Search PubMed⌕ Search

Biomedical subjects

R F Hamman

Publications and source records attributed to R F Hamman.

At least 73 records · Page 4Linked to original sources
PubMed1994

ApoA-IV polymorphism associated with myocardial infarction in obese NIDDM patients. The San Luis Valley Diabetes Study.

Non-insulin-dependent diabetes mellitus (NIDDM) confers myocardial infarction (MI) risk unexplained by known factors. In 356 NIDDM patients and 1,087 people with normal glucose tolerance, we investigated the association between MI risk and polymorphism at codon 360 in the apolipoprotein A-IV (apoA-IV) gene. During 1984-1992, MI was diagnosed in 84 diabetic and in 106 nondiabetic people. The risk of MI did not differ by apoA-IV phenotype in nondiabetic people; however, in NIDDM patients, those with the apoA-IV 1-2 phenotype had 2.8 (95% confidence interval: 1.4-5.6) higher MI risk than those with the 1-1 phenotype, adjusting for age, gender, ethnicity, hypertension, smoking, body mass index, fat centrality, and low-density lipoprotein and high-density lipoprotein cholesterol. The risk of MI was particularly high in obese NIDDM patients with the apoA-IV 1-2 phenotype: 5.1 (2.4-11.2) times that in obese apoA-IV 1-1 NIDDM patients and 7.7 (3.6-16.7) times that in lean nondiabetic people. The effect of apoA-IV 1-2 did not appear to be a part of the insulin-resistance syndrome nor was it dependent on diabetes duration or control. One half of the excess MI risk in the diabetic population studied was explained by the apoA-IV 1-2 phenotype. These results indicate that approximately 17% of NIDDM patients have a high MI risk apoA-IV phenotype that is particularly deleterious in obese patients.

Adult↗
PubMed1994

Dietary fat predicts conversion from impaired glucose tolerance to NIDDM. The San Luis Valley Diabetes Study.

OBJECTIVE: To determine if dietary fat intake measured at a baseline exam in subjects with impaired glucose tolerance (IGT) predicted the subsequent development of non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Based on an oral glucose tolerance test (OGTT) (World Health Organization criteria), we identified 134 eligible subjects with IGT from a geographically based sample of subjects with no prior history of diabetes. One to three years after the baseline exam, 123 subjects (92%) had a repeat OGTT. Diet was assessed by a 24-h diet recall reported before the baseline OGTT. RESULTS: The mean percentage of energy eaten as fat was 43.4% in 20 people subsequently developing NIDDM compared with 40.6% in 43 people remaining IGT and 38.9% in 60 subjects who subsequently reverted to normal glucose tolerance. In comparing the 20 subjects who developed NIDDM with the 103 who remained IGT or normal, an increase in fat intake of 40 g/day was associated with an increase in risk of NIDDM of 3.4-fold (95% confidence interval [CI] 0.8-13.6) adjusted for energy intake, age, sex, ethnicity, and obesity. The odds ratio increased to sixfold (95% CI 1.2-29.8) after adjustment for fasting glucose, insulin, and 1-h insulin. CONCLUSIONS: Fat consumption significantly predicts NIDDM risk in subjects with IGT after controlling for obesity and markers of glucose metabolism.

Adult↗
PubMed1994

Risk factors for distal symmetric neuropathy in NIDDM. The San Luis Valley Diabetes Study.

OBJECTIVE: To investigate risk factors for distal symmetric (sensory) neuropathy among prevalent cases of non-insulin-dependent diabetes mellitus (NIDDM) in a population-based study in southern Colorado. RESEARCH DESIGN AND METHODS: Prevalent neuropathy was identified in 77 of 277 people with NIDDM by a standardized history and neurologic examination. Fifteen known or suspected risk factors for neuropathy were determined without knowledge of neuropathy status. RESULTS: Older age at examination, longer duration of diabetes, higher glycohemoglobin percentage, lower fasting C-peptide, insulin use, and presence of retinopathy and nephropathy (microalbumin > or = 200 micrograms/ml) were all significantly associated with neuropathy. Sex, ethnicity (Hispanic versus non-Hispanic white), height, systolic blood pressure, peripheral vascular disease, cigarette and alcohol use, and serum lipid levels were not significantly associated with neuropathy. In a multivariate logistic model, increasing age (odds ratio [OR] = 1.3, 95% confidence interval [CI] = 1.1-1.6), longer duration of diabetes (OR = 1.3, CI = 1.0-1.6), increased glycohemoglobin percentage (OR = 1.5, CI = 1.1-2.1), and insulin use (OR = 2.8, CI = 1.3-6.1) were associated with neuropathy. Retinopathy (OR = 3.0, CI = 1.2-7.7), but not nephropathy, was important when added to this model. CONCLUSIONS: Worse glycemic control and insulin use were independently associated with neuropathy in people with NIDDM. Whether insulin use represents another marker for severity of the metabolic disturbance or is an independent risk factor for neuropathy requires further study. We could not confirm associations of neuropathy with height, with nephropathy, or with retinopathy, independent of duration of diabetes.

