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Biomedical subjects

S M Haffner

Publications and source records attributed to S M Haffner.

At least 19 recordsLinked to original sources

Lipoprotein(a) concentrations in Mexican Americans and non-Hispanic whites: the San Antonio Heart Study.

There is considerable evidence that lipoprotein(a) (Lp(a)) is a strong independent risk factor for coronary heart disease. Based on their risk factor profile, Mexican Americans have an increased risk of coronary heart disease, yet Mexican Americans have coronary heart disease mortality similar to or lower than that of non-Hispanic whites. The authors therefore attempted to determine whether Mexican Americans had decreased Lp(a) concentrations relative to non-Hispanic whites in the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Lp(a) concentrations (mg/dl) were significantly lower in Mexican Americans (n = 316) than in non-Hispanic whites (n = 242) (men: 10.4 vs. 16.3; women: 11.5 vs. 16.4). In addition, the proportion of persons with Lp(a) concentrations of > or = 30 mg/dl (the threshold at which increased risk of coronary heart disease is believed to occur) was significantly higher in non-Hispanic whites than in Mexican Americans (18.6% vs. 7.6%; Mantel-Haenszel odds ratio (adjusted for sex) = 2.79). Age, obesity, body fat distribution, cigarette smoking, alcohol consumption, and glucose and insulin concentrations were not significantly related to Lp(a) levels. Decreased Lp(a) concentrations may account in part for Mexican Americans' relative protection from coronary heart disease mortality.

Adult

The relation between serum insulin levels and 8-year changes in lipid, lipoprotein, and blood pressure levels.

Hyperinsulinemia is associated with an adverse pattern of cardiovascular risk factors, including obesity, elevated triglyceride levels, low levels of high-density lipoprotein (HDL) cholesterol, and elevated blood pressure. Whether hyperinsulinemia precedes (and perhaps causes) this deterioration in the risk factors or merely accompanies the deterioration is controversial. We therefore examined the 8-year changes in lipids, lipoproteins, and blood pressure as a function of baseline levels of fasting insulin in 1,383 nondiabetic Mexican-American and non-Hispanic white subjects enrolled between October 1979 and November 1982 in the San Antonio Heart Study, a population-based longitudinal study of cardiovascular risk factors and diabetes in San Antonio, Texas. After age and concomitant changes in body mass index were adjusted for, fasting insulin at baseline was found to be correlated positively with 8-year changes in triglyceride levels and negatively with 8-year changes in HDL cholesterol levels (p less than 0.05). Among the non-Hispanic whites, insulin was more strongly correlated with a decline in HDL cholesterol levels in women than in men (p less than 0.001). Fasting insulin was also positively correlated with changes in both systolic and diastolic blood pressure in non-Hispanic whites, but not in Mexican Americans, although these correlations were slightly diminished and no longer achieved statistical significance after subjects receiving antihypertensive medications were excluded. These results support the hypothesis that in nondiabetic subjects, insulin has a direct regulatory effect on triglyceride and HDL cholesterol levels. These data provide evidence for a possible role for insulin in blood pressure regulation, at least in non-Hispanic whites, although further analysis of this issue is warranted.

Adult

Lack of change of lipoprotein (a) concentration with improved glycemic control in subjects with type II diabetes.

Recently, lipoprotein (a) [Lp(a)] has been identified as a major risk factor for coronary heart disease. No data are available on the effect of improved metabolic control on plasma Lp(a) concentrations in subjects with type II diabetes mellitus, a group at high risk for coronary heart disease. We examined the effects of improved metabolic control on plasma lipid and lipoproteins and Lp(a) concentrations in 12 subjects before and after 21 days of tight metabolic control. Glycosylated hemoglobin declined from 8.9% to 6.9% (P less than .002). Lp(a) increased slightly from 21.4 to 25.8 mg/dL (P = .119) with improved metabolic control. There were no significant differences in total, low-density, or high-density cholesterol values, although the decline in triglyceride concentrations was statistically significant. The distribution of apolipoprotein (a) [apo (a)] isoforms in subjects with type II diabetes mellitus was not unusual and the apo (a) isoform patterns did not change with improved metabolic control. Although the number of subjects was small, there was no decline in Lp(a) concentrations with improved control and thus the effect of glycemic control on Lp(a) concentrations may be much smaller in type II than in type I diabetes. These results suggest that diabetic subjects with elevated Lp(a) concentrations should have intensive management of conventional cardiovascular risk factors such as high-density lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), and blood pressure.

