Cholesterol Journal Articles

Record 581 to 600

Aging affects the conformation of cholesterol in the human eye lens
Duindam, J. J., G. F. Vrensen, et al. (1996), Ophthalmic Res 28 Suppl 1: 86-91.
Abstract: The distribution of 3-beta-OH-cholesterol along the optical axis of 20 human eye lenses of different ages was measured using confocal Raman microspectroscopy in combination with the 3-beta-hydroxysteroid-specific probe filipin. This non-destructive technique allow a spatially very detailed study of the distribution of 3-beta-OH-cholesterol in individual lenses. It revealed age-related changes of the 3-beta-OH-cholesterol distribution along the optical axis. The 3-beta-OH-cholesterol was found to be distributed asymmetrically along the optical axis and this distribution was found to change with age. The relative 3-beta-OH-cholesterol content in the anterior part of the lens decreases significantly with increasing age compared with its equal posterior counterpart. Additionally all the lenses have a very low 3-beta-OH-cholesterol content in the central part of their nuclear region, the area where the primary lens fibres are located.

Aging and total cholesterol levels: cohort, period, and survivorship effects
Newschaffer, C. J., T. L. Bush, et al. (1992), Am J Epidemiol 136(1): 23-34.
Abstract: This analysis describes the association of age with the serum total cholesterol level in 5,010 participants in a geriatric health screening program. Cholesterol levels were measured annually in participants monitored for up to 12 years. The association of age with cholesterol level is described via three approaches: cross-sectional analysis, descriptive longitudinal analysis, and longitudinal analysis using statistical modeling. The results were compared to examine the influence of cohort, period, and survivorship effects on the association between age and cholesterol. In cross-sectional analysis, the cholesterol level was fairly constant for the ages of 65 to 75 years, but decreased by 21% over the age range from 75 to 95 years. Descriptive longitudinal analysis suggested that both cohort and period effects were influencing the cross-sectional findings. In longitudinal analysis adjusting for both cohort and period effects, the findings were similar to those from cross-sectional analysis for the ages of 65 to 75 years, but from the ages of 75 to 95 years, cholesterol decreased by only 9%--half as great a decline as that estimated from cross-sectional analysis. When longitudinal data were limited to those with complete follow-up, the predicted decline for the age range from 75 to 95 years was only 6%. Although this flattening of the age trend was suggestive, there was no conclusive evidence that it reflected an association between baseline cholesterol and loss to follow-up.

Aging influences development and progression of early aortic atherosclerotic lesions in cholesterol-fed rabbits
Orlandi, A., M. Marcellini, et al. (2000), Arterioscler Thromb Vasc Biol 20(4): 1123-36.
Abstract: The arterial wall in aged animals shows an increased susceptibility to develop atherosclerotic lesions, although the mechanisms by which aging acts are still unclear. We investigated early aortic lesions in aged rabbits (5 to 6 years old, AH group) and young rabbits (2 months old, YH group) after 2 months of 0.2% cholesterol feeding. Fatty streaks or spots mainly in the proximal segments occupied a relative surface area that was greater in AH than in YH rabbits, although plasma cholesterol and lipoprotein levels did not differ. YH lesions showed an irregular endothelial profile mainly from accumulations of large, rounded, RAM 11-positive macrophagic foam cells. There was a higher percentage of myocytic, CD-5-positive, proliferating, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells and larger accumulation of glycosaminoglycans in AH fatty streaks than in YH lesions. Ligation-mediated polymerase chain reaction confirmed differences in apoptosis. Early fibromuscular coats and subendothelial plasma-like insudate were also observed in AH lesions. Aged-matched normocholesterolemic rabbits showed a diffuse aortic intimal thickening composed of myocytic cells with a synthetic phenotype and extracellular matrix rich in glycosaminoglycans. In addition, in aged rabbits, we observed a spontaneous increase of monocytes adhering to the endothelial surface and a reduced expression of endothelial nitric oxide synthase in areas distant from the branches. These plasma cholesterol-independent spontaneous changes in the aortic wall of aged rabbits seem to act as a multiple atherogenic risk factor. Moreover, age-related differences in the distribution, composition, and proliferative and apoptotic rates represent crucial events during the progression of early fatty streaks to advanced plaques.

