare the performance of the models with the performance of impaired glucose tolerance (15% prevalence) as a predictor of diabetes. The relative risk of being high risk ranged from 12.16 to 35.29, whereas the relative risk of having impaired glucose tolerance ranged from 7.11 to 10.0. The sensitivity of the multiple logistic regression models ranged from 67.7 to 83.3% compared with 56.5 to 62.1% for impaired glucose tolerance. The results indicate that multivariate predictive models perform at least as well, if not better than impaired glucose tolerance in predicting type II diabetes but need not require an oral glucose load. Moreover, the models highlight the complex metabolic and hemodynamic syndrome that precedes diabetes.

Mexican Americans have an increased prevalence and incidence of non-insulin-dependent diabetes mellitus (NIDDM). In addition, Mexican American diabetic subjects have an increased prevalence of retinopathy relative to Caucasian diabetic subjects. In Mexican American diabetic subjects, established risk factors may have a stronger effect on diabetic retinopathy, compared to Caucasian diabetic subjects. In this report, we compare the effect of established risk factors (age at examination, gender, age at diagnosis of diabetes, duration of diabetes, glycemia, type of therapy, systolic and diastolic blood pressure, and hypertension prevalence) between Caucasian diabetic subjects (n = 478), a low-risk population for NIDDM (Wisconsin Epidemiologic Study of Diabetic Retinopathy), and Mexican American diabetic subjects (n = 231), a high-risk population for NIDDM (San Antonio Heart Study). Retinopathy was classified into two categories (any or none) as assessed by seven standard stereoscopic retinal photographs read at the University of Wisconsin Reading Center. Mexican American diabetic subjects in Texas had an increased prevalence of any retinopathy (odds ratio = 1.71, 95% confidence interval: 1.25, 2.34), compared to Caucasian diabetic subjects in Wisconsin. Longer duration of diabetes, more severe glycemia, earlier age at diagnosis, and insulin therapy were associated with diabetic retinopathy in both Mexican Americans and Caucasians. Socioeconomic status was not associated with prevalence of retinopathy. Moreover, the effect of risk factors for retinopathy was similar in both ethnic groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension often occurs in association with NIDDM and IGT. We examined the association of hypertension at baseline to the 8-yr incidence of NIDDM and IGT in 1471 subjects who participated in the San Antonio Heart Study. Subjects who were hypertensive at baseline had a higher incidence of NIDDM (8.9 vs. 4.9%, P = 0.041) and IGT (25.2 vs. 10.0%, P < 0.001) than subjects who were normotensive at baseline. After adjusting for age, sex, ethnicity, obesity, body fat distribution, fasting glucose, and insulin, this excess was eliminated for NIDDM, but not for IGT. Specifically, the adjusted OR for NIDDM in hypertensive versus normotensive patients was 0.73 (95% Cl 0.34-1.58), whereas the adjusted OR for IGT was 1.87 (95% Cl 1.08-3.22). The excess risk of NIDDM in hypertensive patients can be explained by their greater age, obesity, more unfavorable body fat distribution, and hyperinsulinemia, whereas the excess risk of IGT is independent of these factors.

Using random initial parameter estimates, three segregation analysis models of the inheritance of HDL2 in the Berkeley GAW8 data set were maximized 5000 times each. Initial parameter estimates were assumed to be uniformly distributed on intervals formed by parameter boundaries. The three models were unrestricted, environmental, and Mendelian regressive type A models. Likelihood ratio tests of the global maxima rejected the Mendelian model and accepted the environmental model. However, tests using local maxima accepted the Mendelian model and both rejected and accepted the environmental model. Patterns among the initial parameter estimates of convergent runs were examined to develop empirical rules to increase the frequency of convergence. These rules were tested using data on apoAI in the Berkeley GAW8 data set.

Objective: In subjects with NIDDM, diabetic women have a greater relative excess of CHD relative to nondiabetic women than do diabetic men relative to nondiabetic men. This excess in diabetic women is explained partially by the particularly atherogenic pattern of lipoproteins in this group. We hypothesize that diabetic women also may have a higher incidence of hypertension than diabetic men., Research Design and Methods: We examined the effect of NIDDM and IGT relative to NGT on the incidence of hypertension separately in men (n = 844) and women (n = 618) in the 8-yr follow-up of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease., Results: Women had a greater risk of hypertension with worsening glucose tolerance (RR NIDDM/NGT = 2.65 and RR IGT/NGT = 1.94) compared with men (RR NIDDM/NGT = 1.61 and RR IGT/NGT = 0.91). Controlling for other possible confounding variables such as age, obesity, body fat distribution, and fasting insulin concentration did not alter the interaction of sex and glycemia on incidence of hypertension., Conclusions: The especially increased risk of hypertension in women with abnormal glucose tolerance may explain partly the high risk of CHD in this group.

Many studies have shown that hyperinsulinemia and/or insulin resistance are related to various metabolic and physiological disorders including hypertension, dyslipidemia, and non-insulin-dependent diabetes mellitus. This syndrome has been termed Syndrome X. An important limitation of previous studies has been that they all have been cross sectional, and thus the presence of insulin resistance could be a consequence of the underlying metabolic disorders rather than its cause. We examined the relationship of fasting insulin concentration (as an indicator of insulin resistance) to the incidence of multiple metabolic abnormalities in the 8-yr follow-up of the cohort enrolled in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease in Mexican Americans and non-Hispanic whites. In univariate analyses, fasting insulin was related to the incidence of the following conditions: hypertension, decreased high-density lipoprotein cholesterol concentration, increased triglyceride concentration, and non-insulin-dependent diabetes mellitus. Hyperinsulinemia was not related to increased low-density lipoprotein or total cholesterol concentration. In multivariate analyses, after adjustment for obesity and body fat distribution, fasting insulin continued to be significantly related to the incidence of decreased high-density lipoprotein cholesterol and increased triglyceride concentrations and to the incidence of non-insulin-dependent diabetes mellitus. Baseline insulin concentrations were higher in subjects who subsequently developed multiple metabolic disorders. These results were not attributable to differences in baseline obesity and were similar in Mexican Americans and non-Hispanic whites. These results support the existence of a metabolic syndrome and the relationship of that syndrome to multiple metabolic disorders by showing that elevations of insulin concentration precede the development of numerous metabolic disorders.

