Alterations in serum levels of lipids and lipoproteins with indinavir therapy for human immunodeficiency virus-infected patients.

Alterations in lipid metabolism have been associated with the use of protease inhibitors. Sequential lipid analyses were performed on serum samples from human immunodeficiency virus-infected antiretroviral-naive patients who received indinavir in combination with two nucleoside reverse transcriptase inhibitors. Serum levels of cholesterol, triglycerides, high-density lipoproteins (HDLs), and low-density lipoproteins (LDLs) were measured at baseline and at periodic intervals. After 48 weeks of indinavir therapy, mean serum levels +/- SD rose as follows: cholesterol, from 167.2 +/- 36.0 to 206.3 +/- 32.4 mg/dL (P < .0005); triglycerides, from 110.4 +/- 47.5 to 158.4 +/- 72.5 mg/dL (P < .0101); and LDLs, from 106.6 +/- 35.1 to 136.1 +/- 31.6 mg/dL (P = .0029). There was no significant change in the serum HDL fraction. Mean serum lipoprotein (a) levels +/- SD rose from 6.5 +/- 1.4 to 9.6 +/- 2.0 mg/dL after 30 weeks (P = .0695). Potential mechanisms for the noted increases include alterations in serum lipoprotein lipase activity or changes in hepatic lipid metabolism. The clinical significance of these changes remains to be determined.

Changes in women's plasma lipid and lipoprotein concentrations due to moderate consumption of alcohol are affected by dietary fat level.

We studied the impact of substituting ethanol for dietary carbohydrate, in high- and low-fat diets, on plasma lipids and lipoprotein concentrations. During a 12-wk, weight maintaining, controlled feeding study, women consumed only food and beverage provided by the Human Studies Facility of the USDA Beltsville Human Nutrition Research Center. Twenty-six women (age 41-59 y) consumed either a high-fat diet (38% of energy from fat) or a low-fat diet (18% of energy from fat) for 12 wk. The 12-wk feeding period was divided into two 6-wk periods in a cross-over design during which either ethanol or carbohydrate was added to the diet (5% of total daily energy intake). When the women consuming the high-fat diet had ethanol added to their diet, they had 6% lower plasma cholesterol (P = 0.003), 11% lower LDL cholesterol (P = 0.001) and 3% higher HDL cholesterol (P = 0.06) than when they had an equal amount (% energy) of carbohydrate added to their diet. The greater HDL cholesterol concentration was due to a 21% greater the HDL(2) subfraction (P = 0. 001). The ratio of LDL to HDL cholesterol was 14% lower. No significant differences existed in plasma lipids in women consuming the low-fat diet between the periods in which they had ethanol or carbohydrate added to their diet. This study suggests that the decreases in cardiovascular disease risk factors typically seen with moderate alcohol consumption may not be evident in individuals consuming a diet low in fat. Therefore changes in the risk factors associated with a low-fat diet and moderate alcohol consumption do not appear to be additive.

Effects of margarine compared with those of butter on blood lipid profiles related to cardiovascular disease risk factors in normolipemic adults fed controlled diets.

Effects of butter and 2 types of margarine on blood lipid and lipoprotein concentrations were compared in a controlled diet study with 23 men and 23 women. Table spreads, added to a common basal diet, provided 8.3% of energy as fat. Diets averaged 34.6% of energy as fat and 15.5% as protein. Each diet was fed for 5 wk in a 3 x 3 Latin-square design. One margarine (TFA-M) approximated the average trans monoene content of trans fatty acid-containing margarines in the United States (17% trans fatty acids by dry wt). The other margarine (PUFA-M) was free of trans unsaturated fatty acids; it contained approximately twice the polyunsaturated fatty acid content of TFA-M (49% compared with 27% polyunsaturated fatty acids). The tub-type margarines had similar physical properties at ambient temperature. Fasting blood lipids and lipoproteins were determined in 2 samples taken from the subjects during the fifth week of each dietary treatment. Compared with butter, total cholesterol was 3.5% lower (P=0.009) after consumption of TFA-M and 5.4% lower (P< 0.001) after consumption of PUFA-M. Similarly, LDL cholesterol was 4.9% lower (P=0.005) and 6.7% lower (P< 0.001) after consumption of TFA-M and PUFA-M, respectively. Neither margarine differed from butter in its effect on HDL cholesterol or triacylglycerols. Thus, consumption of TFA-M or PUFA-M improved blood lipid profiles for the major lipoproteins associated with cardiovascular risk when compared with butter, with a greater improvement with PUFA-M than with TFA-M.

alpha-Tocopherol concentrations in plasma but not in lipoproteins fluctuate during the menstrual cycle in healthy premenopausal women.