Adult↗
PubMed1994

Ethnic differences in human leukocyte antigen markers of susceptibility to IDDM.

OBJECTIVE: To determine whether genetic differences explain the lower risk of developing insulin-dependent diabetes mellitus (IDDM) for Hispanic versus non-Hispanic white children in Colorado. RESEARCH DESIGN AND METHODS: Hispanic (n = 62) and non-Hispanic white (n = 82) subjects with IDDM identified from the Colorado IDDM Registry and healthy, nondiabetic control subjects were recruited. Human leukocyte antigen (HLA) serologic typing and sequence-specific oligonucleotide typing of DQA1 and DQB1 alleles were performed. RESULTS: HLA and allele associations with IDDM were similar in both ethnic groups. HLA-DR3 and HLA-DR4 were more common in IDDM subjects in both ethnic groups. Subjects with DQBl alleles encoding aspartic acid (Asp) in position 57 were less likely to have IDDM, irrespective of ethnic background. HLA-DR3 was less common among Hispanic subjects than non-Hispanic white control subjects (4.4 vs. 17.5%, Hispanics vs. non-Hispanic whites, P = 0.04). CONCLUSIONS: These data suggest that the lower prevalence of HLA-DR3 in the Hispanic population, a pattern consistent with the presence of Amerindian admixture, may explain the lower rate of IDDM in the Hispanic population.

Adolescent↗
PubMed1994

Patterns and predictors of hypertension incidence among Hispanics and non-Hispanic whites: the San Luis Valley Diabetes Study.

OBJECTIVES: To determine whether Hispanics are at lower risk for the development of hypertension than non-Hispanic Whites. We also examined selected predictors of hypertension incidence and explored the role of markers of insulin resistance in the development of hypertension. DESIGN: A cohort study of a geographically-based sample of Hispanic and non-Hispanic white southern Colorado residents who were re-examined an average of 4 years after their baseline examination. METHODS: These analyses included 664 participants who were normotensive and confirmed nondiabetic by an oral glucose tolerance test at their baseline examination. Hypertension was defined as systolic blood pressure > or = 140 mmHg or diastolic blood pressure > or = 90 mmHg or use of antihypertensive medication. RESULTS: Hispanics and non-Hispanic Whites had similar hypertension incidence rates. The strongest predictors of hypertension incidence were baseline blood pressure and age. Higher baseline heart rates and higher body mass index also predicted hypertension. Increased fasting insulin levels were associated with hypertension incidence among lean participants, though the association disappeared once baseline blood pressure levels were added to the models. Models investigating change in systolic or diastolic blood pressure levels found higher baseline levels of insulin area under the glucose tolerance curve predicted greater increases in systolic blood pressure in non-Hispanic Whites only. CONCLUSIONS: Hypertension incidence rates were similar in Hispanics and non-Hispanic Whites. Higher levels of insulin area were associated with larger increases in systolic blood pressure among non-Hispanic Whites only.

Adult↗
PubMed1993

Ethnic differences in risk factors associated with the prevalence of non-insulin-dependent diabetes mellitus. The San Luis Valley Diabetes Study.

Non-insulin-dependent diabetes mellitus is 2-5 times more common in Hispanics than in non-Hispanic whites in the United States. The authors conducted this case-control study in two Colorado counties from 1984 to 1986 to determine whether known risk factors for non-insulin-dependent diabetes mellitus explained the excess incidence in Hispanics. There were 279 subjects with prevalent diabetes and 488 subjects with normal glucose tolerance who were eligible for this analysis. After adjustment for age and sex, results showed that Hispanics were 3.5 times more likely than non-Hispanic whites to have non-insulin-dependent diabetes mellitus (95% confidence interval 2.4-4.9). The excess risks of diabetes associated with body mass index, subscapular and triceps skinfold thickness, family history of diabetes, and income were similar in Hispanics and non-Hispanic whites, after adjustment for age and sex. However, 1-unit increases in subscapular/triceps skinfold ratio and waist/hip ratio were associated with greater increases in risk among non-Hispanic whites than among Hispanics. When risk factors were entered into logistic regression models simultaneously, higher subscapular skinfolds, a higher waist/hip ratio, family history of diabetes, older age, male sex, and lower income were independently associated with non-insulin-dependent diabetes mellitus in both ethnic groups. No association was found with skin reflectance, a marker for Amerindian admixture. While the excess risk of diabetes in Hispanics was reduced, a significant 1.9-fold excess risk in Hispanics remained. Further studies are needed to understand factors contributing to the excess prevalence of diabetes in Hispanic Americans.