Objective: To assess the extent to which glycemic control by itself results in satisfactory control of diabetic dyslipidemia., Research Design and Methods: A population-based case series consisting of 386 Mexican Americans and 94 non-Hispanic whites with non-insulin-dependent (type II) diabetes was studied. All subjects answered questions about their medical history and care received and underwent a standardized oral glucose tolerance test and measurements of fasting serum lipid and lipoprotein concentrations. Three definitions of dyslipidemia were used: total cholesterol greater than 6.20 mM (240 mg/dl), triglyceride greater than 2.82 mM (250 mg/dl), and high-density lipoprotein cholesterol less than 0.90 mM (35 mg/dl)., Results: Despite having removed subjects receiving lipid-lowering drugs, diabetic subjects who had been previously diagnosed and were under medical care exhibited a lower prevalence of hypertriglyceridemia than those who were newly diagnosed at the time of their survey visit, suggesting that conventional management was associated with a reduced frequency of this dyslipidemia. Among previously diagnosed cases, the prevalence of dyslipidemia rose with worsening glycemic control but there was little association with type of therapy (diet only, oral agents, or insulin) or frequency of physician visits. In general, the prevalence of dyslipidemia in diabetic subjects remained higher than in nondiabetic subjects, despite hypoglycemic therapy., Conclusions: The results suggest that glycemic control by itself does not suffice to control diabetic dyslipidemia and that significant numbers of diabetic subjects will need direct lipid management. Clinical trials are urgently needed to define the optimum management strategy for diabetic dyslipidemia.

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 less than 0.001), more carbohydrate (64-65 vs. 49%, P less than 0.001), and performed more physical activity than San Antonio Mexican Americans. Mexicans appeared to consume more refined sugar than Mexican Americans.(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: To assess the impact of associated conditions (obesity, dyslipidemia, and hypertension) on the glycemic control of non-insulin-dependent diabetes mellitus (NIDDM) patients under home-life conditions., Research Design and Methods: We analyzed the metabolic data of 271 NIDDM patients (89% Mexican American) screened in a population-based survey (the San Antonio Heart Study)., Results: Obesity was present in 77% of the patients, hypertension in 23%, hypertriglyceridemia (serum triglycerides greater than 2.9 mM) in 23%, and hypercholesterolemia (serum total cholesterol greater than 6.5 mM) in 14%. Forty percent of the patients had two or more comorbid conditions. With the use of a multiple linear regression model, which was adjusted for age, sex, ethnicity, distribution of body fat (waist-hip ratio), plasma insulin, and treatment (of both diabetes and hypertension), we found that the presence of higher serum triglyceride concentrations was associated with significantly higher plasma glucose levels both in the fasting state (1.4 mM, P less than 0.001) and 2 h after an oral glucose load (1.2 mM, P = 0.003). The presence of obesity, hypertension, or high serum cholesterol levels was not associated with significant changes in glycemic control. When the entire group was stratified by diabetes treatment (untreated n = 89, diet n = 75, oral agents n = 82, insulin n = 25) and after adjusting for age, sex, ethnicity, and waist-hip ratio, only fasting and 2-h plasma glucose and insulin concentrations were significantly different across treatment groups, with diet and oral agents being associated with higher fasting (P less than 0.001) and postglucose (P less than 0.005) plasma glucose levels and lower plasma insulin concentrations (P less than 0.005) compared with newly diagnosed patients. Neither serum lipids nor blood pressure differed across treatment., Conclusions: In NIDDM patients under home-life conditions, higher serum triglycerides are associated with higher fasting and postglucose hyperglycemia regardless of antidiabetic treatment. The presence of obesity, hypertension, or high serum cholesterol levels is not associated with significant changes in glycemic control.

An unfavourable body fat distribution has been associated with an increased prevalence and incidence of non-insulin dependent diabetes mellitus (NIDDM). The potential utility of assessing body fat distribution in diabetes screening, however, has not been assessed. We compared the impact of upper body fat distribution (assessed by the waist-to-hip ratio (WHR)) and body mass index (BMI) and NIDDM using the population attributable risk approach of Levin in 1965 Mexican Americans from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. The population attributable risk percentage (PAR%) was 52.0% for WHR compared to 43.4% for body mass index. After stratification by BMI, women with a high WHR had a PAR% of approximately 50% and men had a PAR% of 28-58%. For any given cutpoint (e.g. the 10th percentile, 20th percentile, etc.) of WHR used to screen for NIDDM, WHR had both a higher sensitivity and a lower false positive rate than the corresponding cutpoint of BMI. To evaluate the relative contribution of WHR in identifying prevalent cases of NIDDM, multiple logistic regression analyses were performed, and the number of subjects identified as being in the top 20% of the risk score distribution was compared using a model that included WHR and a model that included BMI. In men, BMI did not increase the sensitivity in detecting NIDDM subjects once age was accounted for; WHR increased the sensitivity only slightly. In women, sensitivity was enhanced modestly using both measures, although WHR again was the more sensitive method. These data suggest that WHR is a better single screening measure for NIDDM than BMI.