Because premenopausal women experience cyclic fluctuations of plasma carotenoids and their lipoprotein carriers, it was hypothesized that plasma alpha-tocopherol (A-T) fluctuates by phase of the menstrual cycle. Twelve free-living women, with a confirmed ovulatory cycle, were given a controlled diet for two consecutive menstrual cycles. Blood was drawn during the menses, early follicular, late follicular and luteal phases to simultaneously measure serum hormones, plasma lipoproteins and A-T concentrations, and A-T distribution in the lipoprotein fractions. Plasma A-T concentrations were significantly lower during menses than during the luteal phase by approximately 12% in each controlled diet cycle (P < 0.001). Adjustment for serum cholesterol and triglyceride concentrations did not alter these findings. The distributions of A-T in lipoprotein cholesterol fractions were not significantly different by menstrual phase. From 61 to 62% of A-T was concentrated in the LDL fraction, with another 9-14% in HDL2, 17-22% in HDL3 and the remaining 6-8% in VLDL+ IDL. There were no significant differences in lipoprotein cholesterol fractions by menstrual phase, except for a significant increase (P = 0.03) in HDL2 cholesterol from the early follicular to the late follicular phase. Spearman rank correlations from data during the second controlled diet month showed A-T in HDL2 in the late follicular phase was positively correlated with HDL cholesterol in the early follicular (r = 0.88), late follicular (r = 0.86) and luteal phases (r = 0.86) and with luteal apolipoprotein (ApoA-1) level (r = 0.90), and luteal HDL2 cholesterol (r = 0.83). A-T in HDL3 in the early follicular phase was negatively correlated with HDL2 cholesterol (r = -0.96) and ApoA-1 (r = -0.85), whereas luteal A-T in HDL3 was correlated with luteal HDL3 cholesterol (r = -0.79). Late follicular A-T in VLDL was positively correlated with early follicular HDL3 cholesterol and late follicular HDL3 cholesterol (r = 0.83). Fluctuations of A-T concentrations by phase of the menstrual cycle should be taken into consideration in future research concerning premenopausal women and the risk of chronic disease.

Effect of menstrual cycle phase on the concentration of individual carotenoids in lipoproteins of premenopausal women: a controlled dietary study.

Because premenopausal women experience cyclic fluctuations of plasma carotenoids and their lipoprotein carriers, it is hypothesized that carotenoid concentrations in lipoprotein fractions fluctuate by phase of the menstrual cycle. Nine women ate a standard set of carotenoid-rich foods daily for two cycles under isoenergetic conditions. In the second cycle, hormones and carotenoids in lipoprotein fractions were measured in the early and late follicular and luteal phases. alpha-Carotene concentrations in the LDL fraction were lower in the early than in the late follicular phase (P = 0.03) on the basis of regression analysis. beta-carotene concentrations in the LDL fraction and the HDL2 subfraction were higher in the late follicular than in the luteal phase (P = 0.02 and P = 0.04, respectively). Lutein/zeaxanthin concentrations in the LDL and HDL fractions were higher in the late follicular than in the luteal phase (P = 0.03 and P = 0.02, respectively). In each phase, 80% of alpha-carotene, 82% of beta-carotene, 85% of lycopene, and 64% of lutein/zeaxanthin were distributed in the LDL fraction. Among the hydrocarbon cartenoids, 18% of alpha-carotene and of beta-carotene and 13% of lycopene were distributed in the HDL fraction, with slightly more in the HDL2 than in the HDL3 subfraction. In contrast 34% of lutein/zeaxanthin was distributed in the HDL fraction with more concentrated in the HDL3 than in the HDL2 subfraction. Less than 4% of any carotenoid was found in the VLDL + IDL (intermediate-density-lipoprotein) fractions. Thus, the hydrocarbon carotenoids were highly concentrated in the LDL fraction and xanthophyll was more evenly distributed in the LDL and HDL fractions. The cyclic fluctuations of these carotenoids in lipoprotein fractions add another dimension to the understanding of their transport and physiologic function.

