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Biomedical subjects

B D Mitchell

Publications and source records attributed to B D Mitchell.

At least 109 records · Page 6Linked to original sources

Macrovascular complications in Mexican Americans with type II diabetes.

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)

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Cardiovascular risk factors in confirmed prediabetic individuals. Does the clock for coronary heart disease start ticking before the onset of clinical diabetes?

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.

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Does fasting interval affect the glucose challenge test?

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.

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Relationships between glucose levels and insulin secretion during a glucose challenge test.

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.

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Functional impairment in Mexican Americans and non-Hispanic whites with 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.

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Risk factors for cardiovascular mortality in Mexican Americans and non-Hispanic whites. San Antonio Heart Study.

A lower cardiovascular mortality in Mexican-American men than in non-Hispanic white men has been consistently observed. In contrast, no such ethnic difference has been observed in women. To determine whether this sex-ethnicity interaction in mortality is matched by a corresponding sex-ethnicity interaction in cardiovascular risk factors, the authors compared risk factors between 3,301 Mexican Americans and 1,877 non-Hispanic whites from the San Antonio Heart Study, a population-based study of cardiovascular disease and diabetes conducted in San Antonio, Texas (1979-1988). In both men and women, triglycerides, systolic and diastolic blood pressures, and body mass index (weight (kg)/height (m)2) were higher and high-density lipoprotein cholesterol was lower in Mexican Americans than in non-Hispanic whites. Although Mexican-American men were more likely than non-Hispanic white men to be smokers, Mexican Americans of both sexes smoked, on average, fewer cigarettes per day than non-Hispanic whites. Cardiovascular risk scores, which were constructed from Framingham Study risk equations to summarize the combined effect of multiple risk factors, were higher in Mexican Americans than in non-Hispanic whites of both sexes. The cardiovascular risk profile was less favorable for both Mexican Americans who grew up in Mexico and Mexican Americans who grew up in San Antonio. Although it is possible that in their younger years Mexican Americans had a more favorable cardiovascular risk profile, these results may also indicate that some protective factor, either genetic or life-style, is present in Mexican-American males but absent in non-Hispanic white males.

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Increased prevalence of clinical gallbladder disease in subjects with non-insulin-dependent diabetes mellitus.

The association between non-insulin-dependent diabetes mellitus (NIDDM) and the prevalence of gallbladder disease remains controversial. The authors investigated this association in 1,250 men and 1,656 women from the San Antonio Heart Study (1984-1988) a population-based study of diabetes and cardiovascular disease. A total of 68% of the subjects were Mexican American, a population at high risk for both gallbladder disease and NIDDM. Gallbladder disease was assessed by self-report, and the prevalence of diabetes was determined using National Diabetes Data Group criteria. NIDDM was significantly associated with gallbladder disease in Mexican-American men and women and in non-Hispanic white women. After adjustment for age, body mass index, ratio of waist-to-hip circumference, and ethnicity, using multiple logistic regression, the odds of gallbladder disease in women was 1.6 times higher if NIDDM was present (odds ratio = 1.60, 95% confidence interval 1.08-2.37). Mexican-American women also had a significantly increased prevalence of gallbladder disease relative to non-Hispanic white women (odds ratio = 2.21, 95% confidence interval 1.50-3.28). In nondiabetic women, fasting insulin was significantly related to prevalence of gallbladder disease in univariate analyses, but not in multivariate analyses. The authors conclude that women with diabetes have an increased prevalence of gallbladder disease relative to nondiabetic women and that this association is not explained by the greater adiposity or unfavorable body fat distribution of the diabetic subjects.

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Decreased prevalence of hypertension in Mexican-Americans.

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.

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Incidence of type II diabetes in Mexican Americans predicted by fasting insulin and glucose levels, obesity, and body-fat distribution.

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.

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Cigarette smoking and neuropathy in diabetic patients.

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.

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Overweight and mortality in Mexican Americans.

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)

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Lack of awareness and treatment of hyperlipidemia in type II diabetes in a community survey.

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.

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Type II diabetes mellitus and polymorphism of insulin-receptor gene in Mexican Americans.

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)

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Proteinuria in Mexican Americans and non-Hispanic whites with NIDDM.

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)

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Increased insulin concentrations in nondiabetic offspring of diabetic parents.

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.

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