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Biomedical subjects

S M Haffner

Publications and source records attributed to S M Haffner.

At least 289 records · Page 16Linked to original sources

Association between NIDDM, RH blood group, and haptoglobin phenotype. Results from the San Antonio Heart Study.

We examined seven red cell antigen and 10 polymorphic protein phenotypes in 1237 Mexican Americans randomly selected from three San Antonio neighborhoods. Statistically significant associations were found between non-insulin-dependent diabetes mellitus (NIDDM) and RH blood type (X2 = 32.87, df = 10, P = 0.0003) and haptoglobin phenotype (X2 = 9.15, df = 2, P = 0.010). The haptoglobin association showed a dose effect with a single dose of the haptoglobin-1 allele associated with an approximately 50% increase and a double dose of the haptoglobin-1 allele associated with an approximately 100% increase in NIDDM prevalence. Multivariate analysis indicated statistically significant associations between NIDDM and age, sex, adiposity, and neighborhood of residence. However, even after taking these potential confounding variables into account, there was still a significant, independent association between NIDDM and haptoglobin phenotype. The results suggest that the haptoglobin gene may be in linkage disequilibrium with a major susceptibility gene for NIDDM.

Adult↗

Upper body and centralized adiposity in Mexican Americans and non-Hispanic whites: relationship to body mass index and other behavioral and demographic variables.

Mexican Americans have a higher prevalence of NIDDM, more overall obesity and more centralized adiposity than non-Hispanic whites, but have thus far not been characterized as to whether they have greater upper body adiposity. Waist-to-hip circumferences (WHR, a measure of upper body adiposity) and subscapular-to-triceps skinfold ratios (centrality index, a measure of centralized adiposity) were determined in 725 Mexican Americans and 226 non-Hispanic whites as part of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Mexican American females had higher centrality indices and WHRs than non-Hispanic white females, even after adjustment for demographic (age, menopausal status) and behavioral variables (body mass index, parity, cigarette smoking, alcohol consumption, exercise, and oral contraceptive and estrogen use). Mexican American males had higher centrality indices than non-Hispanic white males, but differences in WHR disappeared after adjustment for overall adiposity (body mass index). Of the demographic and behavioral variables, only age and body mass index were consistently related to regional body fat distribution. The lack of an association between body fat distribution and behavioral variables suggests that genetic factors may play the principal role in determining body fat distribution. Surprisingly, the distributions of centrality index and WHR were relatively independent of one another suggesting that they may be used as distinct, independent predictors of metabolic diseases.

Adipose Tissue↗

Evidence of bimodality of two hour plasma glucose concentrations in Mexican Americans: results from the San Antonio Heart study.

Evidence for bimodality in the distribution of two hour post oral glucose challenge plasma glucose concentrations has come previously primarily from native American and Pacific Island populations having high non-insulin dependent diabetes mellitus (NIDDM) prevalence. Because the National Diabetes Data Group (NDDG) criteria for diagnosing NIDDM rely in part upon the assumption of bimodality, it is important to determine the generality of this phenomenon. We looked for bimodality among Mexican Americans in San Antonio, a population having greater than 50% Caucasian admixture. By fitting both a single normal distribution model and a mixture model of two normal distributions, for each age decade, we found that the mixture model was preferred to the single normal model (p less than 0.001) and that this model fit the data well. The proportion in the upper component (hyperglycemics) increased with each successive age decade. The minimum misclassification cutpoints decreased with age, but all were higher than the 200 mg/dl cutpoint recommended by the NDDG. Use of the NDDG cutpoint, however, improved sensitivity with only a minimal deterioration of specificity. Our findings further generalize the bimodality phenomenon and support the NDDG criteria.

Adult↗

Compositional and metabolic heterogeneity of alpha 2- and beta-very-low-density lipoproteins in subjects with broad beta disease and endogenous hypertriglyceridemia.