Adult↗
PubMed1993

Impact of apolipoprotein E polymorphism in determining interindividual variation in total cholesterol and low density lipoprotein cholesterol in Hispanics and non-Hispanic whites.

The extent of apolipoprotein E (apo E) polymorphism and its effect on eight quantitative risk factors for coronary heart disease (total cholesterol; low density lipoprotein (LDL) cholesterol; total high density lipoprotein and its subfractions, HDL2 and HDL3; triglycerides; fasting glucose and fasting insulin) has been determined in 238 randomly selected Hispanics (120 males and 118 females) and 201 non-Hispanic whites (NHWs) (105 males and 96 females) from the San Luis Valley, Colorado. The frequencies for the E * 2, E * 3 and E * 4 alleles were 0.048, 0.853 and 0.099, respectively, in Hispanics and 0.080, 0.783 and 0.137, respectively, in NHWs. Relatively low frequency of the E * 2 and E * 4 alleles in Hispanics compared with NHWs is consistent with the genetic and anthropologic data that Hispanics have substantial Amerindian admixture. The impact of apo E polymorphism on each quantitative trait was estimated after adjusting for concomitant variables including age, cigarette smoking and body mass index in both genders and pre- or post-menopause status in females. The distribution of eight quantitative traits was analyzed among three common apo E phenotypes, 3-2, 3-3 and 4-3. In Hispanics, significant variability among apo E phenotypes was observed for total cholesterol (P = 0.001) in females only and the apo E polymorphism accounts for 12.4% variation in total cholesterol and 15.2% variation in LDL-cholesterol. In NHWs, significant mean differences among apo E phenotypes were observed for total cholesterol in both males (P = 0.007) and females (P = 0.0004). In NHW males and females, the apo E polymorphism explained 9.2% and 12.4%, respectively, of the variation in total cholesterol, and 15.1% and 6.6%, respectively, of the variation in LDL-cholesterol. In NHWs, borderline significance levels were also noted for phenotype specific differences in HDL2-cholesterol in males (P = 0.04) and females (P = 0.05), for total HDL cholesterol in females (P = 0.02) and HDL3-cholesterol in females (P = 0.06). While the estimated effects of the apo E polymorphism on quantitative traits differ somewhat between Hispanics and non-Hispanic whites, this probably reflects the overall difference in frequencies of the less common alleles in the Hispanics rather than a biological difference in the effects of these alleles on lipid metabolism.

Alleles↗
PubMed1993

Association of a PvuII RFLP at the lipoprotein lipase locus with fasting insulin levels in Hispanic men.

We present results from an association study between RFLPs in the lipoprotein lipase (LPL) gene and lipid and insulin levels. The study population consisted of 102 Hispanic men and 97 Hispanic women. The subjects were genotyped for two previously reported RFLPs detected with the restriction enzymes HindIII and PvuII. The frequencies of the RFLPs in the Hispanic population are similar to those seen in other Caucasian populations. Strong linkage disequilibrium was detected between the sites in Hispanics. Genotypes were used separately in analyses of variance with fasting serum triglycerides, total cholesterol, high density lipoprotein (HDL)-cholesterol, low density lipoprotein (LDL)-cholesterol, HDL2/HDL3-cholesterol, and insulin levels, as well as two measures of adiposity: waist-hip ratio and body mass index. Men and women were analyzed separately. Mean fasting insulin levels of the LPL PvuII genotypes were significantly different from each other in Hispanic men. The mean fasting insulin level of men who were homozygous for the presence of the PvuII site (+/+) was 9.20 +/- 0.24 mu units/ml, men who were heterozygous had a mean level of 10.54 +/- 0.20 mu units/ml, and men who were homozygous for the absence of the site (-/-) had a mean of 12.91 +/- 0.30 mu units/ml. This effect was not seen in Hispanic women. These results suggest that the regulation of LPL by insulin may be different in Hispanics with different LPL PvuII genotypes.