The prevalence of hypertension has been reported to be lower in Mexican-Americans (MAs) than in non-Hispanic whites (NHWs). This finding is paradoxical since, compared to NHWs, MAs are generally more obese, and generally have a higher prevalence of non-insulin-dependent diabetes mellitus (NIDDM), both of which are risk factors for hypertension. Thus far, no data exist on the incidence of hypertension in MAs. We therefore determined the 8-year incidence of hypertension (defined as a diastolic blood pressure greater than or equal to 95 mm Hg or current treatment with antihypertensive medications) in 1462 subjects (867 MAs and 595 NHWs) who were normotensive at baseline and who subsequently participated in the 8-year follow-up of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Hypertension developed in 79 MAs (9.1%) and 55 NHWs (9.2%). The age-adjusted odds ratio (OR) for ethnicity (MA/NHW) was 0.83 (95% CI = 0.48, 1.44) in men and 1.25 (95% CI = 0.76, 2.04) in women. After adjusting for age, gender, body mass index, NIDDM, and level of educational attainment using multiple logistic regression, Mexican-Americans had an incidence of hypertension similar to non-Hispanic white (OR = 0.80, 95% CI = 0.52, 1.22). The similar incidence of hypertension in MAs is in striking contrast to the markedly increased incidence of NIDDM in this ethnic group relative to non-Hispanic whites. The cause of the relative protection from hypertension in MAs is unknown.

Objective: To determine whether dietary protein intake is correlated with clinical proteinuria in subjects with non-insulin-dependent diabetes mellitus (NIDDM)., Research Design and Methods: Cross-sectional analysis of data obtained from the San Antonio Heart Study, a population-based survey of diabetes and cardiovascular risk factors. Subjects were enrolled in two phases: phase 1 between 1979 and 1982 and phase 2 between 1984 and 1988. This study was based on 376 NIDDM subjects who had both urinalysis and complete dietary protein intake information available. Dietary protein intake was measured by 24-h dietary recall in phase 1 and by food-frequency questionnaire in phase 2. An early-morning spot urine was obtained from study subjects. Clinical proteinuria was defined as greater than or equal to 1 on Ames Albustix test., Results: In phase 1, the subjects with negative or trace proteinuria had a mean protein intake of 79.9 g/day compared with 72.1 g/day for subjects with greater than or equal to 1 proteinuria. In phase 2, the mean protein intake was 72.2 g/day in the negative/trace group and 65.3 g/day in the greater than or equal to 1 proteinuria group. In multivariate analysis, adjusting for age, sex, ethnicity, systolic blood pressure, and 2-h blood glucose, we were again unable to detect a significant correlation between dietary protein intake and clinical proteinuria., Conclusions: These data do not support the hypothesis that high-protein intake is a risk factor for clinical proteinuria in NIDDM subjects. Therefore, any recommendation for protein restriction in the diets of NIDDM subjects, before the development of NIDDM-related nephropathy, must be made with caution.

The prevalence of diabetes recorded in population surveys in the American region varies from < 1% (rural Mapuche Indians aged 20 years and over, Chile) to almost 50% (Pima Indians aged 20 years and over, United States of America). The prevalence of non-insulin-dependent diabetes mellitus (NIDDM) was approximately 2.5 times higher among Mexican Americans than in non-Hispanic white Americans. In the Mexican Americans, prevalence followed a sociocultural gradient: 16% in low-income barrios, about 10% in middle-income neighbourhoods and 5% in high-income suburbs in San Antonio, Texas. Data from the Hispanic Health and Nutrition Examination Survey indicate prevalence of diabetes in the age range 45-74 years of 24% for Mexican Americans, 26% for Puerto Ricans and 16% for Cuban Americans, compared to 12% for non-Hispanic whites. Figures for a low-income district of Mexico City show a 36% lower prevalence than for Mexican Americans in the USA. Prevalence in Brazil is approximately 7% in subjects aged 30-69 years. Black Americans have a relatively high prevalence of NIDDM, though not as high as the Mexican Americans. There is evidence that complications of diabetes may vary between populations, and that they may be particularly severe in Mexican Americans, and higher in black than in white Americans. The extent to which these differences relate to access to health care and treatment remains to be clarified.

Mexican Americans have a high prevalence of diabetes relative to non-Hispanic whites, but paradoxically experience a lower prevalence of myocardial infarction and lower cardiovascular mortality (at least in men). To determine whether Mexican Americans might be more resistant to the atherogenic effects of diabetes than non-Hispanic whites, we examined the associations between diabetes and myocardial infarction and selected coronary heart disease (CHD) risk factors in these two ethnic groups. The study population consisted of 5149 Mexican Americans and non-Hispanic whites who were 25 to 64 years old and recruited from the San Antonio Heart Study, a population-based study of cardiovascular risk factors and diabetes conducted between 1979 and 1988. Diabetic men were more than twice as likely to have an electrocardiography (ECG)-documented myocardial infarction than were nondiabetic men, while diabetic women were more than three times as likely to have a myocardial infarction than were nondiabetic women. In both sexes the association between myocardial infarction and diabetes was nearly identical between the two ethnic groups. In both ethnic groups diabetes was also more strongly associated with conventional CHD risk factors (e.g., triglycerides, systolic blood pressure, and high-density-lipoprotein cholesterol) in women than in men. Furthermore, these associations were at least as strong, if not stronger, in Mexican Americans as in non-Hispanic whites. Thus, these data provide no evidence to suggest that Mexican Americans are resistant to the lipid-altering effects of diabetes. We conclude that the protective effect against CHD conferred by Mexican American ethnicity may be obscured in part by the high prevalence of diabetes in this ethnic group.