Blood Glucose

Lack of association between lipoprotein (a) concentrations and coronary heart disease mortality in diabetes: the Wisconsin Epidemiologic Study of Diabetic Retinopathy.

Recently, considerable data have suggested that lipoprotein (a) [Lp(a)] is a strong independent risk factor for coronary heart disease. Since Lp(a) is increased in both insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), this study examined the relationship of Lp(a) concentrations to coronary heart disease (CHD) mortality in the 4-year follow-up of the Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR). Twenty-four older-onset subjects and 11 younger-onset subjects who died of CHD (cases) before the age of 70 were matched by age, gender, and type of diabetes to subjects who remained alive (controls). The distribution and mean levels of Lp(a) in the cases and controls were very similar, suggesting a lack of association between Lp(a) concentrations and CHD mortality. Although the number of subjects was small, caution should be used in extrapolating results on Lp(a) relationships in nondiabetic subjects to diabetic subjects.

Biomarkers

Metabolism of apolipoprotein B in members of a family with accelerated atherosclerosis: influence of apolipoprotein E-3/E-2 pattern.

Familial combined hyperlipidemia (FCHL) appears to be the most common, simply inherited hyperlipidemia strongly associated with coronary heart disease. In the family examined in this study, two of the siblings who met diagnostic criteria for FCHL had extensive clinical atherosclerosis before age 30, unusually premature for this form of hyperlipidemia. Lipoproteins and low-density lipoprotein (LDL) apolipoprotein (apo) B metabolism were characterized in these siblings in an attempt to gain insight into the cause of the rapid atherosclerosis in the two siblings so affected. LDL apo B production rates were very high in all three siblings (25 to 30 mg/kg/d), consistent with FCHL. beta-Very-low-density lipoprotein-beta (beta-VLDL) was present in the plasma of both siblings with accelerated atherosclerosis. The isoapolipoprotein E pattern in both of these siblings was E-3/E-2. In the third sibling, who was free of premature clinical atherosclerosis and lacked plasma beta-VLDL, the pattern was E-3/E-3. Thus, the heterozygote apo E-3/E-2 pattern may be related to the accumulation of beta-VLDL in persons with a very high apo B production rate. The abnormal accumulation of beta-VLDL may be one of the possible explanations for the rapid, premature atherosclerosis in the two siblings with FCHL in this kindred. Both male members in this kindred also had low levels of high-density lipoproteins, and thus may have had an additional risk of developing atherosclerosis due to this lipoprotein abnormality as well.

Adult

Relationship of sex hormone-binding globulin to lipid, lipoprotein, glucose, and insulin concentrations in postmenopausal women.

Sex hormones play a major role in determining the risk of cardiovascular disease. While several studies have shown that reduced sex hormone-binding globulin (SHBG) is associated with increased insulin and triglyceride and decreased high-density lipoprotein cholesterol (HDLC) in premenopausal women, little data are available for postmenopausal women. We hypothesized that in postmenopausal women decreased SHBG would be associated with an atherogenic pattern of cardiovascular risk factors. We measured SHBG, lipids, lipoproteins, glucose, and insulin concentrations, and systolic and diastolic blood pressure in 101 postmenopausal women. SHBG was negatively associated with triglyceride (r = -.21) and insulin (r = -.47) concentrations and positively associated with HDLC concentrations (r = .47). After adjustment for overall adiposity (body mass index) and upper body adiposity (as measured by the ratio of waist to hip circumferences), SHBG was still associated with HDLC and insulin, but not with triglyceride. Sex hormones were not related to systolic and diastolic blood pressure. The results may help to explain an association of increased androgenicity, as measured by a lower SHBG concentration, with diabetes and risk of cardiovascular disease in older women.