Adult↗
PubMed1993

The role of dietary fiber in the etiology of non-insulin-dependent diabetes mellitus. The San Luis Valley Diabetes Study.

To investigate the hypothesis that a low intake of dietary fiber could increase the risk of developing non-insulin-dependent diabetes mellitus (NIDDM), we ascertained prior dietary intake of 242 persons with known diabetes and 460 persons without a prior diagnosis of diabetes among 20- to 74-year-old residents of two counties in southern Colorado from 1984 to 1986. When persons with diabetes were compared to nondiabetic controls, a higher reported fiber intake prior to diagnosis was found among persons with diabetes. A decrease in fiber of 10 g/d was associated with a decrease in risk of NIDDM of 0.75 (95% confidence interval: 0.59 to 0.96), rather than an increase as hypothesized. However, when the diabetic group was limited to those with diabetes for less than 5 years, this association was no longer present. Two further analyses were carried out on 1317 persons without a prior diagnosis of diabetes seen between 1984 and 1988. Among these persons, current fiber intake was inversely associated with fasting plasma insulin concentration. However, fiber explained less than 1% of the variation in fasting insulin levels. When persons with previously undiagnosed NIDDM were compared to normal controls, the odds ratio relating a decrease in fiber consumption of 10 g/d to NIDDM was 1.21 (95% confidence interval: 0.70 to 2.10) adjusting for calorie and carbohydrate intake. All analyses were adjusted for age, sex, ethnicity, and body mass index. The inconsistent findings reported here do not support the hypothesis that increasing dietary fiber intake could reduce the future occurrence of NIDDM.

Adult↗
PubMed1993

Waist-hip ratio measurement location influences associations with measures of glucose and lipid metabolism. The San Luis Valley Diabetes Study.

The ratio of waist to hip circumference is widely used to characterize fat distribution patterns but the locations for measurement are not standardized. Between 1986 and 1988, we measured two waist and two hip circumferences on 616 Hispanic and non-Hispanic white subjects, aged 30 to 74 years. Intraclass correlation coefficients, based on repeat measurements of 38 subjects, showed that minimum waist and maximum hip circumferences attained or exceeded the level of repeatability seen with the landmark-based circumference measures. Sex-specific partial correlation coefficients, adjusted for age and body mass index, indicated wide variation in the magnitudes of associations of the two waist-hip ratios with measures of insulin, high-density-lipoprotein cholesterol, triglycerides, and diastolic blood pressure. Models with simple waist circumference generally produced partial correlation coefficients of equal or greater magnitude compared to the coefficients seen with the waist-hip ratio.

Adult↗
PubMed1993

Association of lipoprotein lipase gene variation with the physiological components of the insulin-resistance syndrome in the population of the San Luis Valley, Colorado.

OBJECTIVE: To cross-sectionally evaluate the presence of clustering of the insulin-resistance syndrome components. Tests were conducted for association of the HindIII restriction site polymorphism at the lipoprotein lipase locus with clustering of the physiological components of the insulin resistance syndrome. RESEARCH DESIGN AND METHODS: DNA samples of 370 normoglycemic Hispanics and 520 normoglycemic non-Hispanic whites from the San Luis Valley, Colorado, were amplified by the polymerase chain reaction. Lipids and glucose were determined by the standard procedures. Cross-tabulation and chi 2 analysis were used. RESULTS: The insulin-resistance syndrome components (elevated fasting insulin, reduced high-density lipoprotein cholesterol, and elevated triglycerides) appeared together in individuals of this population sample more often than expected by chance. Individuals in the population with the (+/+) lipoprotein lipase-HindIII restriction of fragment-length polymorphism genotype were more likely to have elevated fasting insulin and triglycerides and a reduced high-density lipoprotein-cholesterol level than subjects with the (+/-) genotype (odds ratio = 2.3, 95% confidence interval 1.38-3.98). CONCLUSIONS: As expected from the physiological function of lipoprotein lipase, the primary association of lipoprotein lipase genotypes is with triglyceride and high-density lipoprotein-cholesterol levels. This appears to be the first reported genetic association with the insulin-resistance syndrome and may reflect genotype specific differences in the regulation of lipoprotein lipase by insulin.

Base Sequence↗
PubMed1993

Blood pressure, insulin, and C-peptide levels in San Luis Valley, Colorado.