Mexican-American men experience lower rates of cardiovascular mortality and have a lower prevalence of nonfatal myocardial infarction than do non-Hispanic white men. To see if this ethnic difference exists for other cardiovascular end points, we compared the prevalence of angina pectoris, as assessed by the Rose Angina Questionnaire, between Mexican Americans (n = 3272) and non-Hispanic whites (n = 1848) examined in the San Antonio Heart Study, a population-based survey of cardiovascular disease and diabetes conducted in San Antonio, Texas, between 1979 and 1988. Contrary to our expectations, angina prevalence was approximately twice as high in Mexican Americans as in non-Hispanic whites, with age-adjusted odds ratios of 2.01 (95% confidence interval (CI), 1.13 to 3.58; P = .02) in men and 1.84 (95% CI, 1.26 to 2.70; P = .001) in women. After controlling for age, body mass index, diabetes status, cigarette smoking, and educational level by logistic regression analysis, angina prevalence remained statistically associated with Mexican American ethnicity in men, but not women. There was little ethnic difference in the proportion of Mexican-American and non-Hispanic white subjects who reported nonspecific chest pain (chest pain not meeting the Rose criteria), suggesting that the ethnic difference in angina prevalence was not an artifact of reporting bias. This was further supported by the fact that the conventional cardiovascular risk factors were more strongly associated with angina prevalence in Mexican Americans than in non-Hispanic whites. These data suggest that Mexican-American men experience high rates of angina despite low rates of myocardial infarction. Future studies should investigate ethnic factors that may have differential effects on the various manifestations of coronary heart disease.

Mexican Americans have a threefold greater prevalence of non-insulin-dependent (type II) diabetes mellitus than non-Hispanic whites in the San Antonio Heart Study, a population-based study of diabetes. In addition, Mexican-American diabetic subjects (n = 365) have greater fasting glycemia than non-Hispanic white diabetic subjects (P less than 0.001). Despite these findings, and despite a higher prevalence of microvascular complications among Mexican Americans, there does not appear to be a marked difference in prevalence of macrovascular complications between Mexican-American and non-Hispanic white diabetic subjects. Mexican-American diabetic subjects have only a moderate excess of peripheral vascular disease (as judged by ankle-arm blood pressure ratios) relative to non-Hispanic white diabetic subjects (sex-adjusted Mantel-Haenszel odds ratio 1.84, 95% confidence interval 0.75-4.49). Mexican-American diabetic subjects actually reported fewer myocardial infarctions than non-Hispanic white diabetic subjects (sex-adjusted Mantel-Haenszel odds ratio 0.73, 95% confidence interval 0.31-1.71). Duration was not associated with either peripheral vascular disease or myocardial infarction. Severity of glycemia was only mildly associated with presence of peripheral vascular disease and negatively associated with self-reported myocardial infarction. This latter finding may represent a survival bias in that more severe diabetic subjects have already died and are not ascertained in a prevalence study. The absence of an ethnic difference in the prevalence of macrovascular disease contrasts with our previous reports from the San Antonio Heart Study, in which the prevalence of both retinopathy and proteinuria was observed to be higher in Mexican-American diabetic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence from migrant population studies and secular trend data indicates that environmental factors play a role in the etiology of non-insulin-dependent (type II) diabetes. These environmental factors appear to be concomitants of the process whereby traditional populations become "modernized" or "westernized" and include increased intake of total calories, fat, and sucrose, decreased intake of total and complex carbohydrates, including fiber, and decreased physical exercise. There also appears to be a "postmodernization" process, which we have characterized as the "descending limb of the curve." In Mexican Americans in San Antonio, the prevalence of type II diabetes declines with acculturation to the values, attitudes, and behaviors of "postmodernized" American society. However, examination of the dietary and exercise concomitants of this process revealed a mixed picture. There was some suggestion that Mexican-American women, although not men, had entered onto the descending limb of the curve. However, Native American genetic admixture in Mexican Americans also covaried with affluence and acculturation in such a way that the declining prevalence of diabetes could as easily be due to genetic factors as to environmental factors. The "pancreatic exhaustion" theory holds that resistance to insulin action is a principal lesion leading to hypersecretion of insulin, hyperinsulinemia, and eventual islet cell failure and clinical diabetes. This theory predicts that prediabetic subjects will be hyperinsulinemic. In conformity with this theory, we have shown that subgroups of the Mexican-American population, defined on the basis of family history of diabetes, who would be expected a priori to be enriched with prediabetic subjects, are hyperinsulinemic as predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

In a population-based survey of 2,930 subjects, prevalence rates for obesity, Type 2 (non-insulin-dependent) diabetes mellitus, impaired glucose tolerance, hypertension, hypertriglyceridaemia, and hypercholesterolaemia were 54.3, 9.3, 11.1, 9.8, 10.3 and 9.2%, respectively. The prevalence, however, of each of these conditions in its isolated form (free of the other five) was 29.0% for obesity, 1.3% for Type 2 diabetes, 1.8% for impaired glucose tolerance, 1.5% for hypertension, 1.0% for hypertriglyceridaemia, and 1.7% for hypercholesterolaemia. Two-by-two associations were even rarer. The large differences in prevalence between isolated and mixed forms indicate a major overlap among the six disorders in multiple combinations. In the isolated form, each condition was characterized by hyperinsulinaemia (both fasting and 2 h after oral glucose), suggesting the presence of insulin resistance. In addition, in any isolated condition most of the variables categorising other members of the sextet were still significantly altered in comparison with 1,049 normal subjects. In the whole of the subjects who presented with one or another disorder (1,881 of 2,930 or 64%), marked fasting and post-glucose hyperinsulinaemia was associated with higher body mass index, waist:hip ratio, fasting and post-glucose glycaemia, systolic and diastolic blood pressure, serum triglycerides and total cholesterol levels, and with lower HDL-cholesterol concentrations (all p less than 0.001). We conclude that (1) insulin sensitivity, glucose tolerance, blood pressure, body fat mass and distribution, and serum lipids are a network of mutually interrelated functions; and (2) an insulin resistance syndrome underlies each and all of the six disorders carrying an increased risk of coronary artery disease.