Aging per se is an independent risk factor for cholesterol gallstone formation in gallstone susceptible mice
Wang, D. Q. (2002), J Lipid Res 43(11): 1950-9.
Abstract: Cholesterol gallstones occur rarely in childhood and adolescence and increase linearly with age in both genders. To explore whether aging per se increases cholesterol saturation of bile and gallstone prevalence, and to investigate age-related changes in hepatic and biliary lipid metabolism, we studied gallstone-susceptible C57L mice and resistant AKR mice of both genders fed 8 weeks with a lithogenic diet containing 1% cholesterol, 0.5% cholic acid, and 15% butter fat starting at (young adult) 8, (older adult) 36, and (aged) 50-weeks-of-age. After the 8-week feeding, gallstone prevalence, gallbladder size, biliary lipid secretion rate, and HMG-CoA reductase activity were significantly greater but cholesterol 7alpha-hydroxylase activity was lower in C57L mice of both genders compared with AKR mice. Increasing age augmented biliary secretion and intestinal absorption of cholesterol, reduced hepatic synthesis and biliary secretion of bile salts, and decreased gallbladder contractility, all of which increased susceptibility to cholesterol cholelithiasis in C57L mice. We conclude that aging per se is an independent risk factor for cholesterol gallstone formation. Because aging increases significantly biliary cholesterol hypersecretion and gallstone prevalence in C57L mice carrying Lith genes, it is highly like that Longevity (aging) genes can enhance lithogenesis of Lith (gallstone) genes.

Agreement study of methods based on the elimination principle for the measurement of LDL- and HDL-cholesterol compared with ultracentrifugation in patients with liver cirrhosis
Gomez, F., J. Camps, et al. (2000), Clin Chem 46(8 Pt 1): 1188-91.

AHA Science Advisory. Stanol/sterol ester-containing foods and blood cholesterol levels. A statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association
Lichtenstein, A. H. and R. J. Deckelbaum (2001), Circulation 103(8): 1177-9.
Abstract: Considerable attention in the recent past has focused on the potential benefits or adverse effects of butter versus different types of margarines, usually with respect to their relative content of polyunsaturated, saturated, and trans fatty acids, and the impact of these on low-density lipoprotein (LDL) cholesterol levels. Recently, a new class of margarines and other fat-derived products (eg, salad dressings, mayonnaise) containing plant-derived sterols that are intended for use to lower blood cholesterol levels have been introduced into the food supply. These products are being marketed as adjuncts to low-saturated-fat and low-cholesterol diets to maximize reductions in LDL cholesterol levels achievable by dietary means.

AHA Science Advisory: Lyon Diet Heart Study. Benefits of a Mediterranean-style, National Cholesterol Education Program/American Heart Association Step I Dietary Pattern on Cardiovascular Disease
Kris-Etherton, P., R. H. Eckel, et al. (2001), Circulation 103(13): 1823-5.

Albumin decrement in depression and cholesterol decrement in mania
Swartz, C. M. (1990), J Affect Disord 19(3): 173-6.
Abstract: Within all psychiatric inpatients over a 4-year period, on admission depressives showed serum albumin 5.4% lower (P less than 0.001) than non-psychiatric controls. Similarly, manics showed cholesterol 10% lower (P less than 0.0005) and serum calcium/protein ratio 2.2% higher (P less than 0.05) than controls. These deviations suggest a tendency towards dietary aberrations in these patients of potential medical significance. These tests had shown the most distinct variation with diagnosis on split-half discriminant function analysis of routine chemistry and hematology tests of 107 patients with mania, 132 with depression, 67 with schizophrenia, 18 with schizoaffective illness, and 83 non-psychiatric controls admitted for elective surgery.

Alcohol and atherogenesis: effect of low and high doses of ethanol on rat blood cholesterol
Bozhko, G., V. S. Chursina, et al. (1992), Vopr Med Khim 38(2): 44-7.
Abstract: Alterations in content of cholesterol and specific radio-activity of erythrocyte lipoproteins were studied in rats after administration of labelled sterol under conditions of acute and chronic influence of low 0.6 g/kg and high 4.0 g/kg doses of ethanol. Both these doses caused a decrease in content of high density lipoproteins (HDL) after single ethanol administration, while content of apoB containing lipoproteins as well as binding of labelled sterol with erythrocytes were elevated after long-term ethanol treatment. Atherogenicity index was increased after single and chronic administration of either low or high doses of ethanol. In chronic administration of low doses of ethanol specific radioactivity of HDL was decreased, thus suggesting that cholesterol acceptor function of these particles was lowered.