OBJECTIVE: To explore the associations between blood pressure and both fasting insulin and C-peptide levels. RESEARCH DESIGN AND METHODS: A cross-sectional analysis was conducted of 895 normoglycemic members of a bi-ethnic community in Colorado who were selected from a control group recruited for a geographically based study of diabetes mellitus prevalence and risk factors. All subjects included in this study had normal glucose tolerance as judged by a 75-g oral glucose tolerance test interpreted using World Health Organization criteria. None of the subjects were taking antihypertensive medication. Multiple linear regression analysis was used to examine relationships between fasting insulin and C-peptide levels and blood pressure. RESULTS: Among all subjects, diastolic blood pressure was found to significantly increase with increasing levels of both hormones (insulin coefficient = 0.197, P = 0.013; C-peptide coefficient = 0.0436, P = 0.004), whereas systolic blood pressure was significantly related to fasting C-peptide level (coefficient = 0.0295, P = 0.050). These relationships were similar in magnitude for both Hispanic and non-Hispanic white subjects, but were diminished among women and subjects with a higher body mass index. CONCLUSIONS: Higher fasting insulin and C-peptide levels are associated with higher blood pressure, but these relationships are modified by sex and degree of obesity.

Adult↗
PubMed1993

Reproductive history, glucose tolerance, and NIDDM in Hispanic and non-Hispanic white women. The San Luis Valley Diabetes Study.

OBJECTIVE: To ascertain whether childbearing would decrease oral glucose-stimulated insulin and C-peptide levels and increase the risk of NIDDM and impaired glucose tolerance in a population of Hispanic and non-Hispanic white women residing in the San Luis Valley of Colorado. Several investigators have related childbearing to subsequent abnormal glucose tolerance. RESEARCH DESIGN AND METHODS: In a population-based case-control epidemiological study, diabetic patients 20-74 yr of age (n = 196) and randomly sampled control women subjects (n = 735) underwent a glucose tolerance test, a physical examination, and an in-person standardized interview. The relations between the live-birth number and fasting and oral glucose stimulated glucose, insulin and C-peptide concentrations, and NIDDM and impaired glucose tolerance were estimated using linear or logistic regression to adjust for extraneous variables. RESULTS: In women selected as control subjects, the live-birth number was related to a significant decrease in the sum of 1- and 2-h C-peptide concentrations (coefficient = -0.077, P < 0.001) and the logarithm of the sum of 1- and 2-h insulin concentrations (coefficient = -0.014, P = 0.02). After adjustment for subscapular skin-fold thickness, the relative odds of NIDDM for the live-birth number, which was small and of borderline significance, diminished (odds ratio = 1.04 for one birth, P = 0.18). Findings were similar for impaired glucose tolerance. CONCLUSIONS: Childbearing was related to lower C-peptide and insulin levels in Hispanic and non-Hispanic women of the San Luis Valley. It had little apparent effect on later risk of NIDDM or impaired glucose tolerance.

Adult↗
PubMed1993

Two DNA polymorphisms in the lipoprotein lipase gene and their associations with factors related to cardiovascular disease.

Lipoprotein lipase (LPL) plays a crucial role in plasma lipoprotein processing by catalyzing the hydrolysis of core triglycerides of chylomicrons and very low density lipoproteins. Several polymorphic restriction sites have been reported in the LPL gene, including those identified by the enzymes HindIII and PvuII. We have determined the HindIII and PvuII polymorphisms in diabetic (D) and non-diabetic (ND) Hispanics (D = 195; ND = 384) and non-Hispanic Whites (D = 76; ND = 539) from the San Luis Valley, Colorado. Both polymorphisms showed comparable gene frequencies between diabetics and non-diabetics, and between the two ethnic groups. The HindIII and PvuII polymorphisms were in strong linkage disequilibrium in both Hispanics and non-Hispanic Whites (P < 0.001). We estimated whether the two DNA polymorphisms have significant impact in determining interindividual differences in plasma levels of total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, fasting glucose, and fasting insulin. Plasma triglyceride levels varied significantly among the HindIII genotypes in the normoglycemic sample. There was a clear gene dosage effect among the three HindIII genotypes, with the (-/-) genotype having the lowest and the (+/+) genotype having the highest triglyceride levels; these levels were intermediate in the (+/-) genotype. The average effect of the (-) allele of the HindIII polymorphism was to lower triglycerides by 12.85 mg/dl in non-Hispanic White males, 8.06 mg/dl in non-Hispanic White females, 10.91 mg/dl in Hispanic males, and 12.47 mg/dl in Hispanic females. The HindIII polymorphism also showed a significant association with HDL-cholesterol levels in the normoglycemic sample.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Early exposure to cow's milk and solid foods in infancy, genetic predisposition, and risk of IDDM.