Plasma lipoprotein (a) levels in men and women consuming diets enriched in saturated, cis-, or trans-monounsaturated fatty acids.

Studies that have shown adverse effects of trans-unsaturated fatty acids on plasma lipoprotein (a) [Lp(a)] levels have used levels of trans-fatty acid that are higher than those in the average U.S. diet. This study was conducted to clarify the effects on Lp(a) of trans-fatty acids levels commonly found in U.S. diets. Lp(a) levels were measured in a double-blind study of 29 men and 29 women who ate 4 controlled diets in random order for 6 weeks each. Fatty acids represented 39% to 40% of energy. The diets were: (1) Oleic (16.7% of energy as oleic acid); (2) Moderate trans (3.8% of energy as trans-monoenes, approximately the trans content of the U.S. diet); (3) High trans (6.6% of energy as trans-monoenes); (4) Saturated (16.2% of energy as lauric plus myristic plus palmitic acids). The Saturated diet lowered Lp(a) levels significantly (by 8% to 11%). Compared to the Oleic diet, the trans diets had no adverse effect on Lp(a) levels when all subjects were considered collectively. A subset with initially high levels of Lp(a) (> or = 30 mg/dL), however, responded to the High trans diet with a slight (5%) increase in Lp(a) levels relative to the Oleic and Moderate trans diets. Thus, in amounts commonly found in the typical U.S. diet, saturated fatty acids consistently decrease Lp(a) concentrations. The adverse effects of replacing cis- with trans-fatty acids are only suggestive and are restricted to high trans intakes in subjects with high Lp(a) levels.

Estrogen replacement therapy and coagulation: relationship to lipid and lipoprotein changes.

OBJECTIVE: To examine the relationship of estrogen-induced changes in lipids and lipoproteins with alterations in the coagulation system. METHODS: Coagulation and lipid indices were measured in 31 postmenopausal women, ages 40-60 years, after a 3-month course of 0.625-mg conjugated equine estrogen. We analyzed changes in variables from baseline to 3 months using t tests for paired samples or the Wilcoxon matched-pairs signed-rank test. RESULTS: Unopposed estrogen replacement therapy produced statistically significant decreases in antithrombin-III antigen (P = .006) and activity (P = .001) and total protein S (P = .003) and a significant increase in protein C antigen (P = .017). C4b-binding protein also decreased significantly from baseline to 3 months (P < .001). Mean fibrinogen level decreased by 18.2 mg/dL, not a statistically significant change (P = .213). Estrogen produced the expected statistically significant changes in lipids and lipoproteins. Several correlations between changes in lipids and lipoproteins and coagulation indices were statistically significant. Protein C antigen and activity changes correlated directly with high-density lipoprotein cholesterol changes (r = .52, P < or = .005; r = .38, P < or = .05; respectively), and protein C antigen also correlated directly with increases in apoprotein A-I (r = .54, P < or = .005). Triglyceride changes correlated directly with changes in protein C antigen (r = .36, P < or = .05) and activity (r = .49, P < or = .005) and inversely with C4b-binding protein (r = -.58, P < or = .01). Apoprotein B was correlated with free protein S (r = .48, P < or = .01). CONCLUSIONS: Although several estrogen-induced changes may decrease atherosclerotic potential and hypercoagulability, others may promote coagulability. These divergent effects may be manipulated pharmacologically by other estrogen compounds or by the addition of various progestins.

The fluctuation of plasma carotenoid concentrations by phase of the menstrual cycle: a controlled diet study.