Analysis of Variance

Eight-year incidence of hypertension in Mexican-Americans and non-Hispanic whites. The San Antonio Heart Study.

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.

Adult

Relationship of insulin clearance and secretion to insulin sensitivity in non-diabetic Mexican Americans.

The antecedents of type II diabetes, while still controversial, are thought to involve decreased insulin sensitivity and compensatory hypersecretion of insulin. Mexican Americans have a three-fold excess risk of type II diabetes and non-diabetic Mexican Americans are characterized by hyperinsulinaemia and insulin resistance. Few data exist, however, on whether there are defects in insulin secretion and/or clearance in this population. We examined insulin sensitivity, secretion and clearance using combined insulin and C-peptide measurements analysed by the minimal model technique of Bergman and colleagues in 10 non-obese, normoglycaemic Mexican Americans and 11 age, sex and obesity-matched non-Hispanic whites. Mexican Americans had significantly decreased insulin sensitivity (SI 4.06 s. 7.56, P = 0.017), higher first phase insulin secretion (1.03 nM vs. 0.72 nM) and decreased insulin clearance (0.099 vs. 0.161) than non-Hispanic whites. Thus, normal Mexican Americans have higher rather than lower insulin secretion suggesting that lower insulin sensitivity may be an early defect in this ethnic group. In addition, they have reduced insulin clearance. Moreover, insulin sensitivity and insulin clearance were positively correlated. We thus speculate that decreased insulin clearance may represent a further autoregulatory mechanism in addition to increased insulin secretion to compensate for decreased insulin sensitivity.

Adult

Clustering of cardiovascular risk factors in confirmed prehypertensive individuals.

Numerous studies have indicated that hypertensive subjects have an atherogenic lipoprotein pattern, hyperinsulinemia, and impaired glucose tolerance relative to normotensive individuals. These abnormalities could be due to adverse effects of certain antihypertensive agents, to pathophysiological concomitants of the hypertensive state itself, or to both. In this report, we describe the cardiovascular risk factor profile of 1,440 subjects who were normotensive and were not taking any antihypertensive medications when first examined and who subsequently participated in the 8-year follow-up of the San Antonio Heart Study. Hypertension developed in 130 subjects during the follow-up period. At baseline these prehypertensive individuals had significantly higher levels of blood pressure, fasting total and low density lipoprotein cholesterol, triglyceride, glucose, and insulin, and 2-hour glucose than those who remained free of hypertension. In addition, they had higher body mass indexes, a less favorable body fat distribution, and lower levels of high density lipoprotein cholesterol. In multiple linear regression analyses, baseline levels of triglyceride and blood pressure remained significantly higher and high density lipoprotein cholesterol remained significantly lower in the subjects who later converted to hypertension than in those who remained normotensive. Although baseline insulin levels were also higher in the prehypertensive subjects, this difference was not statistically significant. In nonobese subjects, however, those with high baseline insulin concentrations had an increased incidence of hypertension compared with those with low insulin concentrations. The present results suggest that the cluster of atherogenic changes associated with hypertension actually precede the development of the hypertensive state.

Adult

Hyperdynamic circulation and the insulin resistance syndrome ("syndrome X").