The catabolism of alpha 2- and beta-very-low-density lipoproteins (VLDL) was studied in normolipidemic and hyperlipidemic subjects to determine whether differences in the catabolism of these subfractions are due to their composition. alpha 2-VLDL (cholesterol/triglyceride ratio, 00.18 +/- 0.06; and apoprotein E/C ratio, 0.27 +/- 0.22, n = 4) and beta-VLDL (cholesterol/triglyceride ratio, 0.67 +/- 0.13; and apoprotein E/C ratio, 1.05 +/- 0.52, n = 4) were isolated from subjects with broad beta disease, iodinated, and injected in five normolipidemic subjects, six with broad beta disease, and five with endogenous hypertriglyceridemia. VLDL, intermediate (IDL) and low-density lipoprotein (LDL) apoprotein (apo)-B radioactivity (tetramethylurea insoluble) following injection of 125I-labeled alpha 2- and beta-VLDL decayed biphasically in all subjects, and this decay in normolipidemic subjects was more rapid than in subjects with broad beta disease (P = 0.004) or endogenous hypertriglyceridemia (P = 0.004 for alpha 2- and P = 0.010 for beta-VLDL). The residence times, however, for the delipidation chain in alpha 2-VLDL were similar in all the subjects and varied from three to six hours. The decay of radioactivity in beta-VLDL in subjects with broad beta disease was much slower (residence time, 36.9 +/- 24.4 hr, n = 7) than in normolipidemic subjects (residence time, 7.56 +/- 4.6 hr, n = 5) or in subjects with endogenous hypertriglyceridemia (residence time, 10.6 +/- 4.65, n = 4). The residence time for alpha 2-VLDL was longer than for beta-VLDL in all subjects, suggesting that alpha 2-VLDL is a precursor to beta-VLDL. To test this directly, iodinated alpha 2-VLDL was injected into a subject with broad beta disease and the radioactivity in the subfractions was followed. The radioactivity from alpha 2-VLDL was transferred into beta-VLDL supporting, the notion that alpha 2-VLDL generated some beta-VLDL. Nicotinic acid treatment of a subject with broad beta disease accelerated the catabolism of alpha 2- and beta-VLDL without changing the VLDL composition.

Adult↗

Dietary intakes of essential nutrients among Mexican-Americans and Anglo-Americans: the San Antonio Heart Study.

Dietary intakes of essential nutrients were measured as part of a population-based investigation of diabetes and cardiovascular risk factors in Mexican-Americans and Anglo-Americans in San Antonio, Texas. Twenty-four hour dietary recalls were conducted on 2134 individuals residing in three socioeconomically distinct neighborhoods: low-income, middle-income, and upper-income. Mean intakes of calcium, vitamin A and vitamin C were significantly lower among Mexican-Americans than among Anglos. Intake of vitamin C was most affected by socioeconomic status. Females of both ethnic groups consumed less than their RDA for calcium and iron. Intakes of B vitamins, phosphorus, and potassium were adequate, with few ethnic or socioeconomic differences.

Adult↗

Dietary intakes of macronutrients among Mexican Americans and Anglo Americans: the San Antonio heart study.

Twenty-four-hour dietary recalls were obtained on 1254 Mexican Americans (MA) and 916 Anglo Americans (AA), aged 25 to 64, as part of the San Antonio heart study, a population-based survey of cardiovascular risk factors from 1979 to 1982. In order to separate the effects of ethnicity from those of socioeconomic status (SES), we sampled subjects in three distinct neighborhoods: a low income MA neighborhood (barrio), a middle income neighborhood, and an upper income, predominantly Anglo, neighborhood. Intakes of protein, fat, and carbohydrate were similar to those found in other dietary surveys (NHANES, LRC). MA females living in the barrio consumed more cholesterol than either Anglos or MAs living in the other two neighborhoods. In MA males, the rise in the Hegsted Score with increasing SES paralleled the rise in LDL cholesterol with rising SES reported previously by our group. Females consumed a less atherogenic diet than males.

Adult↗

Prevalence, detection, and control of hypertension in a biethnic community. The San Antonio Heart Study.