This is the first controlled diet study to examine the fluctuation of plasma carotenoids, lipoproteins, and serum hormone concentrations by phase of the menstrual cycle. Nonsmoking, premenopausal women (n = 12) with confirmed ovulatory cycles were given a standard diet with 10 mg total carotenoids/d for two cycles under isoenergetic conditions. Blood was drawn for simultaneous measurement of carotenoids, lipoproteins, and hormones on menses days 1-2, 4-6, 11 through 1 d after the luteinizing hormone surge, and 7-8 d after the surge, representing the menses, early and late follicular, and midluteal phases, respectively. Regression modeling with adjustment for plasma cholesterol concentrations was used to compare mean individual and total plasma carotenoid concentrations by phase of the cycle. Plasma carotenoid concentrations were at their lowest at menses and significantly higher thereafter, except for alpha-carotene. Compared with plasma concentrations at menses, beta-carotene peaked (increased by 9%, P = 0.01) in the late follicular phase. Plasma lutein/zeaxanthin and anhydrolutein concentrations were higher by 8-11% (P < or = 0.006) and by 15-31% (P < or = 0.02), respectively, during the last three phases. Plasma lycopene and phytofluene concentrations peaked (increased by 12%, P = 0.004; and by 21%, P = 0.006, respectively) at the midluteal phase. This cyclic fluctuation may affect the estimation of the plasma carotenoid-disease relation in studies of premenopausal women.

Cyclic changes in lipoprotein and apolipoprotein levels during the menstrual cycle in healthy premenopausal women on a controlled diet.

Lipoprotein, apolipoprotein (apo), and hormone levels were measured in 12 healthy women over three consecutive menstrual cycles, one free-living and two under controlled dietary conditions. Serum hormone levels were measured to identify menstrual cycle phases (menses, early follicular, late follicular, and midluteal). After stabilization for one cycle on the controlled diet, ANOVA modeling of the second controlled-diet cycle revealed that low-density lipoprotein (LDL) cholesterol levels in the midluteal phase were significantly lower (by 7%) than in the early follicular phase. High-density lipoprotein (HDL) cholesterol levels during the late follicular phase were higher (by 6%) than menses levels. Differences in the HDL-cholesterol and apoA-I fluctuations resulted in a higher proportion of HDL-cholesterol to apoA-I during the late follicular phase than that during the menses phase. The ratios of LDL cholesterol/HDL cholesterol and apoB/apoA-I in the early follicular phase were greater by 5.6% and 6.0%, respectively, than those in the midluteal phase. Fluctuations in total cholesterol, triglyceride, apoA-I, and apoB did not reach significance. Thus, the cyclic fluctuations of LDL and HDL cholesterol need to be considered in the screening and medical monitoring of women with borderline lipoprotein levels, as well as in the design and the interpretation of results of studies involving premenopausal women.

Corn oil and beef tallow elicit different postprandial responses in triglycerides and cholesterol, but similar changes in constituents of high-density lipoprotein.

OBJECTIVE: The study was designed to compare, in a homogeneous, normolipidemic population, the postprandial responses of plasma lipids, in particular, high-density lipoprotein (HDL) constituents, after administration of a polyunsaturated fat and a more saturated fat. METHODOLOGY: Emulsions of 100 g corn oil (CO) and 100 g beef tallow (BT) were given in a crossover protocol to 12 male subjects (21-24 years). Plasma cholesterol (TC), triglycerides (TG), and HDL lipid and protein constituents were measured at 0, 2, 4, 7 and 10 hours. RESULTS: A postprandial increase in TG at 2 hours after CO ingestion (96%) was twice that with BT (48%); TG returned to near fasting levels at 10 hours after ingestion of either fat. Areas under the TG response curves for CO and BT were 6.29 +/- 1.67 and 1.75 +/- 0.60 mmol x hour/L (mean +/- SE), respectively. TC and low-density lipoprotein cholesterol (LDL-C) levels were unchanged at 10 hours after CO ingestion, but they were increased 8.1% and 9.3%, respectively, with BT. Both fats increased HDL TG at 2-4 hours, and both similarly increased HDL free cholesterol, cholesterol ester, phospholipid, apolipoproteins A-I and A-II, and lipoprotein (A-I) levels at 7-10 hours. Changes in HDL were predominantly in HDL3. CONCLUSIONS: The increase in LDL-C with BT at 10 hours suggests that levels may be abnormally elevated in "fasting" samples, dependent on the amount and type of fat in a prior meal. The increase in LDL-C is consistent with short-term regulation of hepatic LDL-receptor activity and/or LDL synthesis. Similar increases in HDL constituents at 7-10 hours after CO or BT, despite the difference in TG responses, suggests differences in the metabolism of chylomicrons and/or HDL due to the type of fat ingested.

