Relation of lipoprotein subclasses as measured by proton nuclear magnetic resonance spectroscopy to coronary artery disease.

Although each of the major lipoprotein fractions is composed of various subclasses that may differ in atherogenicity, the importance of this heterogeneity has been difficult to ascertain owing to the labor-intensive nature of subclass measurement methods. We have recently developed a procedure, using proton nuclear magnetic resonance (NMR) spectroscopy, to simultaneously quantify levels of subclasses of very low density (VLDL), low density (LDL), and high density (HDL) lipoproteins; subclass distributions determined with this method agree well with those derived by gradient gel electrophoresis. The objective of the current study of 158 men was to examine whether NMR-derived lipoprotein subclass levels improve the prediction of arteriographically documented coronary artery disease (CAD) when levels of lipids and lipoproteins are known. We found that a global measure of CAD severity was positively associated with levels of large VLDL and small HDL particles and inversely associated with intermediate size HDL particles; these associations were independent of age and standard lipid measurements. At comparable lipid and lipoprotein levels, for example, men with relatively high (higher than the median) levels of either small HDL or large VLDL particles were three to four times more likely to have extensive CAD than were the other men; the 27 men with high levels of both large VLDL and small HDL were 15 times more likely to have extensive CAD than were men with low levels. In contrast, adjustment for levels of triglycerides or HDL cholesterol greatly reduced the relation of small LDL particles to CAD. These findings suggest that large VLDL and small HDL particles may play important roles in the development of occlusive disease and that their measurement, which is not possible with routine lipid testing, may lead to more accurate risk assessment.

Black/white differences in leukocyte subpopulations in men.

BACKGROUND: Although counts of leukocytes differ substantially between blacks and whites, and are predictive of ischaemic heart disease (IHD), racial differences in counts of leukocyte subpopulations have received less attention. METHODS: We examined black/white differences in leukocyte subpopulations among 3467 white and 493 black 31-45 year-old-men who had previously served in the US Army. Laboratory determinations were performed at a central location during 1985-1986. RESULTS: Black men had an 840 cell/microliter (or 15%) lower mean total leukocyte count than did white men, largely due to a 960 cell/microliter (or 25%) lower mean neutrophil count. Although black men also had a 20% lower mean monocyte count (= 70 cells/microliter) than did white men, their mean lymphocyte count was 10% higher (approximately = 200 cells/microliter). Counts of various leukocyte subpopulations were associated with cigarette smoking, haemoglobin levels, platelet counts, and several other characteristics, but black/white differences in counts of neutrophils, lymphocytes, monocytes and other subpopulations could not be attributed to any of the examined covariates. CONCLUSIONS: Despite the relatively low counts of leukocytes and neutrophils among black men, their lymphocyte counts are generally higher than those among white men. It is possible that black/white differences in counts of various cell types may influence race-specific rates of IHD, and future studies should attempt to assess the importance of leukocyte subpopulations in the development of clinical disease.

Cigarette smoking and leukocyte subpopulations in men.

Because of previously reported associations among the total leukocyte count, cigarette smoking, and risk of cardiovascular disease, we examined the relation of cigarette smoking to various leukocyte subpopulations among 3467 men aged 31 to 45 years. The median total leukocyte count was 36% higher (7840 vs. 5760 cells/mL) among current cigarette smokers than among men who had never smoked, and both stratification and regression analyses were used to examine independent associations with leukocyte subpopulations. At equivalent counts of other subpopulations, CD4+ lymphocytes and neutrophils were the cell types most strongly associated with cigarette smoking; each standard deviation change in counts of these subpopulations increased the odds of current (vs. never) smoking by approximately threefold. Furthermore, whereas 15% of the 238 men with relatively low (< 25 percentile) counts of both neutrophils and CD4+ lymphocytes were cigarette smokers, 96% of the 249 men with relatively high counts of both subpopulations were current smokers. Counts of T lymphocytes also tended to be higher among the 32 men with self-reported ischemic heart disease than among other men. These results, along with previous reports of immunologically active T lymphocytes in atherosclerotic plaques, suggest that this subpopulation may be of particular interest in studies examining the relation of leukocytes to cardiovascular disease.