A survey was carried out on a random sample of 1,288 Mexican Americans and 929 Anglos living in three socially distinct neighborhoods in San Antonio, Texas. Hypertension was defined as diastolic blood pressure greater than or equal to 95 mmHg or currently taking antihypertensive medication. Overall age-adjusted prevalence rates of hypertension were similar for Mexican-American and Anglo men (10.0 and 9.8%, respectively); for women, the Mexican-American rate was slightly lower than that for Anglos (7.8 and 9.7%, respectively). After adjustment for obesity differences, Mexican Americans have a tendency toward lower hypertension rates than Anglos of the same socioeconomic level. Only among women was a decline in the prevalence of hypertension with increasing socioeconomic status observed. Mexican Americans have a higher proportion of newly diagnosed hypertension, and, among previously diagnosed cases, a lower proportion are on antihypertensive medication than Anglos. The rates of hypertension control found in this survey are among the highest reported in the United States at the community level. Despite this, Mexican Americans still lag somewhat behind Anglos of the same socioeconomic level in awareness, treatment, and degree of hypertension control, suggesting the possibility of sociocultural barriers to adequate medical care.

Adult↗

Coffee consumption, diet, and lipids.

Recent reports suggest that coffee consumption is associated with increased serum cholesterol and triglyceride concentrations. The authors examined the association between serum lipids and coffee consumption and other caffeinated beverages as part of a population-based study of 1,228 women and 923 men, aged 25-64 years, in San Antonio, Texas, studied between October 1979 and November 1982. The study confirmed a positive relationship between coffee consumption and both total and low density lipoprotein cholesterol in both sexes which persisted after adjustment for age, ethnicity, obesity, cigarette smoking, and alcohol consumption. Neither tea nor cola consumption was associated with changes in serum lipids, suggesting that caffeine alone does not exert a direct effect on lipid levels. The possibility was examined that the coffee-cholesterol relationship might be due to a more atherogenic diet consumed by heavy coffee drinkers. In men, per cent calories from both total and saturated fat and dietary cholesterol intake increased with increased coffee consumption. Similar trends were not observed in women, however. The positive relationship between coffee and cholesterol may therefore be due to confounding effects of other aspects of the diet.

Adult↗

Retarded chylomicron apolipoprotein-B catabolism in type 2 (non-insulin-dependent) diabetic subjects with lipaemia.

To define the kinetics of chylomicron apolipoprotein-B catabolism in diabetic subjects with lipaemia, autologous chylomicrons (Sf 400) harvested from plasma following an oral fat load were radioiodinated and re-injected. The radioactivity in the tetramethylurea-insoluble, non-lipid Sf greater than 400 lipoprotein fraction was followed in serial samples over 60-72 h on a fat-free, isocaloric diet in: (1) five normal subjects; (2) four hypertriglyceridaemic, non-diabetic subjects; and (3) five diabetic patients (one subject, No. 3, was studied twice). The plasma apolipoprotein-B decay curve for the Sf 400 fraction disclosed biphasic disappearance: a rapid first phase (residence time 0.8-1.9 h) accounting for the large majority of removal (60%-95%) and a slower second phase (residence time 3.6-47.6 h), accounting for the remainder. Total chylomicron apolipoprotein-B residence times were similar in normolipidaemic (1.8-7.3 h) and hypertriglyceridaemic (2.3-10.3 h) non-diabetic subjects and the mildly hypertriglyceridaemic diabetic patients (5.6 and 5.8 h). In the untreated lipaemic diabetic subjects (Nos. 1 and 2), only a single, much slower phase was observed (total chylomicron apolipoprotein-B residence time 38.5-58 h). Adipose tissue biopsy in one of these subjects (No. 1) disclosed profoundly low lipoprotein lipase activity. The lipaemic diabetic subject (No. 3) studied early during treatment showed an intermediate pattern. These studies suggest a key role for insulin-dependent, lipoprotein lipase-mediated triglyceride hydrolysis in the removal of chylomicrons from plasma.

Adipose Tissue↗

Preliminary report: kinetic studies on the modulation of high-density lipoprotein, apolipoprotein, and subfraction metabolism by sex steroids in a postmenopausal woman.