This study describes the prevalence of overweight in 2013 Mexican Americans and 928 non-Hispanic whites, aged 25-65 y, who participated in phase 2 of the San Antonio Heart Study, 1984-1988, and examines differences in overall obesity and body fat distribution among diverse Mexican American subgroups defined by neighborhood, socioeconomic status (SES), and assimilation to mainstream US society. Prevalence of overweight was greater in Mexican Americans than in non-Hispanic whites, and the ethnic difference was greater in women than in men. In Mexican Americans the effects of SES and assimilation on overall obesity and body fat distribution differed by sex group. In men SES and cultural assimilation were associated with less favorable body fat distribution. In women SES and assimilation were associated with lower overall obesity and more favorable body fat distribution. Interventions to reduce obesity in Mexican Americans should take these subgroup differences into account.

Hyperinsulinaemia links non-insulin dependent diabetes (NIDDM), obesity, and hypertension, each an insulin-resistant state in its own right. Insulin resistance predicts the occurrence of NIDDM, and plays a major role in its pathogenesis. We tested the hypothesis that hyperinsulinaemia may also predict hypertension in a sample (n = 2905) of the mixed population of San Antonio, in which hyperinsulinaemia and NIDDM are more prevalent among Mexican-Americans than non-Hispanic whites. Whilst in the whole sample the hypertensives had significantly (P less than 0.001) higher plasma insulin concentrations than the normotensives, high blood pressure was significantly (P less than 0.01) more frequent among non-Hispanic whites than Mexican-Americans regardless of diabetes status. After adjusting for factors (age, sex, body mass, and body fat distribution) known to affect insulin levels, a direct relationship between post-glucose plasma insulin concentrations and prevalence of hypertension was still present in both ethnic groups. In Mexican-Americans, however, the standardized prevalence of hypertension was significantly (P less than 0.001) lower at any given insulin concentration. Post-glucose plasma glucose levels also were directly related to hypertension prevalence in both groups; again, the regression line was shifted downward and, furthermore, less steep (P less than 0.02) in Mexican-Americans, suggesting relative protection against the negative effect of hyperglycaemia on blood pressure. Dyslipidaemia (higher total cholesterol and triglyceride, and lower HDL-cholesterol concentrations) was strongly associated with hyperinsulinaemia and blood pressure in both ethnic groups. After adjusting for plasma insulin, only hypertriglyceridaemia was associated with high blood pressure, with no inter-ethnic difference.(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: To determine whether Mexican Americans have an increased incidence of non-insulin-dependent (type II) diabetes mellitus relative to non-Hispanic whites. Currently, no study has reported on the incidence of this disorder in Mexican Americans., Research Design and Methods: We determined the 8-yr incidence of type II diabetes in 617 Mexican Americans and 306 non-Hispanic whites who participated in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Forty Mexican Americans (6.5%) and 6 non-Hispanic whites (2%) developed type II diabetes, as defined by World Health Organization criteria. The age-adjusted ethnic odds ratio (OR; Mexican Americans/non-Hispanic whites) for diabetes incidence was 8.13 (95% confidence interval [C1] 1.10-59.9) in men and 3.62 (95% CI 1.37-9.55) in women. We adjusted for age, sex, ethnicity, body mass index, and level of educational attainment with multiple logistic regression analyses., Results: Mexican Americans continued to show a statistically significant increase in diabetes incidence (OR 2.72, 95% CI 1.02-7.28). Obesity and age were also positively related to diabetes incidence in this analysis (P less than 0.001). In addition, subjects with at least some college education had a lower incidence of diabetes than those with less than a high school education (OR 0.51, 95% CI 0.26-0.99)., Conclusions: The incidence of type II diabetes in Mexican Americans is greater than in non-Hispanic whites, a difference that is not explained by ethnic differences in obesity, age, or level of educational attainment.

Mexican-American men experience reduced cardiovascular mortality compared with non-Hispanic white men. There is no corresponding ethnic difference in cardiovascular mortality in women. The difference in men could result either from a lower incidence of cardiovascular disease or a lower case fatality rate among Mexican-Americans. Although the incidence of cardiovascular disease in Mexican-Americans is unknown, we have collected data on prevalence of myocardial infarction in 5,148 individuals examined in the San Antonio Heart Study, a population-based survey of cardiovascular disease conducted between 1979 and 1988 in Mexican-Americans and non-Hispanic whites aged 25-64 years. Myocardial infarction was assessed by Minnesota-coded electrocardiograms and by a self-reported history of a physician-diagnosed heart attack. For both end points, the age-adjusted prevalence of myocardial infarction was lower in Mexican-American men than in non-Hispanic white men. After adjustment for age and diabetes status (present/absent), the odds of a myocardial infarction, as defined by either criterion, was approximately one third lower in Mexican-American men than in non-Hispanic white men (p = 0.06). In women, the prevalence of both myocardial infarction end points was slightly higher in Mexican-Americans than in non-Hispanic whites, although neither of these differences was significant. Although the ethnic differences in prevalence in this study were not statistically significant, their pattern parallels the pattern in the mortality due to cardiovascular diseases. Therefore, the results support the hypothesis that the reduced cardiovascular mortality rate observed in Mexican-American men reflects a lower incidence of myocardial infarction rather than a reduced case fatality rate because the latter would result in a higher prevalence.