Correlates of leukocyte counts in men.

Because of previously reported associations between a high leukocyte count and risk of ischemic heart disease (IHD), we examined the relation of leukocyte counts to various characteristics among 3591 white and 506 black 31- to 45-year-old men. The mean leukocyte count was approximately 1000 cells/microL higher among whites than among blacks, and approximately 1900 cells/microL higher among current smokers than among nonsmokers. The leukocyte count was also higher among men who had recently stopped smoking and among men who reported their general health as poor or fair. Independent of these relations, the leukocyte count was associated positively with the platelet count (r = 0.29), triglyceride level (r = 0.21), heart rate (r = 0.15), and use of corticosteroids and beta-blockers; and inversely with alcohol consumption and prothrombin time (r = -0.10). The examined characteristics could together account for 37% of the variability in leukocyte counts. These relatively strong associations indicate that it may be difficult to disentangle the relation of the leukocyte count to IHD from that of other risk factors.

The relation of documented coronary artery disease to levels of total cholesterol and high-density lipoprotein cholesterol.

Recommendations for identifying persons at high risk for coronary heart disease are based primarily on levels of total and low-density lipoprotein cholesterol. We examined whether, given knowledge of these levels, information on the high-density lipoprotein cholesterol level would improve the prediction of arteriographically documented coronary artery disease among 591 men. We found that even at levels of total and low-density lipoprotein cholesterol considered desirable, high-density lipoprotein cholesterol was inversely related to disease severity. For example, among the 112 men with a total cholesterol level <180 mg per dl, the mean occlusion score (representing the overall severity of disease) was 107 among men with a high-density lipoprotein cholesterol level < or = 30 mg per dl vs a mean score of 52 among men with levels > or = 45 mg per dl. Furthermore, men with low levels of both low-density lipoprotein cholesterol (< 110 mg per dl) and high-density lipoprotein cholesterol (< or = 30 mg per dl) had as much occlusive disease as did men with high levels of both lipoprotein fractions. Given information on the ratio of high-density lipoprotein cholesterol to total cholesterol, the actual levels of the lipoprotein fractions did not improve disease prediction. Our results emphasize the importance of considering high-density lipoprotein cholesterol when assessing coronary heart disease risk.

Alcohol-related hospitalizations of elderly people. Prevalence and geographic variation in the United States.

OBJECTIVE: To determine the prevalence, geographic variation, and charges to Medicare of alcohol-related hospitalizations among elderly people in the United States. DESIGN: A cross-sectional prevalence study using 1989 hospital claims data from the Health Care Financing Administration (HCFA). Rates were determined using (1) hospital claims records from the HCFA's Medicare Provider Analysis and Review Record (MEDPAR) database for all Medicare Part A beneficiaries aged 65 years and older; (2) county population estimates for 1985 from the Bureau of the Census; and (3) per capita consumption of alcohol by state in 1989 as estimated by the US Department of Health and Human Services. SETTING: Data include all hospital inpatient Medicare Part A beneficiaries aged 65 years and older in the United States in 1989. RESULTS: The prevalence of alcohol-related hospitalizations among people aged 65 years and older nationally in 1989 was 54.7 per 10,000 population for men and 14.8 per 10,000 for women. Comparison with hospital records showed that MEDPAR data had a sensitivity of 77% to detect alcohol-related hospitalizations. There was considerable geographic variation; prevalence ranged from 18.9 per 10,000 in Arkansas to 77.0 per 10,000 in Alaska. A strong correlation existed between alcohol-related hospitalizations and per capita consumption of alcohol by state (Spearman correlation coefficient, .64; P < .0001). In 1989, the hospital-associated charges to Medicare for all admissions where the primary diagnosis was alcohol related (N = 33,039) totaled $233,543,500. Median charge per hospital stay was $4514. CONCLUSIONS: Alcohol-related hospitalizations among elderly people are common; rates were similar to those for myocardial infarction as detected by the same method. The charges to Medicare for this preventable problem are considerable. Ecological analysis suggests that per capita consumption in the total US population predicts alcohol-related hospitalizations in the elderly population.