Alcohol and coronary heart disease: the roles of HDL-cholesterol and smoking
Manttari, M., L. Tenkanen, et al. (1997), J Intern Med 241(2): 157-63.
Abstract: OBJECTIVES: To study the role of HDL-cholesterol (HDLc) in the causal pathway mediating the effect of alcohol on coronary heart disease (CHD). DESIGN: Cox proportional hazard models were used to compare the relative CHD risks in various HDLc-smoking categories. SETTING: A prospective, multicentre, placebo-controlled, double-blind CHD primary prevention trial with gemfibrozil in primary (occupational) health care units, the Helsinki Heart Study. SUBJECTS: Dyslipidaemic middle-aged men with available alcohol consumption data (1924 of 2035) in the placebo arm of the 5-year study. MAIN OUTCOME MEASURES: Seventy-seven (of 84) cases of nonfatal myocardial infarction or cardiac death. RESULTS: A U-shaped association was detected between alcohol consumption and CHD. The protection was found both in subjects with low (mean 0.94 mmol L-1) and normal (mean 1.25 mmol L-1) HDLc with corresponding reductions of 23% and 36% in relative risks. In contrast to previous data, alcohol offered virtually no protection against CHD in non-smokers. In subjects consuming more than 800 g pure ethanol annually, the CHD incidence was 6/1000 in subjects with more than three weekly drinking occasions, compared to 11/1000 in 'weekend' drinkers. CONCLUSIONS: Our results confirm the protective effect of alcohol against CHD. However, in contrast to previous data the effect in our population is restricted to smokers and the role of HDLc in mediating the effect is less central than suggested previously.

Alcohol consumption and insulin concentrations. Role of insulin in associations of alcohol intake with high-density lipoprotein cholesterol and triglycerides
Mayer, E. J., B. Newman, et al. (1993), Circulation 88(5 Pt 1): 2190-7.
Abstract: BACKGROUND. The relation between alcohol intake and insulin levels may explain, in part, the reported associations of alcohol with cardiovascular disease risk factors, including high-density lipoprotein (HDL) cholesterol, triglycerides, blood pressure, and glucose levels, each of which has been recognized as a component of the insulin resistance syndrome. METHODS AND RESULTS. Subjects included nondiabetic participants of the Kaiser Permanente Women Twins Study (1989 through 1990). Usual alcohol intake was assessed as part of a food frequency questionnaire. For women from twin pairs in which both twins drank (n = 338), an increment of 12 g of alcohol per day (about one drink) was associated with an 8% lower 2-hour post-glucose-load insulin (P <.01) in a multiple regression analysis for twin data, adjusted for age, body mass index, waist-to-hip ratio, total caloric intake, and family history of diabetes. With genetic influences removed by matched analysis of the subset of 98 monozygotic twin pairs, an intrapair difference of 12 g of alcohol per day was associated with a 12.4% intrapair decrement in postload insulin (P <.01). Inverse associations were also seen for fasting insulin. Alcohol consumption was inversely associated with postload glucose but not with fasting glucose in unmatched (P =.05) and matched (P =.005) analyses. A significant positive association of alcohol intake with high-density lipoprotein cholesterol and an inverse relation of alcohol intake with triglycerides were each independent of insulin levels (P < or =.02 in the matched models). Neither systolic nor diastolic blood pressures were related to alcohol consumption in this sample, perhaps because of the rather low level of alcohol intake in the study population (median, 4 g/d). CONCLUSIONS. Within the range of light to moderate drinking habits, alcohol consumption was inversely related to fasting and postload insulin levels. This relation did not explain associations of alcohol intake with lipid levels and may instead reflect an additional mechanism by which moderate alcohol consumption impacts cardiovascular disease risk.