The insulin resistance syndrome ("syndrome X") consists of hyperinsulinemia, glucose intolerance, dyslipidemia, and hypertension, although the inclusion of hypertension has been challenged. Insulin has biological effects that could produce a hyperdynamic circulation. We therefore postulated that an insulin-induced hyperdynamic circulation is an early feature of the insulin resistance syndrome and that this circulatory abnormality leads to later fixed hypertension. The San Antonio Heart Study cohort, a population-based cohort of 3,301 Mexican Americans and 1,857 non-Hispanic whites, was used to define individuals who were hyperdynamic (pulse pressure and heart rate in the upper quartile of their respective distributions), intermediate, and hypodynamic (pulse pressure and heart rate in the bottom quartile). The characteristics of the insulin resistance syndrome were then examined according to these three hemodynamic categories. We also examined the 8-year incidence of hypertension and of type II diabetes according to these hemodynamic categories. A hyperdynamic circulation was associated with statistically significant increases in body mass index (BMI) (p < 0.001), subscapular-to-triceps skinfold ratio (p = 0.042), triglyceride (p = 0.002), 2-hour glucose (p = 0.002), and fasting and 2-hour insulin (p = 0.019 and 0.006). When hemodynamic status was examined separately in lean (BMI < 27 kg/m2) and obese (BMI > or = 27 kg/m2) individuals, the above effects persisted, although they were somewhat attenuated. The odds ratio for the hyperdynamic state as a predictor of future hypertension was 1.66, although this was not statistically significant (p = 0.304). The odds ratio for predicting future type II diabetes was 3.97, which was statistically significant (p = 0.047).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Increased lipoprotein(a) concentrations in chronic renal failure.

Subjects with chronic renal failure have a greatly increased risk of coronary heart disease and dyslipidemia. Relatively few studies have examined the relationship of chronic renal failure to lipoprotein (Lp)(a) concentrations, an important risk factor for coronary heart disease. Diabetic subjects have been reported to have both increased Lp(a) concentrations and an increased risk of renal failure, thereby possibly confounding the Lp(a)-renal failure association. The association between Lp(a) and chronic renal failure in 359 control subjects and 111 subjects with renal failure was examined. Lp(a) (in milligrams per deciliter) was elevated in subjects with chronic renal failure, regardless of ethnicity (Mexican Americans, 19.8 +/- 2.7 versus 14.1 +/- 1.3; P = 0.03; non-Hispanic white patients, 24.9 +/- 3.0 versus 16.3 +/- 1.2; P = 0.006;). These differences persisted after adjustment for diabetes and ethnicity (P < 0.001). The type of treatment for chronic renal failure (diet, hemodialysis, or peritoneal dialysis) did not have an effect on Lp(a) concentrations. Lp(a) levels were not correlated with the level of creatinine in subjects with chronic renal failure. Thus, the elevation of Lp(a) levels in renal failure must occur early in renal failure, or alternatively, elevated Lp(a) levels may promote progression to chronic renal failure. These results indicate that Lp(a) concentrations are increased in chronic renal failure and may increase the risk for coronary heart disease in these subjects.

Cohort Studies

Lp(a) concentrations in NIDDM.

NIDDM patients have a two- to fourfold increased risk of CHD relative to nondiabetic subjects. This excess risk is explained only partially by increased levels of standard risk factors. We compared the plasma concentrations of Lp(a) in NIDDM patients (n = 260) and nondiabetic subjects (n = 336) who participated in a population-based study (San Antonio Heart Study). Lp(a) was measured using a monoclonal anti-Lp(a) antibody. NIDDM patients and nondiabetic subjects had similar Lp(a) concentrations for both men (13.6 +/- 1.5 vs. 16.1 +/- 1.4 mg/dl) and women (12.6 +/- 0.8 vs. 15.9 +/- 1.3 mg/dl) (P = 0.361). Duration of diabetes and level of fasting glycemia were not significantly related to Lp(a) concentrations. Lp(a) levels were significantly higher in patients who had higher total and LDL cholesterol levels. We conclude that in a large population-based study, Lp(a) levels are not increased in NIDDM patients.

Analysis of Variance

Genetic and environmental determinants of type II diabetes in Mexico City and San Antonio.

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)

Adult

Prospective analysis of the insulin-resistance syndrome (syndrome X).

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.

Adult

Greater effect of glycemia on incidence of hypertension in women than in men.

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.

Blood Glucose

Impact of associated conditions on glycemic control of NIDDM patients.

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.

Blood Glucose

Does glycemic control of type II diabetes suffice to control diabetic dyslipidemia? A community perspective.

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.

Adult

Public health significance of upper body adiposity for non-insulin dependent diabetes mellitus in Mexican Americans.

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.

Adipose Tissue