Effects of alcohol consumption on lipoproteins of premenopausal women. A controlled diet study.

A substantial portion of American women consume alcohol, but controlled studies of alcohol-induced changes in lipoproteins of women are rare. In this study, the effects of alcohol consumption (equivalent to two drinks per day) on the lipoprotein profiles of 34 premenopausal women were measured while controlling subjects' diet and various other potentially confounding variables including phase of the menstrual cycle. Alcohol and no-alcohol treatments were administered in a crossover design, and blood samples were obtained during the early follicular phase of the third month of treatment. With alcohol, HDL cholesterol levels increased 10%, LDL levels decreased 8%, and levels of lipoprotein(a) were unchanged. The increase in HDL cholesterol was due to an increase in both HDL2 and HDL3, and the overall size of HDL particles was increased. HDL particles containing apolipoprotein (apo) A-I and apoA-II as well as those containing apoA-I but no apoA-II were elevated in response to alcohol. Although these observations are limited to a single phase of the menstrual cycle, the alcohol-induced changes in lipoproteins are consistent with changes that are thought to confer protection against coronary heart disease.

Dietary trans fatty acids: effects on plasma lipids and lipoproteins of healthy men and women.

Effects of cis and trans monounsaturated fatty acids (TFA) and saturated fatty acids were assessed in 29 men and 29 women consuming controlled diets. Subjects ate each diet for 6 wk in a Latin square design. The diets, each with 39-40% of energy as fat were: 1) high oleic (16.7% of energy as oleic acid), 2) moderate TFA (3.8% of energy as TFA), 3) high TFA (6.6% of energy as TFA), 4) and saturated (16.2% of energy as lauric+myristic+palmitic acids). Compared with the oleic diet, LDL cholesterol increased 6.0%, 7.8%, and 9.0% after moderate TFA, high TFA, and saturated diets, respectively. HDL cholesterol was unchanged after moderate TFA, but was slightly lower (2.8%) after high TFA. HDL cholesterol after the saturated diet was 3.5% higher than after the oleic diet. Changes in apolipoproteins B and A-I corresponded with changes in the lipoprotein cholesterols. Thus, compared with oleic acid, dietary TFAs raise LDL cholesterol, but to a slightly lesser degree than do saturates, and high TFA concentrations may result in minor reductions of HDL cholesterol.

Quantitative and qualitative changes in lipids, lipoproteins, apolipoprotein A-I, and sex hormone-binding globulin due to two doses of conjugated equine estrogen with and without a progestin.

OBJECTIVE: To determine whether the quantitative and qualitative effects on lipoproteins differ between two doses of conjugated equine estrogen before and after progestin administration. METHODS: We randomized 103 postmenopausal women into a control group and into two groups receiving either 0.625 mg or 1.25 mg of conjugated equine estrogen for 4 months and then the same estrogen dose plus cyclic medroxyprogesterone acetate for 8 months. RESULTS: Both estrogen doses similarly lowered (P < .01) low-density lipoprotein (LDL) cholesterol and raised (P < .01) high-density lipoprotein (HDL) cholesterol, apolipoprotein A-I, triglyceride levels of all lipoproteins, and sex hormone-binding globulin capacity. Cyclic addition of the progestin reduced HDL cholesterol (P < .01) and apolipoprotein A-I (P < .05), but not LDL cholesterol in either estrogen group. A greater lowering of HDL cholesterol (P < .05) in response to the progestin was seen with the 0.625-mg dose of estrogen. Estrogen-induced triglyceride enrichment of HDL and LDL was not reversed by the progestin. CONCLUSION: The only significant quantitative difference in lipoprotein levels between the doses of conjugated equine estrogen before or after administration of medroxyprogesterone acetate was a greater decline in HDL cholesterol levels with the lower dose after 4 months of the progestin. This difference was not sustained over time. There were no differences between doses in the estrogen-induced triglyceride enrichment of lipoproteins, and these qualitative changes were not affected by the progestin.

Effects of unopposed conjugated equine estrogen on lipoprotein composition and apolipoprotein-E distribution.