Using a case-control study design, we examined the hypothesis that early exposure to cow's milk and solid foods increased the risk of IDDM. An infant diet history was collected from 164 IDDM subjects from the Colorado IDDM Registry with a mean birth year of 1973, and 145 nondiabetic population control subjects who were frequency matched to diabetic subjects on age, sex, and ethnicity. Early exposure was defined as exposure occurring before 3 mo of age. After controlling for ethnicity, birth order, and family income, more diabetic subjects were exposed early to cow's milk (OR 4.5, 95% CI 0.9-21.4) and solid foods (OR 2.5, CI 1.4-4.3) than control subjects. To examine this association while accounting for the genetic susceptibility to IDDM, we defined individuals as high and low risk by an HLA-DQB1 molecular marker. Early exposure to cow's milk was not associated with elevated risk for IDDM in low-risk individuals. Relative to unexposed low-risk individuals, early exposure to cow's milk was strongly associated in individuals with a high risK marker (OR 11.3, CI 1.2-102.0). Similar findings were observed for early exposure to solid foods. These data indicate that early exposure to cow's milk and solid foods may be associated with increased risk of IDDM. The inclusion of HLA-encoded risk in the analyses demonstrates the combined effect of genetic and environmental factors.

Adult↗
PubMed1993

Excess incidence of known non-insulin-dependent diabetes mellitus (NIDDM) in Hispanics compared with non-Hispanic whites in the San Luis Valley, Colorado.

Non-insulin-dependent diabetes mellitus is between two and five times more prevalent among Hispanic Americans than among non-Hispanic whites (NHW). Incidence data for Hispanic populations will help to determine whether this excess prevalence is due to increased incidence, survivorship, or other factors. Incident cases were identified through concurrent surveillance of all local medical practices from 1983 to 1988 in two southern Colorado counties in which the population was 46% Hispanic. All identified subjects were invited for an oral glucose tolerance test. Among the subjects who attended clinic, 83% were confirmed as having diabetes, using WHO criteria. The standardized average annual incidence rates per 1000 for confirmed non-insulin-dependent diabetes, accounting for nonresponse, were 3.7 and 1.6 for Hispanic and NHW males, and 4.5 and 1.2 for Hispanic and NHW females, respectively. The age and nonresponse adjusted rate ratio comparing Hispanics to NHWs was 3.1 (95% CI: 2.3-4.2), indicating a significant excess risk of diabetes incidence for the Hispanic population in southern Colorado. Peak age-specific incidence among Hispanics occurred in persons 50 to 59 years old, a decade earlier than among NHWs. These results are consistent with data from the Mexican-American population in Texas and suggest that the previously observed excess in diabetes prevalence is due to higher incidence rates. The earlier age-specific peak in incidence has also been observed in Mexican-American and American Indian populations, suggesting that risk factors may operate at earlier ages.

Adult↗
PubMed1993

Is the risk of coronary heart disease lower in Hispanics than in non-Hispanic whites? The San Luis Valley Diabetes Study.

A less favorable cardiovascular risk factor profile, but paradoxically lower coronary heart disease mortality and prevalence have been reported for Hispanic men compared to non-Hispanic white men. Since mortality and prevalence data are susceptible to bias, the patterns of coronary heart disease incidence, as well as prevalence and mortality, were investigated in a biethnic Hispanic and non-Hispanic white population of the San Luis Valley in Colorado. Little evidence was found for lower incidence, prevalence, or mortality due to coronary heart disease among Colorado Hispanics without diabetes. The risk of coronary heart disease among diabetic Hispanics appeared, however, to be approximately 50% lower than among non-Hispanic whites, especially in men. Adjustment for selected cardiovascular risk factors (age, gender, diabetes, hypertension, cigarette smoking, body mass index, and high-density lipoprotein cholesterol and triglycerides levels) did not change this ethnic pattern. The plausible explanations of a lower coronary heart disease risk among diabetic Hispanics, compared to non-Hispanic whites, include both biologic mechanisms and artifacts due to deficiencies of mortality classification or differential access to health care. The existing evidence is insufficient to conclude that the risk of coronary heart disease in the general population differs between Hispanics and non-Hispanic whites. The ethnic patterns of coronary heart disease incidence should be investigated further through population-based incidence studies.

Adult↗