The relationship between fasting interval and glucose screening was assessed in a prospective study of 153 non-diabetic pregnant patients undergoing a standard 50g glucose challenge test. An interval of less than 3 hours after the last meal was found to be associated with a significantly greater insulin response as opposed to a fasting interval of more than 3 hours (121.3 pmol/l vs. 83.5 pmol/l, p less than .001) and a greater insulin/glucose index (0.92 vs. 0.66, p less than .001), with no difference in plasma glucose. Overall, obese patients had a higher glucose response than non-obese, but only higher insulin levels (107 pmol/l vs. 69 pmol/l, p less than .001) and insulin/glucose index (0.79 vs. 0.59, p less than .02) when the fasting interval was greater than 3 hours. Our data suggest that the fasting interval can influence insulin response during a glucose challenge test and the aberration in insulin secretion may effect screening results, especially in the high-risk gravida with glucose abnormality.

The relationship between glucose and insulin levels was examined in a prospective study of 153 pregnant patients without diabetes who underwent a standard 50 gm glucose challenge test. One hundred eighteen women had normal screening results (glucose level less than 140 mg/dl) and 35 had abnormal screening values but a normal oral glucose tolerance test. Abnormal responders had greater insulin levels (149 vs 82 pmol/L, p less than 0.0001), and a higher insulin/glucose index (0.96 vs. 0.72, p less than 0.007). Patients with glucose levels less than 100 mg/dl had significantly lower insulin/glucose indices. Overall, obese patients had significantly greater glucose and insulin measurements than did nonobese women, but there was no difference within normal and abnormal groups. Glucose levels accounted for 52% of the insulin output and 29% of the insulin/glucose index variance. Neither age, parity, nor obesity contributed significantly to insulin levels in the multiple regression model. Therefore the accepted threshold for glucose screening reflects abnormal insulin output and this aberration may be indicative of the primary defect in gestational diabetes.

Microalbuminuria is associated with progression to renal disease in insulin-dependent diabetes and with increased mortality in noninsulin-dependent diabetes. In contrast, few studies have addressed the effect of microalbuminuria on cardiovascular risk in nondiabetics. We, therefore, determined the level of microalbuminuria in 316 nondiabetic subjects from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Microalbuminuria (greater than or equal to 30 mg/l) was found in 42 of these 316 subjects (13%). Subjects with microalbuminuria had significantly higher blood pressure, triglyceride concentration, sum of insulin concentrations during a glucose tolerance test, and prevalence of hypertension and of self-reported myocardial infarction than subjects without microalbuminuria. When subjects with hypertension were excluded (n = 27), normotensive subjects with microalbuminuria (n = 31) still had significantly higher triglyceride concentrations and insulin sum than normotensive subjects without microalbuminuria (n = 258), suggesting that an increased atherogenic risk factor pattern exists even in normotensive subjects with microalbuminuria. Microalbuminuria may be a marker for cardiovascular risk, although it is not certain whether microalbuminuria causes these metabolic changes or results from some metabolic disturbance such as insulin resistance.

Relatively few studies of hypertension have been carried out in Mexican-Americans, a population characterized by high rates of obesity and non-insulin-dependent diabetes mellitus. We therefore compared the prevalence of hypertension according to four different definitions in 3,297 Mexican-Americans and in 1,873 non-Hispanic whites from the San Antonio Heart Study, a population-based study of cardiovascular disease and diabetes. By all four definitions, the crude prevalence of hypertension in both sexes was lower in Mexican-Americans than in non-Hispanic whites, although only two of the eight pairwise comparisons were statistically significant. However, after adjusting for the potentially confounding effects of age, body mass index, and non-insulin-dependent diabetes mellitus, Mexican-Americans did have a statistically significant lower prevalence of both systolic and diastolic hypertension than did non-Hispanic whites in both sexes (odds ratios ranging from 0.66 to 0.71 depending on the definition of hypertension). The cause of this lower prevalence is unknown, but study of this ethnic group with elevated levels of risk factors for hypertension (obesity, hyperinsulinemia, and diabetes) may provide additional insights into the etiology of hypertension.

The Geriatric Research Center (GRC) table of desirable weights is based on the mortality experience of holders of 4.2 million policies issued by 25 life insurance companies in the USA and Canada. The GRC table defines optimum weight-for-height as the weight range which is associated with below average mortality for a given age and height group. People who fall outside this range, i.e. overweight or underweight, experience above average mortality for their age and height group. We classified 3176 Mexican Americans and 1841 non-Hispanic whites who participated in the San Antonio Heart Study according to the GRC table and found that Mexican Americans were less likely than non-Hispanic whites to be underweight and more likely to be overweight. The two effects did not offset one another, however, and fewer Mexican Americans were found to be in the 'just right' range. If the mortality experience of the population which generated the GRC table (largely non-Hispanic) applied to Mexican Americans, these results imply that Mexican Americans should have higher mortality rates than non-Hispanic whites. Vital statistics data from the state of Texas for the years 1979-81, however, fail to corroborate this prediction. Beyond age 45 years, an age range in which obesity and obesity-related disorders would be expected to exert an important influence on mortality, age-specific and age-adjusted all cause mortality was at last as good if not better in Mexican Americans than in non-Hispanic whites. These results could not be explained by ethnic differences in body fat distribution, since fat was less favorably distributed in Mexican Americans.(ABSTRACT TRUNCATED AT 250 WORDS)

Although type II diabetes is associated with both microvascular and macrovascular complications, duration of diabetes and severity of glycemia are strongly associated only with the former. Since prediabetic individuals are hyperinsulinemia, and since hyperinsulinemia may be a cardiovascular risk factor, we hypothesized that prediabetic individuals might have an atherogenic pattern of risk factors even before the onset of clinical diabetes, thereby explaining the relative lack of an association of macrovascular complications with either glycemic severity or disease duration. We documented the cardiovascular risk factor status of 614 initially nondiabetic Mexican Americans who later participated in an 8-year follow-up of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Individuals who were nondiabetic at the time of baseline examination, but who subsequently developed type II diabetes (ie, confirmed prediabetic subjects, n = 43), had higher levels of total and low-density lipoprotein cholesterol, triglyceride, fasting glucose and insulin, 2-hour glucose, body mass index, and blood pressure, and lower levels of high-density lipoprotein cholesterol than subjects who remained nondiabetic (n = 571). Most of these differences persisted after adjustment for obesity and/or level of glycemia, but were abolished after adjustment for fasting insulin concentration. When subjects with impaired glucose tolerance at baseline (n = 106) were eliminated, the more atherogenic pattern of cardiovascular risk factors was still evident (and statistically significant) among initially normoglycemic prediabetic subjects. These results indicate that prediabetic subjects have an atherogenic pattern of risk factors (possibly caused by obesity, hyperglycemia, and especially hyperinsulinemia), which may be present for many years and may contribute to the risk of macrovascular disease as much as the duration of clinical diabetes itself.