To investigate the effects of estrogens and androgens on the metabolism of high density lipoproteins (HDL) and low density lipoproteins (LDL), a normolipidemic postmenopausal woman was studied under the following conditions: (1) during supplementation with ethinyl estradiol (0.06 mg/d); (2) without sex steroid therapy; (3) during treatment with stanozolol, an androgenic, anabolic steroid (6 mg/d). During these manipulations HDL and LDL cholesterol levels fluctuated widely but reciprocally: during estrogen supplementation HDL increased while LDL decreased; during stanozolol HDL-C decreased while LDL-C increased. Simultaneous changes in post-heparin plasma hepatic triglyceride lipase activity paralleled those of LDL (and opposed those of HDL), decreasing with estrogen and increasing with stanozolol. During all three phases, autologous 125I-HDL turnover studies disclosed similarities between HDL2 and apolipoprotein A-I metabolism and between HDL3 and apolipoprotein A-II metabolism. In the untreated state the residence times of HDL2 and apo A-I were only half those of HDL3 and apo A-II. During estrogen treatment HDL2 and apo A-I, residence times were selectively prolonged, coming to resemble those of HDL3 and apo A-II, which remained unchanged. By contrast, during stanozolol treatment HDL3 and apo A-II residence times were selectively reduced, coming to resemble those of HDL2 and apo A-I, which remained unchanged. Apo A-I levels increased on estrogen and decreased on stanozolol, while apo A-II remained stable. Hence, estrogen increased HDL primarily by retarding the catabolism of the HDL2 subfraction rich in apo A-I, whereas stanozolol decreased HDL by accelerating the catabolism of HDL3, relatively rich in apo A-II.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein A-I↗

Chylomicron and very low-density lipoprotein apolipoprotein B metabolism: mechanism of the response to stanozolol in a patient with severe hypertriglyceridemia.

Studies of simultaneous autologous 131I-chylomicron (Sf greater than 400) and 125I-very low density lipoprotein (VLDL) (Sf 20 to 400) apolipoprotein B (apo B) were performed both before (triglyceride level c 1500 mg/dL) and during treatment with stanozolol, a 17 alpha-methyl anabolic androgenic steroid (triglyceride level c 750 mg/dL) in a 74-year-old woman with a past history of recurrent chylomicronemic pancreatitis. Both before and during stanozolol treatment chylomicron apo B disappeared rapidly and directly, little appearing in VLDL and virtually none in intermediate (IDL) or low density lipoproteins (LDL). Multicompartmental analysis indicated that the great majority of chylomicron apo B was removed via an extremely rapid compartment (estimated fractional catabolic rate [FCR], 5.0/h), accounting for 66% before and 88% during stanozolol treatment. The remaining 131I-apo B decayed biphasically, with total Sf greater than 400 residence times of 8.6 hours before and 3.7 hours during stanozolol treatment. Hence, despite a moderately depressed adipose tissue lipoprotein lipase activity, the subject's hypertriglyceridemia did not appear to proceed solely from retarded chylomicron removal, nor was the dramatic decrease in triglyceride in response to stanozolol a function only of the acceleration of such removal. VLDL apo B kinetics were analyzed by a multicompartmental model featuring a rapid, stepwise delipidation chain which proceeds either rapidly to IDL and LDL or to a slowly turning over compartment within VLDL. While VLDL. apo B synthesis remained essentially constant, the major effect of stanozolol was a substantial reduction in the fraction of VLDL apo B diverted to this slowly turning over compartment, which decreased from 5.0% before to 1.2% during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Down-regulation of the low-density lipoprotein receptor by dietary cholesterol.

To determine the effect of dietary cholesterol on the low-density lipoprotein (LDL) receptor of circulating mononuclear cells, nine adults (six men, three women) consumed a natural diet consisting of 45% of the calories as carbohydrate, 40% as fat, and 15% as protein, polyunsaturated/saturated fatty acid ratio 0.80 to 0.84, and either 137 +/- 25 mg cholesterol per day (low cholesterol phase) or 1034 +/- 25 mg cholesterol per day (high cholesterol phase). The study lasted 2 months with 1 month in each phase and used a cross-over design. The levels of plasma triglyceride, plasma cholesterol, very low-density and high-density lipoprotein cholesterol, and apolipoproteins B, A-I, and A-II were similar in the two diet phases. The high cholesterol diet was associated with an 11 +/- 9% increase (p less than 0.02) in LDL cholesterol level and a 41 +/- 14% decrease in LDL receptor activity (p less than 0.05, n = 6). The percentage decrease in LDL receptor activity correlated with the percentage increase in LDL cholesterol (r = -0.796, p = 0.06, n = 6). Thus, high levels of dietary cholesterol can down-regulate the LDL receptor in humans.