Administration of conjugated equine estrogen to 31 postmenopausal women for 3 months produced 14.6% and 9.4% decreases in low density lipoprotein cholesterol (LDL-C) and apolipoprotein-B (apoB), and 11.5%, 12.7%, and 9.6% increases in high density lipoprotein cholesterol (HDL-C), apoA-I and apoA-II, respectively. Phospholipids of HDL2 and HDL3 were increased 57.9% and 19.3%, respectively, while relatively small increases in cholesterol of the two subfractions were not significant. Compositions of LDL and HDL and its subfractions were altered substantially with estrogen treatment. The proportion of LDL triglyceride to LDL-C was increased. The phospholipid content in both the HDL2 and HDL3 subfractions (compared to cholesterol) was increased significantly (34.8% and 10.7%, respectively), while the triglyceride content was increased only in the HDL2 subfraction (43.6%). Estrogen use also caused a 9.1% reduction in total apoE levels and a redistribution of apoE to the very low density lipoprotein (VLDL) from the LDL plus HDL fraction, resulting in a significant 19.5% decrease in apoE in the LDL plus HDL fraction. Changes in apoE in the VLDL fraction were associated positively with changes in the cholesterol levels of the VLDL fraction and inversely with changes in LDL-C and apoB levels, while changes in apoE in the LDL plus HDL fraction were associated positively with changes in the levels of HDL-C. Thus, estrogen causes alterations in lipoproteins that could potentially affect their metabolism and/or function.

Erythrocytes from magnesium-deficient hamsters display an enhanced susceptibility to oxidative stress.

Previous studies in our laboratory have indicated a role for free radical participation in magnesium deficiency cardiomyopathy. We have demonstrated the ability of various antioxidant drugs and nutrients to protect against magnesium deficiency-induced myocardial injury. In this study, we have examined erythrocytes from normal and magnesium-deficient animals and compared their susceptibility to an in vitro oxidative stress. Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group also received vitamin E in doses of 10 and 25 mg as subcutaneous implants. Erythrocytes obtained after 14 days on the diet were exposed to an exogenous hydroxyl (.OH) radical generating system (dihydroxyfumarate not equal to Fe3+ ADP) at 37 degrees C for 20 min. Erythrocyte crenation was observed and quantified by scanning electron microscopy. Lipid peroxidation, hemolysis (%), and intracellular glutathione levels were determined. In addition, serum lipid changes and membrane phospholipids were characterized. Our data demonstrate that erythrocytes from magnesium-deficient animals are more susceptible to free radical injury, supporting our hypothesis that magnesium deficiency reduces the threshold antioxidant capacity.

Plasma lipid and lipoprotein concentrations of men consuming a low-fat, high-fiber diet.

This study assessed the influence of a low-fat, high-fiber diet on blood lipid concentrations of 42 men with desirable or moderately elevated cholesterol concentrations. A low-fat diet (19% fat, 4% saturated fatty acids, 4.6 g fiber/MJ) was compared with a high-fat diet (41% fat, 15% saturated fatty acids, 2.0 g fiber/MJ) and with subjects' self-selected diets. Substituting the low-fat for the high-fat diet decreased total, low-density-lipoprotein, and high-density-lipoprotein cholesterol by 17-20%. Lipid changes between 6 and 10 wk were minor. A reduction in plasma cholesterol of greater than 0.52 mmol/L was achieved with the low-fat diet in 59% of men changing from their self-selected diets and in 79% changing from the high-fat diet. Percent reduction was independent of subjects' cholesterol classification. Results indicate that significant reductions in plasma cholesterol can be achieved by the majority of men committing to a low-fat, high-fiber diet.

Effects of conjugated equine estrogen with and without three different progestogens on lipoproteins, high-density lipoprotein subfractions, and apolipoprotein A-I.

The effects of conjugated equine estrogen and subsequent cyclical progestogen supplementation on lipoprotein and apolipoprotein A-I levels were investigated in three groups of postmenopausal women. Unopposed conjugated equine estrogen (0.625 mg) lowered total cholesterol 4-8% and low-density lipoprotein (LDL) cholesterol 12-19% below pre-treatment levels in all three groups. Levels of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I were increased 9-13 and 9-18%, respectively, with unopposed estrogen. The increase in HDL cholesterol was mainly due to increases in the high-density lipoprotein2 (HDL2) subfraction. Addition of medroxyprogesterone acetate, norethindrone acetate, or d,l-norgestrel at doses shown previously to provide protection against endometrial hyperplasia reversed some of the beneficial estrogen effects, reducing levels of HDL cholesterol 14-17%, HDL2 cholesterol 22-37%, and apolipoprotein A-I 11-15% from those obtained with unopposed estrogen. The LDL cholesterol levels fell 12-19% with unopposed estrogen but remained 7-12% below baseline when progestogens were added. These observations demonstrate that after 3 months of treatment, all three progestogens reversed some of the favorable effects of unopposed estrogen on lipoproteins but permitted a continued modest reduction in LDL cholesterol.