We studied whether lifetime cigarette smoking is associated with the presence of diabetic neuropathy. The research design consisted of a case-control study conducted from a referral-based diabetes clinic at a major medical center. The patients were a 65% sample (163 insulin-dependent diabetes mellitus [IDDM] and 166 non-insulin-dependent diabetes mellitus [NIDDM] patients) of all patients admitted during a 26-mo period. Neuropathy was diagnosed on the basis of signs and symptoms. Smoking history was obtained by mailed questionnaire (66% response rate). Diabetes duration, HbA1, age, sex, peripheral vascular disease, hypertension history, and lifetime alcohol consumption were measured as covariates. The prevalence of neuropathy was 49 and 38% in IDDM (n = 113) and NIDDM (n = 104) patients, respectively. In IDDM, but not NIDDM, current or ex-smokers were significantly more likely to have neuropathy than individuals who had never smoked (odds ratio 2.46, P = 0.02), and the prevalence of neuropathy increased with increasing number of pack-years smoked (P less than 0.001). After adjustment for covariates, IDDM patients smoking greater than or equal to 30 pack-yr were 3.32 times more likely to have neuropathy than patients smoking less than this amount (95% confidence interval 1.15-9.58, P = 0.026). Cigarette smoking was associated with the presence of neuropathy in this clinic-based population of IDDM patients. The hypothesis that cigarette smoking is associated with diabetic neuropathy should be investigated further, both prospectively and in a more representative population.

Few data exist on predictors of non-insulin-dependent (type II) diabetes mellitus. We examined body mass index (BMI), ratio of subscapular-to-triceps skin fold (centrality index), and fasting glucose and insulin concentrations as predictors of decompensation to type II diabetes in Mexican Americans, a population at high risk for this disorder. Twenty-eight of 474 initially nondiabetic Mexican Americans developed type II diabetes after 8 yr of follow-up. Converters to diabetes were older and had higher BMIs, centrality indices, and fasting glucose and insulin concentrations than nonconverters. Subjects in the highest quartile of the insulin distribution had 6.6 times the risk of developing type II diabetes as subjects in the remaining three quartiles combined (95% confidence interval [CI] = 3.14-13.7). In multivariate analysis, fasting glucose (odds ratio [OR] = 5.80, 95% CI = 2.57-13.1) and insulin (OR = 3.12, 95% CI = 1.36-7.14) remained significantly related to conversion to diabetes. However, BMI and centrality index, which were significantly related to conversion in the univariate analysis, were no longer significant in the multivariate analysis once glucose and insulin concentrations were taken into consideration, suggesting that the effect of these variables may be mediated by insulin resistance. Nearly half of the incident cases developed in a subset of the population who were simultaneously in the highest quartile of both fasting insulin and glucose concentrations (population-attributable risk 44.2%). Our results support the insulin resistance/pancreatic exhaustion theory of type II diabetes.

There are virtually no data available describing the functional status of diabetic individuals. We therefore measured functional status using the Sickness Impact Profile (SIP) in 393 diabetic subjects and 486 nondiabetic control subjects identified from the San Antonio Heart Study, a population-based study of diabetes among Mexican Americans and non-Hispanic whites. The SIP is a validated instrument that assesses the presence of health-related behavior changes and activity restrictions in 12 different categories. Functional impairment, defined as a SIP score of 2.0% or greater, was present among 36.6% of diabetic subjects. Following adjustments for age, Mexican Americans were 1.63 times more likely to experience functional impairment that non-Hispanic whites, although this difference was not statistically significant (95% confidence interval: 0.92-2.89). The categories in which subjects experienced impairment varied widely, but the category with the highest prevalence of impairment was "eating" (greater than 40%). The prevalence of functional impairment was 45.9% among diabetic subjects with vascular complications, 31.8% among diabetic subjects without complications, and 16.7% among nondiabetic control subjects. Among all diabetic subjects impairment increased with age, duration of diabetes, fasting glucose, and BMI, and with insulin use and the presence of hypertension. In a multiple logistic regression model these factors (with the exception of insulin use) remained associated with the presence of functional impairment even after adjustment for the presence of vascular complications. If the factors responsible for this excess of functional impairment can be identified, an intervention might be designed which can lead to improvement in the quality of life for diabetic individuals.

Insulin resistance is thought by many to be the primary defect that results in non-insulin-dependent diabetes mellitus (NIDDM). An implication of this theory is that prediabetic persons have higher serum insulin levels than normal subjects. We assessed serum insulin concentrations in a cohort of 1497 nondiabetic Mexican Americans, a population at high risk for NIDDM, according to whether their parents or siblings had diabetes. It was assumed that prediabetic persons would be more likely to have strong family histories of diabetes. We found a stepwise increase in fasting insulin levels in nondiabetics with neither, one, or both parents with diabetes (69.8, 77.8, and 94.6 pmol per liter, respectively; P = 0.002). Similar results were observed for insulin sum (the total of insulin concentrations in the fasting state and at 30, 60, and 120 minutes after a 75-g oral glucose load). The differences in insulin sums according to family history remained statistically significant in analyses of covariance, which controlled for variations in body-mass index, body-fat distribution, and level of blood glucose. Subjects without diabetes who had a diabetic sibling had higher fasting concentrations of insulin than subjects without a diabetic sibling (83.2 vs. 69.6 pmol per liter), but the difference was not statistically significant. We conclude that prediabetic persons, who would be expected to be more numerous in kindreds with progressively stronger family histories of diabetes, have hyperinsulinemia. This supports the insulin-resistance hypothesis.