Adult↗

Sex difference in the effects of sociocultural status on diabetes and cardiovascular risk factors in Mexican Americans. The San Antonio Heart Study.

The authors postulated that as Mexican Americans became more affluent and/or acculturated to "mainstream" United States life-style they would progressively lose their "obesity-related" pattern of cardiovascular risk factors which were defined as: obesity, diabetes, hypertriglyceridemia and low levels of high density lipoprotein cholesterol. This hypothesis was tested in 1979-1982 in the San Antonio Heart Study, a population-based study on 1,288 Mexican Americans and 929 Anglos living in three San Antonio neighborhoods: a low-income barrio, a middle-income transitional neighborhood, and a high-income suburb. The study population comprised 25-65-year-old men and nonpregnant women. In Mexican American women, all of the "obesity-related" risk factors fell sharply with rising socioeconomic status. In Mexican American men, by contrast, diabetes was the only "obesity-related" risk factor which fell with rising socioeconomic status. Moreover, it fell less steeply, there being an approximately twofold difference in diabetes prevalence between the barrio and the suburbs in men compared to a fourfold difference in women. Also, total and low density lipoprotein cholesterol rose with rising socioeconomic status in Mexican American men, but not in Mexican American women. "Obesity-related" risk factors were generally higher in Mexican Americans of both sexes than in their Anglo neighbors who were of similar socioeconomic status. These results suggest that cultural factors exert a stronger influence on diabetes and cardiovascular risk factors in Mexican Americans than do purely socioeconomic factors.

Adult↗

Prevalence of diabetes in Mexican Americans. Relationship to percent of gene pool derived from native American sources.

We have estimated the prevalence of non-insulin-dependent diabetes mellitus (NIDDM) in Mexican Americans and Anglos in three San Antonio neighborhoods. The age-adjusted NIDDM rates (both sexes pooled) for Mexican Americans were 14.5%, 10%, and 5% for residents of a low-income barrio, a middle-income transitional neighborhood, and a high-income suburb, respectively. In Mexican American women, though not in men, obesity also declined from barrio to suburbs. We have previously shown, however, that, although obesity is an important cause of NIDDM in Mexican Americans, there is a two- to fourfold excess in the rate of NIDDM in this ethnic group over and above that which can be attributed to obesity. We therefore speculated that genetic factors might also contribute to excess NIDDM in this ethnic group. The percent native American admixture of Mexican Americans as estimated from skin color measurements was 46% in the barrio, 27% in the transitional neighborhood, and 18% in the suburbs. The NIDDM rates in Mexican Americans thus paralleled the proportion of native American genes. Furthermore, the San Antonio Mexican American rates were intermediate between the NIDDM rates of "full-blooded" Pima Indians (49.9%), who presumably have close to 100% native American genes, and the San Antonio Anglo population (3.0%) and the predominantly Anglo HANES II population (3.1%), both of which presumably have few if any native American genes. The association of genetic admixture with NIDDM rates suggests that much of the epidemic of NIDDM in Mexican Americans is confined to that part of the population with a substantial native American heritage.

Adult↗

Does obesity explain excess prevalence of diabetes among Mexican Americans? Results of the San Antonio Heart Study.

Obesity and Type 2 (non-insulin-dependent) diabetes mellitus are common in the Mexican American population. It is not clear whether this is merely a specific instance of the more general phenomenon of excess Type 2 diabetes and obesity among poor people, or whether Mexican Americans have a discrete genetic susceptibility to Type 2 diabetes. The latter consideration arises because Mexican Americans are of mixed native American and European ancestry and native Americans may have a genetic predisposition to Type 2 diabetes which Mexican Americans could share. We studied 936 Mexican Americans and 398 Anglo-Americans randomly selected from three socially and culturally distinct neighborhoods in San Antonio, Texas. Three categories of obesity--lean, average, and obese--were defined using the Anglo-American distribution of the sum of the triceps and subscapular skinfold. Mexican Americans were two to four times as likely to fall into the obese category as Anglo-Americans, but within categories, the two ethnic groups were closely matched in terms of sum of skinfolds. The prevalence of Type 2 diabetes, however, was significantly greater in Mexican Americans than in Anglo-Americans even when the comparisons were made within the three obesity categories. The summary prevalence ratio, controlling for obesity, was 2.54 for men (p = 0.004) and 1.70 for women (p = 0.036). Thus, lean Mexican Americans are still at greater risk of Type 2 diabetes than equally lean Anglo-Americans. Conversely, although Type 2 diabetes prevalence increases as expected with increasing obesity in both ethnic groups, obese Anglo-Americans are still relatively protected compared with equally obese Mexican Americans. Plasma glucose was significantly higher in Mexican Americans than in Anglo-Americans even after controlling for obesity. These results indicate that, although obesity contributes to Type 2 diabetes in Mexican Americans, it does not by itself explain the entire excess prevalence rate.