Cholesterol and coronary artery disease: age as an effect modifier.

An elevation of serum cholesterol has been one of the more frequently cited risk factors for coronary heart disease, found in both case-control and cohort studies. As a result, this country has undertaken massive screening of adults older than 20 years of age in an attempt to identify those persons with cholesterol levels greater than 200 mg/dl, and follow up with an active approach for intervention. The suggested cutpoints for borderline (200-240 mg/dl), and definite (> or = 240 mg/dl) hypercholesterolemia have been applied to all age groups despite suggestions of a diminution of risk conferred by cholesterol in the elderly. This study of 2544 white men undergoing coronary angiography shows that for all men, aged 25-84 years, plasma cholesterol levels were associated with an increase in coronary artery occlusion (rs = 0.15, p < 0.01). However, when stratified by age, this association held only for the younger men, the association diminishing to near zero in the oldest age group. The negative interaction between cholesterol levels and age in predicting coronary artery disease proved highly significant (p < 0.001) in multivariable linear regression analysis, suggesting that cholesterol levels are much less predictive of coronary artery disease in the elderly as compared to the young. These results point to the need for a more finely tuned set of criteria for the evaluation of hypercholesterolemia, one that takes into account the age of the screenee.

The relation of prothrombin times to coronary heart disease risk factors among men aged 31-45 years.

Although levels of coagulation factor VII and fibrinogen are predictive of cardiovascular disease, relatively little data describe hemostatic characteristics in healthy populations. The cross-sectional associations between the prothrombin time, a measure of the activity of the extrinsic and common pathways of coagulation, and traits associated with the risk of cardiovascular disease were therefore examined among 3,604 white and 514 black, male, US Army veterans aged 31-45 years. The prothrombin time measurements, performed in 1985 and 1986, were precise, with an intraclass correlation of 0.98 (202 pairs). Overall, the mean prothrombin time was 12.4 seconds (standard deviation, 0.4 seconds), and 11 percent of the men had a value of less than 12 seconds. Many of the observed associations with the prothrombin time paralleled those that have been reported with clotting factor VII and fibrinogen. The mean prothrombin time was 0.15 seconds shorter among whites than among blacks and was 0.2 seconds shorter among current cigarette smokers than among men who had never smoked. Inverse associations were also seen with relative weight and with levels of total cholesterol and triglycerides (r = -0.09 to -0.16). All associations were statistically significant at the 0.01 level, and the examined characteristics could jointly account for about 12 percent of the variability in prothrombin times. Additional data on characteristics related to coagulation may help elucidate the natural history of cardiovascular disease and aid in the design of clinical trials.

Alcohol produces dose-dependent antiatherogenic and atherogenic plasma lipoprotein responses.