Mexican Americans have a threefold greater prevalence of non-insulin-dependent diabetes mellitus (NIDDM) than non-Hispanic Whites as found in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. In addition, Mexican-American diabetic subjects have higher levels of glycemia than non-Hispanic White diabetic subjects. We therefore hypothesized that the prevalence of clinical proteinuria would be greater among Mexican-American diabetic subjects (n = 317) than among non-Hispanic White diabetic subjects (n = 67). Clinical proteinuria, defined as greater than or equal to 1+ on the Ames Albustix test, was 2.82 times more prevalent in Mexican-American diabetic subjects compared with non-Hispanic White diabetic subjects adjusting for age and duration (95% confidence interval [CI] = 1.05, 7.55; P = .039). After controlling for other possible confounding variables (i.e., glycemia, systolic blood pressure, smoking, and insulin use), the excess of proteinuria in Mexican-American diabetic subjects was only slightly attenuated, although the statistical significance became borderline (odds ratio [OR] = 2.59, 95% CI = 0.91, 7.32; P = .072). The prevalence of microalbuminuria (greater than 30 mg/L) was also significantly higher in Mexican-American diabetic subjects than in non-Hispanic White diabetic subjects (OR = 3.54, 95% CI = 1.28, 9.81; P = .015). We also compared previously diagnosed Mexican-American diabetic subjects (n = 243) from San Antonio with previously diagnosed non-Hispanic White diabetic subjects in Wisconsin (n = 476).(ABSTRACT TRUNCATED AT 250 WORDS)

Serum insulin concentrations are higher in persons with a positive parental history of diabetes than in persons without such a history. Since hyperinsulinemia is associated with both an increased prevalence of hypertension and an atherogenic pattern of serum lipids and lipoproteins, we hypothesized that among nondiabetic persons, a parental history of diabetes would be associated with an atherogenic pattern of cardiovascular risk factors. In the San Antonio Heart Study, a population-based study of cardiovascular disease and diabetes, we examined 549 nondiabetic persons with a parental history of diabetes and 1167 nondiabetic persons without such a history. Compared to persons without a parental history of diabetes, those with such a history had a more atherogenic pattern of cardiovascular risk factors, including higher body mass index, higher systolic and diastolic blood pressures, higher serum insulin and triglyceride concentrations, and lower levels of high density lipoprotein cholesterol. After adjustment for serum insulin concentration, body mass index, and waist-to-hip ratio, the differences in lipids, lipoproteins, and blood pressure between the two parental history groups were no longer statistically significant. Since persons with a parental history of diabetes are more likely to be prediabetics, the present results suggest that prediabetics have an increased risk of coronary heart disease even before they become diabetic. This phenomenon may help explain why the duration of clinical diabetes is only weakly associated with the risk of coronary heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular disease is the leading cause of morbidity, disability, and death among patients with type II (non-insulin-dependent) diabetes mellitus. Moreover, hyperlipidemia is also common among these patients. Despite this, there are virtually no data regarding the level of awareness and treatment of hyperlipidemia among diabetic subjects at the community level. We therefore examined 374 Mexican-Americans and 86 non-Hispanic whites with type II diabetes identified in an epidemiologic survey that involved 3279 Mexican-Americans and 1847 non-Hispanic whites who resided in San Antonio, Tex. More than 40% of the diabetic subjects were hyperlipidemic according to the criteria of the National Cholesterol Education Program, and an additional 23% had hypertriglyceridemia and/or low levels of high-density lipoprotein cholesterol. By contrast, less than one fourth of the nondiabetic subjects were hyperlipidemic. Only approximately 25% of non-Hispanic whites with diabetes were aware of their hyperlipidemia, and less than 10% were receiving treatment. Awareness and treatment were even less frequent among Mexican-Americans with diabetes. Community physicians should be encouraged to give early attention to the management of lipid disorders in their diabetic patients.

Resistance to insulin action is a well-established feature of type II (non-insulin-dependent) diabetes and is believed by many to contribute to the etiology of this condition. We therefore characterized restriction-fragment-length polymorphisms of the insulin-receptor gene with the restriction enzyme Rsa 1 in 242 Mexican Americans and non-Hispanic Whites with type II diabetes and 202 age-, sex-, and ethnicity-matched control subjects who participated in a population-based study in San Antonio. Alleles of 6.7 kilobases (kb) (A allele), 6.2 kb (B allele), and 3.4 kb (C allele) were identified. The C allele was observed in Mexican Americans only, where its frequency among nondiabetic control subjects was 17.7%. Diabetic Mexican Americans were twice as likely as control subjects to be homozygous for the C allele. The crude odds ratio for diabetes in CC homozygotes compared with the other two genotypes was 2.22, although this result was not statistically significant (chi 2 = 1.57, P = .21). The Mantel-Haenszel odds ratio, adjusting for age, however, indicated a 4.71-fold increased risk of diabetes among Mexican Americans with the CC genotype compared with Mexican Americans without this genotype (chi 2 = 5.38, P = .020). The age of onset of diabetes was also slightly younger in CC homozygote cases (45.4 +/- 9.2 yr) than in CX or XX cases (47.7 +/- 9.0 and 48.6 +/- 9.6 yr, respectively), although this difference was not statistically significant (P .467).(ABSTRACT TRUNCATED AT 250 WORDS)