Adult↗

Studies on the metabolic mechanism of reduced high density lipoproteins during anabolic steroid therapy.

To explore the mechanism whereby stanozolol, a 17 alpha-methyl androgenic anabolic steroid, depresses high density lipoproteins (HDL), 6 subjects, aged 46-71 yr (4 postmenopausal women and 2 men), underwent paired studies of 125I-HDL turnover (including HDL2 and HDL3 and Apo A-I and A-II) and postheparin plasma (PHP) lipolytic activity (hepatic triglyceride lipase, HTGL, and lipoprotein lipase LPL) before and during treatment with stanozolol, 6 mg/day. While total cholesterol and triglyceride levels did not change during stanozolol, HDL-cholesterol decreased from 59 +/- 18 mg/dl (x +/- SD) to 29 +/- 7 mg/dl (p less than 0.01) and low density lipoprotein (LDL)-cholesterol increased from 160 +/- 36 mg/dl to 181 +/- 42 mg/dl (p less than 0.02). PHP-HTGL increased from 111 +/- 47 nmole/min/ml to 369 +/- 202 nmole/min/ml (p less than 0.04), while PHP-LPL did not change. At baseline the residence time of HDL2 (4.00 +/- 1.04 day) was shorter than that of HDL3 (6.79 +/- 1.00 day) (p less than 0.001). Residence times of both declined on stanozolol, to 3.25 +/- 0.83 day and 4.00 +/- 0.29 day, respectively (0.1 less than p less than 0.2); however, only the reduction in residence time of HDL3 was statistically significant (p less than 0.001). At baseline the residence time of apo A-I (4.93 +/- 1.32 day) was shorter than that of A-II (6.85 +/- 1.98 day) (p less than 0.025); on stanozolol these declined to 3.19 +/- 0.41 (p less than 0.02) and 5.10 +/- 1.13 (p = 0.07), respectively, still significantly different from each other (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Ethnic differences in health knowledge and behaviors related to the prevention and treatment of coronary heart disease. The San Antonio Heart Study.

From a public health perspective, Mexican Americans are widely recognized as an understudied population. Available evidence suggests that Mexican Americans shared equally with non-Hispanic Caucasians (Anglo Americans or "Anglos") in the national decline in coronary heart disease (CHD) mortality during 1970-1976. This finding is somewhat unexpected in view of Mexican Americans' relatively lower socioeconomic status, and it suggests that studying this ethnic group may be strategic in understanding which factors have operated to produce the decline in general. Data obtained from a random sample of Mexican Americans and Anglos residing in three socioeconomically and culturally distinct neighborhoods in San Antonio, Texas, indicated that Anglos were significantly more informed than Mexican Americans about CHD prevention and generally reported engaging in more behaviors specifically aimed toward prevention than did Mexican Americans. Levels of knowledge were not particularly high in either ethnic group; moreover, reported behavior lagged considerably behind knowledge. While Mexican Americans were significantly less likely than Anglos to volunteer knowledge about major heart attack symptoms, there were negligible ethnic differences in awareness of the need for prompt utilization of medical treatment resources when a heart attack actually occurs. Awareness of the need for prompt action was notably high among both ethnic groups. Although limitations in the nature and scope of the data dictate that these findings should be interpreted with caution, the results tend to argue in the direction that prompt access to medical treatment when coronary emergencies occur may have made a relatively greater contribution to the CHD mortality decline in both Mexican Americans and Anglos than did changes in life-style. Much additional data are needed, however, before a definitive explanation of the decline will be possible.

Coronary Disease↗