A comprehensive assessment of lipoprotein compositional/metabolic response to incremental caloric ethanol (EtOH) doses ranging from low to moderate to high was undertaken using male squirrel monkeys. Control monkeys were maintained on a chemically defined, isocaloric liquid diet, while experimental primates wee fed increasing doses of alcohol (6, 12, 18, 24, 30, and 36% of energy) substituted isocalorically for carbohydrate at 3-month intervals. Liver function tests and plasma triglyceride were normal for all animals. Plasma cholesterol showed a transient increase at the 12% caloric dose that was attributed solely to an increase in high density lipoprotein (HDL). A more pronounced increase in plasma sterol, beginning at 24% and continuing to 36% EtOH, was the result of increments in both HDL and low density lipoprotein (LDL) cholesterol, although the contribution by the latter was substantial primarily at the 36% dose. Plasma apolipoprotein elevations (HDL apolipoprotein A-I, LDL apolipoprotein B) generally accompanied the lipoprotein lipid increases, although the first atherogenic response for LDL became manifest as a significant increase in apolipoprotein B at 18% EtOH calories. Postheparin plasma lipoprotein lipase was not affected by dietary alcohol, whereas hepatic triglyceride lipase activity showed significant increases at higher (24 and 36%) EtOH doses. Plasma lecithin-cholesterol acyltransferase activity was normal at the 6 and 12% EtOH doses, but exhibited a significant reduction beginning at 18% and continuing to 36% EtOH. Alterations in these key lipoprotein regulatory enzymes may represent the underlying metabolic basis for the observed changes in lipoprotein levels and our earlier findings of HDL2/HDL3 subfraction modifications. Results from our study indicate that in squirrel monkeys, moderate (12%) EtOH caloric intake favors an antiatherogenic lipoprotein profile (increases HDL, normal LDL levels, and lecithin-cholesterol acyltransferase activity), whereas higher doses (24-36%) produce both coronary-protective (increases HDL) and atherogenic (increases LDL) responses. Moreover, the 18% EtOH level represents an important transition dose which signals early adverse alterations in lipoprotein composition (increases apolipoprotein B) and metabolism (decreases lecithin-cholesterol acyltransferase).

Effect of ethanol on low density lipoprotein and platelet composition.

The present study was designed to investigate the effect of ethanol (EtOH) dose on low density lipoprotein (LDL) and platelet composition. Male squirrel monkeys were divided into three groups designated Control, Low, and High EtOH, and fed isocaloric liquid diets containing 0%, 12%, and 24% of calories as EtOH, respectively. After four months of treatment, monkeys fed the 12% alcohol dose had LDL and platelet cholesterol concentrations similar to Controls. By contrast, platelet membranes from High EtOH animals contained significantly more cholesterol which was associated with higher levels of plasma LDL cholesterol and apolipoprotein B. Blood platelet count, size, and mass were similar for all groups and circulating platelet aggregates were absent in the two alcohol cohorts. Despite elevations in platelet cholesterol mass and thromboxane A2 (TXA2) precursor, phospholipid arachidonate, platelet responsiveness, measured as thromboxane formed in response to a collagen challenge in vitro, and the cholesterol/phospholipid molar ratio, were not significantly altered by high dose alcohol. Normal platelet activity in High EtOH monkeys may have resulted from a significant increase in the platelet phospholipid polyunsaturated/saturated fatty acid ratio and a non-significant increase in platelet phospholipid mass, both of which would have a fluidizing effect on platelet membranes. Our data indicate that low EtOH intake has no effect on platelet composition and function while unfavorable platelet cholesterol enrichment following consumption of high dose ethanol may arise from elevations in plasma LDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of drinking pattern on plasma lipoproteins and body weight.

The effect of drinking pattern on plasma lipoproteins and body weight was examined in three groups of squirrel monkeys: (1) controls fed isocaloric liquid diet; (2) regular drinkers given liquid diet containing ethanol (EtOH) substituted isocalorically for carbohydrate at 12% of calories daily; and (3) binge drinkers fed 6% EtOH calories daily for a four-day period followed by three days of 20% EtOH to mimic a weekend bout drinking cycle. The number of calories offered per day was the same for all groups, and the average weekly EtOH consumption (12% calories) was identical for the two alcohol treatments. The entire study lasted six months. There were no significant differences in plasma cholesterol, triglyceride or liver function tests. Regular drinkers had the highest high density lipoprotein2/high density lipoprotein3 (HDL2/HDL3) protein and apolipoprotein A-I/B ratios of any group and exhibited a significant elevation in the molar plasma lecithin:cholesterol acyltransferase (LCAT) rate (nmol/min/ml). Binge drinking produced a selective increase in low density lipoprotein (LDL) cholesterol and apolipoprotein B, and a depression in the fractional LCAT rate (% esterified/min). During the course of the study, controls ate 92% of their diet while the alcohol groups each consumed 95% of the liquid diet. Despite this difference, body weight and Quetelet index (weight/height2) decreased progressively in the order controls greater than regular drinkers greater than binge drinkers. Results from our study indicate that moderate, regular daily consumption of EtOH at 12% of calories causes a modest reduction in body weight and produces a coronary protective lipoprotein profile (increases HDL2/HDL3, increases apolipoprotein A-I/B, low LDL cholesterol). By contrast, when this same average weekly dose is concentrated in a binge cycle, unfavorable alterations in lipoprotein composition (increases LDL cholesterol, increases apolipoprotein B) and metabolism (decreases LCAT activity) occur along with weight loss and depletion of body fat. These studies point to the value of the squirrel monkey model in evaluating both favorable and pathophysiological effects of chronic EtOH intake.