Alcohol consumption and its relation to lipid-based cardiovascular risk factors among middle-aged women: the role of HDL(3) cholesterol
Sillanaukee, P., T. Koivula, et al. (2000), Atherosclerosis 152(2): 503-10.
Abstract: To study the association of alcohol consumption and lipid-based cardiovascular risk factors among middle-age women, cross-sectional analysis among 274 middle-aged healthy women with different drinking habits and a follow-up analysis of alcoholic women during abstinence was performed. Serum total cholesterol, low and high-density lipoprotein cholesterol (LDL and HDL cholesterol), triglycerides (TG), apolipoproteins A1 (Apo A1) and B (Apo B), and HDL-cholesterol subfractions 2 (HDL(2)) and 3 (HDL(3)) were measured. All lipid values except LDL cholesterol positively correlated with self-reported alcohol consumption. When alcoholics were excluded the correlation was significant only for HDL cholesterol, HDL(3), and Apo A1. The increasing trend of HDL cholesterol, HDL(3) and Apo A1 were clearly seen first in women consuming >20-40 g/day of absolute alcohol. Alcohol consumption >40 g/day increased all lipid values except LDL cholesterol. Abstinence for 2 weeks caused a significant decrease in HDL(3) cholesterol, and an increase in LDL cholesterol and Apo B. The results indicate that among middle-aged women the Apo A1 and HDL cholesterol via its HDL(3) but not HDL(2) subfraction might play a role in the beneficial coronary consequences associated with moderate alcohol consumption. However, the increasing beneficial trend first appears when daily drinking exceeds 20 g/day.

Alcohol consumption is associated with enrichment of high-density lipoprotein particles in polyunsaturated lipids and increased cholesterol esterification rate
Perret, B., J. B. Ruidavets, et al. (2002), Alcohol Clin Exp Res 26(8): 1134-40.
Abstract: BACKGROUND: Alcohol consumption is associated with high levels of high-density lipoproteins (HDLs). Moreover, changes in the fatty acid patterns of red blood cell phospholipids and plasma lipids have been observed in drinkers. The objectives of this study were to characterize the composition of HDL particles with respect to lipid molecular species in regular wine drinkers and to assess the functional properties of those HDLs as regards key steps of reverse cholesterol transport. METHODS: Forty-six subjects were recruited in the frame of a population study performed in Toulouse, southern France, and a nutritional investigation, including daily alcohol consumption, was performed. Subjects were sorted according to their daily alcohol intake (0, < or =35, and >35 g/day), mostly as red wine. The plasma HDL fraction was isolated, and neutral lipid molecular lipids and phospholipid fatty acids were analyzed by gas liquid chromatography. Efflux of cellular cholesterol and rates of cholesterol esterification and cholesteryl ester transfers between lipoproteins were assayed in a cell-plasma incubation system. RESULTS: Wine drinking, at 47 g/day, was associated with an increase in HDL cholesterol and apolipoprotein A-I, but not with triglycerides. Isolated HDL displayed a 27% increase in all cholesteryl ester molecular species. The particles were also enriched in unsaturated phospholipids and, particularly, in those containing arachidonic (+30%) and eicosapentaenoic (+90%) acids. The plasma cholesterol esterification rate, reflecting lecithin cholesterol acyl transferase activity on HDL, was found to be higher (+27%) in drinkers than in nondrinkers, whereas the rate of cellular cholesterol efflux to plasma was identical. CONCLUSIONS: Regular wine consumption is associated with high levels of polyunsaturated lipids in HDL and with increases in the cholesterol esterification rate.

Alcohol consumption raises HDL cholesterol levels by increasing the transport rate of apolipoproteins A-I and A-II
De Oliveira, E. S. E. R., D. Foster, et al. (2000), Circulation 102(19): 2347-52.
Abstract: BACKGROUND: Moderate alcohol intake is associated with lower atherosclerosis risk, presumably due to increased HDL cholesterol (HDL-C) concentrations; however, the metabolic mechanisms of this increase are poorly understood. METHODS AND RESULTS: We tested the hypothesis that ethanol increases HDL-C by raising transport rates (TRs) of the major HDL apolipoproteins apoA-I and -II. We measured the turnover of these apolipoproteins in vivo in paired studies with and without alcohol consumption in 14 subjects. The fractional catabolic rate (FCR) and TR of radiolabeled apoA-I and -II were determined in the last 2 weeks of a 4-week Western-type metabolic diet, without (control) or with alcohol in isocaloric exchange for carbohydrates. Alcohol was given as vodka in fixed amounts ranging from 0.20 to 0.81 g. kg(-1). d(-1) (mean+/-SD 0.45+/-0.19) to reflect the usual daily intake of each subject. HDL-C concentrations increased 18% with alcohol compared with the control (Wilcoxon matched-pairs test, P=0.002). The apoA-I concentrations increased by 10% (P=0.048) and apoA-II concentrations increased by 17% (P=0.005) due to higher apoA-I and -II TRs, respectively, whereas the FCR of both apoA-I and -II did not change. The amount of alcohol consumed correlated with the degree of increase in HDL-C (Pearson's r=0.66, P=0.01) and apoA-I TR (r=0.57, P=0.03). The increase in HDL-C also correlated with the increase in apoA-I TR (r=0.61, P=0.02). CONCLUSIONS: Alcohol intake increases HDL-C in a dose-dependent fashion, associated with and possibly caused by an increase in the TR of HDL apolipoproteins apoA-I and -II.