Comparison of psyllium hydrophilic mucilloid and cellulose as adjuncts to a prudent diet in the treatment of mild to moderate hypercholesterolemia.

The effects of the administration of 5.1 g of psyllium or placebo (cellulose) twice daily for 16 weeks were compared as adjuncts to a prudent diet in the management of moderate hypercholesterolemia in a parallel, double-blind study. Psyllium decreased the total cholesterol level by 5.6% and the low-density lipoprotein cholesterol level by 8.6%, whereas the levels were unchanged in the placebo group. The high-density lipoprotein cholesterol level decreased during the diet stabilization period in both groups and returned to near-baseline values by week 16. Plasma triglyceride levels did not change substantially in either group. Subject compliance to treatment was greater than 95%. These data suggest that psyllium hydrophilic mucilloid in a twice-daily regimen may be a useful and safe adjunct to a prudent diet in the treatment of moderate hypercholesterolemia.

Anti-inflammatory drugs in experimental atherosclerosis. 7. Spontaneous atherosclerosis in WHHL rabbits and inhibition by cortisone acetate.

The Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal model for familial hypercholesterolemia, has a deficiency in low density lipoprotein (LDL) receptor binding and exhibits elevated plasma lipoprotein levels and spontaneous atherosclerosis. Since atherosclerotic plaque formation has a number of features in common with the inflammatory process, we have investigated the effect of dietary supplementation with an anti-inflammatory steroid (cortisone acetate, 5 mg daily for 3 months) on atherosclerosis using the WHHL rabbit as a model. Atherosclerotic plaque formation in cortisone-fed animals was reduced by about 60% compared to control WHHL rabbits. Steroid administration increased circulating cholesterol levels modestly and triglycerides were increased about 6-fold. While very low density lipoprotein (VLDL)-cholesterol was increased, LDL-cholesterol levels were decreased and the particle was more triglyceride-enriched as well as less dense. Steroid-fed animals also exhibited decreased platelet aggregation and increased aortic 15-lipoxygenase activity. The histological observations showed typical fibrous plaques in aortas of both control and cortisone-fed rabbits, with intima thickened by foamy macrophages and subcellular lipoproteinaceous debris covered by a fibrous cap. These findings thus indicate that steroids reduce the rate of plaque initiation or progression but do not significantly change the histological appearance of the lesion.

High density lipoprotein cholesterol levels among US adults by selected demographic and socioeconomic variables. The Second National Health and Nutrition Examination Survey 1976-1980.

The distribution of serum high density lipoprotein cholesterol (HDL cholesterol) levels was determined on a nationally representative sample of 9,625 adults aged 20-74 years, as part of the Second National Health and Nutrition Examination Survey, 1976-1980 (NHANES II). Mean HDL cholesterol levels were higher in women compared with men (an age-adjusted difference of 8.9 mg/dl for whites and 4.4 mg/dl for blacks). HDL cholesterol levels were higher in blacks compared with whites (an age-adjusted difference of 7.4 mg/dl for men and 2.8 mg/dl for women). All differences were statistically significant (p less than 0.01). These relations remained after stratification by age, income, poverty index, education, body mass index, alcohol consumption, cigarette smoking, and physical activity. For whites, HDL cholesterol levels were highest in the highest category of earnings, whereas blacks generally had lower levels of HDL cholesterol with increased earnings. In a multivariate model, important predictors of higher HDL cholesterol levels were being female, being black, and reporting a higher frequency of alcohol consumption. Less strongly related were age, years of education, and reported high physical activity. Smoking and body mass index were strongly negatively related to HDL cholesterol levels. The findings in this national study support previous findings in selected populations in the United States.