Relation of serum testosterone levels to high density lipoprotein cholesterol and other characteristics in men.

Although levels of high density lipoprotein (HDL) cholesterol in males decrease during adolescence and after treatment with testosterone derivatives, several studies have reported that levels of HDL cholesterol are positively associated with endogenous levels of testosterone in men. This association was further examined using data collected during 1985 and 1986 from 3,562 white and 500 black men who ranged in age from 31 to 45 years. Black men had higher mean levels of both HDL cholesterol (8 mg/dl) and total testosterone (33 ng/dl) than white men, and positive associations were observed between testosterone and HDL cholesterol levels (r = 0.22, whites; r = 0.26, blacks). In addition, levels of testosterone were related positively to alcohol consumption and cigarette smoking and negatively to age, Quetelet index, and use of beta-blockers. We used stratification and regression analyses to determine if any of these characteristics could account for the positive association between levels of HDL cholesterol and total testosterone. Although controlling for most factors had little influence, adjusting for Quetelet index reduced the strength of the association between levels of testosterone and HDL cholesterol by approximately 30%. These findings suggest that the positive association between levels of testosterone and HDL cholesterol may not be causal. Multivariable analyses that control for obesity and other potentially confounding characteristics should be used in studies that assess the relation of testosterone levels to coronary heart disease.

Sustained coronary-risk-factor reduction after gastric bypass for morbid obesity.

Lipids and clinical changes including diabetes and hypertension were monitored in morbidly obese patients after Roux-Y gastric bypass. Total cholesterol (Chol), high-density-lipoprotein (HDL) cholesterol, and triglycerides at 1 and at 5-7 y postoperatively in 33 patients and at 1 y in 23 patients (including apolipoproteins A-I and B) were compared with preoperative concentrations. Mean concentrations of Chol and both apolipoproteins were unchanged. Elevated serum triglycerides became normal, and reduced concentrations persisted at 5-7 y in men (p less than 0.025). HDL-cholesterol concentrations increased at 1 y (p less than 0.01) and remained higher at 5-7 y in women. Ratios of Chol to HDL cholesterol were lower at 1 y (p less than 0.01) in both men and women. Diabetes (9 patients) and hypertension (22 patients) also were reduced at 1 y (p less than 0.01) and remained lower at 5-7 y. A mean 61% of excess weight was lost in 1 y whereas a 12% weight gain occurred by 5-7 y. The beneficial changes in most coronary risk factors lasted 5-7 y after surgery.

Body fat distribution and male/female differences in lipids and lipoproteins.

The role of body fat distribution, as assessed by the ratio of waist-to-hip circumferences (WHR), in statistically explaining differences in levels of lipoproteins between men and women was studied using data collected in 1985-1986 from employed adults (mean age, 40 years). As compared with the 415 women, the 709 men had higher mean levels of triglycerides (+38 mg/dl) and apolipoprotein B (+11 mg/dl) as well as lower mean levels of high density lipoprotein (HDL) cholesterol (-15 mg/dl) and apolipoprotein A-I (-19 mg/dl). Additionally, men were more overweight, consumed more alcohol, and exercised more frequently than women but were less likely to smoke cigarettes. Controlling for these characteristics, however, did not alter the differences in lipoprotein levels between men and women. In contrast, adjustment for WHR (which was greater among men) reduced the sex differences in levels of apolipoprotein B (by 98%), triglycerides (by 94%), HDL cholesterol (by 33%), and apolipoprotein A-I (by 21%). Similar results were obtained using analysis of covariance, stratification, or matching; at comparable levels of WHR, differences in lipid and lipoprotein levels between men and women were greatly reduced. Although these results are based on cross-sectional analyses of employed adults and need to be replicated in other populations, the findings emphasize the relative importance of body fat distribution. Whereas generalized obesity and body fat distribution are associated with lipid levels, fat distribution (or a characteristic influencing fat patterning) can be an important determinant of sex differences in levels of triglycerides, HDL cholesterol, and apolipoproteins B and A-I.

Cigarette smoking and non-fatal myocardial infarction in women: is the relation independent of coronary artery disease?

The relation of cigarette smoking to both coronary disease and non-fatal myocardial infarction was examined in a cross sectional study of 1053 women who underwent coronary arteriography. As compared with the 489 women who had never smoked cigarettes, ever-smokers (mean duration of smoking, 25 years) were 1.6 times as likely to have significant stenotic disease and were 1.9 times as likely to have suffered a myocardial infarction. These associations were strongest in women under 50 years of age, with odds ratios of 3.5 for coronary artery disease and 4.5 for myocardial infarction. Although the extent of stenotic disease and prior myocardial infarction were strongly associated, women who smoked cigarettes remained at increased risk of a myocardial infarction even after their increased coronary artery disease had been taken into account. For example, heavy smokers (greater than 30 pack-years) were 2.3 times as likely to have had a myocardial infarction as were non-smokers; controlling for the extent of stenotic disease (in addition to age and other risk factors) reduced the estimated relative risk to only 1.9. Stratified analyses showed that this increased risk for clinical disease among smokers was evident at all levels of occlusion, even among women with minimal stenotic disease. These results, collected at the time of arteriography, suggest that non-atherogenic mechanisms may be important in the aetiology of myocardial infarction among women who smoke cigarettes.

Risk factors and the anatomic distribution of coronary artery disease.

Differences in the importance of risk factors according to the anatomic location of coronary artery disease (CAD) were assessed in 4722 men and 1069 women who underwent arteriography. Examined characteristics included total and high-density lipoprotein (HDL)-cholesterol, triglycerides, obesity, smoking, alcohol consumption, diabetes, and hypertension. Of these risk factors, the ratio of total to HDL-cholesterol showed the highest correlation with the overall severity of CAD (r = 0.24, men; r = 0.38, women); in contrast, its relation to left main (LM) disease was much lower (r = 0.10, men; r = 0.08 women) than were correlations with stenotic disease in the left anterior descending, circumflex, and right coronary arteries. Other risk factors also showed weaker associations with LM disease than with stenoses in other vessels, and none was related to increased LM disease after controlling for disease in other vessels. For example, as compared with men who had no significant CAD, those with 1-, 2-, and 3-vessel disease had mean increases in total cholesterol of 12, 18, and 19 mg/dl, respectively. In contrast, after adjusting for disease in other vessels, LM disease (present in 293 men) was associated with only a 4 mg/dl increase in mean cholesterol levels (P = 0.20). These results indicate that the relation of risk factors to CAD differs according to the location of the stenotic disease, and that LM disease is poorly predicted by the standard risk factors.

Calcium intake and the relationship of dietary sodium and potassium to blood pressure.

Using First National Health and Nutrition Examination Survey (NHANES I) data, we studied the relationships of dietary sodium, potassium, and alcohol to blood pressure in relation to levels of dietary calcium intake. At low Ca intakes (less than 400 mg/d for men and less than 800 mg/d for women) the ratio of Na to K (Na:K) was significantly related to blood pressure (p less than 0.01) after controlling for age, body mass index (BMI), race, and gender. At higher Ca intakes neither Na:K nor any other nutrient (with the exception of alcohol) was related to either systolic or diastolic blood pressures. Na:K was more strongly related to blood pressure than either nutrient alone and low Ca intakes were necessary for the Na:K-blood pressure relationship to be evident. Interaction of these three dietary factors in relation to blood pressure was evident in all race and gender groups. Associations of age, BMI, gender, and alcohol with blood pressure were not affected by Ca levels.

Body composition of patients with spinal cord injury.

Body composition of 10 control subjects and 37 spinal cord injured (SCI) patients was measured by dilution of 3H2O and Na2 35SO4. SCI patients were classified into four groups by ascending level of lesion, low and high paraplegics and low and high quadriplegics. The studies show diminishing total body water, intracellular water, lean body mass and body cell mass and increasing fat mass with higher spinal lesions. No differences in body weight or extracellular water were observed so that the ratio of extracellular water/total body water was increased as the level of injury increased.

Black/white differences in risk factors for arteriographically documented coronary artery disease in men.

Although the leading cause of death among black men in the United States is coronary artery disease (CAD), risk factors have not been well documented in black populations. Therefore, possible racial differences in the relation of several characteristics to the extent of CAD were assessed in 4,722 white and 169 black men who underwent arteriography. Associations between an occlusion score (ranging from 0 to 300), reflecting the severity of CAD, and levels of total and high-density lipoprotein (HDL) cholesterol, triglycerides, cigarette smoking, alcohol intake, relative weight, systemic hypertension and diabetes mellitus were examined. Most risk factors were significantly related to the extent of CAD in both races, but lipid levels showed stronger associations with CAD among blacks: correlations between CAD and total cholesterol were 0.16 (whites) vs 0.29 (blacks) and associations with HDL cholesterol were -0.22 (whites) vs -0.49 (blacks). In addition, at adverse levels of certain risk factors, blacks had more extensive CAD than did whites: mean occlusion scores were 148 (whites) and 238 (blacks) at HDL cholesterol levels less than 30 mg/dl. As assessed by multiple linear regression, however, only triglyceride levels were differentially related to CAD between whites (beta = 0) and blacks (beta = 0.47), p less than 0.01 for racial contrast. These results document the importance of risk factors in black men and indicate black/white differences in the relation of triglycerides to CAD.

Plasma lipoprotein alterations in squirrel monkeys (Saimiri sciureus) during ethanol administration and abstinence.

The time course of lipoprotein changes during ethanol (EtOH) consumption followed by abstinence was examined in 3 groups of male squirrel monkeys: 1) controls fed isocaloric liquid diet; 2) low EtOH monkeys given liquid diet with vodka substituted isocalorically for carbohydrate at 12% of calories; and 3) high EtOH animals fed diet plus vodka at 24% of calories. After 2 weeks, high EtOH monkeys showed significant elevations in total plasma cholesterol which continued to increase at 4 weeks and then declined at 8 weeks. These elevations were the result of increases in both low density (LDL)- and high density lipoprotein (HDL)-cholesterol. Low EtOH monkeys had a modest increase in total cholesterol throughout 8 weeks which was attributed to increments in HDL-cholesterol alone. During abstinence, total, HDL- and LDL-cholesterol concentrations decreased rapidly in the high EtOH group and were similar to control values after 4 days. HDL-cholesterol showed a more gradual decline in animals fed 12% EtOH while LDL-cholesterol remained low and not significantly different from controls. Liver function tests were normal for all animals. Our results indicate that low-dose EtOH favors a coronary protective lipoprotein profile (increases HDL, decreases LDL) in squirrel monkeys while the higher alcohol regimen causes both favorable and unfavorable alterations in plasma lipids which quickly revert to control levels during abstinence.