Alcohol consumption stimulates early steps in reverse cholesterol transport
van der Gaag, M. S., A. van Tol, et al. (2001), J Lipid Res 42(12): 2077-83.
Abstract: Alcohol consumption is associated with increased HDL cholesterol levels, which may indicate stimulated reverse cholesterol transport. The mechanism is, however, not known. The aim of this study was to evaluate the effects of alcohol consumption on the first two steps of the reverse cholesterol pathway: cellular cholesterol efflux and plasma cholesterol esterification. Eleven healthy middle-aged men consumed four glasses (40 g of alcohol) of red wine, beer, spirits (Dutch gin), or carbonated mineral water (control) daily with evening dinner, for 3 weeks, according to a 4 x 4 Latin square design. After 3 weeks of alcohol consumption the plasma ex vivo cholesterol efflux capacity, measured with Fu5AH cells, was raised by 6.2% (P < 0.0001) and did not differ between the alcoholic beverages. Plasma cholesterol esterification was increased by 10.8% after alcohol (P = 0.008). Changes were statistically significant after beer and spirits, but not after red wine consumption (P = 0.16). HDL lipids changed after alcohol consumption; HDL total cholesterol, HDL cholesteryl ester, HDL free cholesterol, HDL phospholipids and plasma apolipoprotein A-I all increased (P < 0.01). In conclusion, alcohol consumption stimulates cellular cholesterol efflux and its esterification in plasma. These effects were mostly independent of the kind of alcoholic beverage

Alcohol consumption, serum low density lipoprotein cholesterol concentration, and risk of ischaemic heart disease: six year follow up in the Copenhagen male study
Hein, H. O., P. Suadicani, et al. (1996), Bmj 312(7033): 736-41.
Abstract: OBJECTIVES: To investigate the interplay between use of alcohol, concentration of low density lipoprotein cholesterol, and risk of ischaemic heart disease. DESIGN: Prospective study with controlling for several relevant confounders, including concentrations of other lipid fractions. SETTING: Copenhagen male study, Denmark. SUBJECTS: 2826 men aged 53-74 years without overt ischaemic heart disease. MAIN OUTCOME MEASURE: Incidence of ischaemic heart disease during a six year follow up period. RESULTS: 172 men (6.1%) had a first ischaemic heart disease event. There was an overall inverse association between alcohol intake and risk of ischaemic heart disease. The association was highly dependent on concentration of low density lipoprotein cholesterol. In men with a high concentration (> or = 5.25 mmol/l) cumulative incidence rates of ischaemic heart disease were 16.4% for abstainers, 8.7% for those who drank 1-21 beverages a week, and 4.4% for those who drank 22 or more beverages a week. With abstainers as reference and after adjustment for confounders, corresponding relative risks (95% confidence interval) were 0.4 (0.2 to 1.0; P<0.05) and 0.2 (0.1 to 0.8; P<0.01). In men with a concentration <3.63 mmol/l use of alcohol was not associated with risk. The attributable risk (95% confidence interval) of ischaemic heart disease among men with concentrations > or = 3.63 mmol/l who abstained from drinking alcohol was 43% (10% to 64%). CONCLUSIONS: In middle aged and elderly men the inverse association between alcohol consumption and risk of ischaemic heart disease is highly dependent on the concentration of low density lipoprotein cholesterol. These results support the suggestion that use of alcohol may in part explain the French paradox.

Alcohol consumption, S-LDL-cholesterol and risk of ischemic heart disease. 6-year follow-up in The Copenhagen Male Study
Hein, H. O., P. Suadicani, et al. (1997), Ugeskr Laeger 159(26): 4110-6.
Abstract: A high intake of saturated fat is associated with an increase in serum low density lipoprotein cholesterol (LDL) and an increase in risk of ischaemic heart disease (IHD). In some parts of France a high intake of fat is not associated with increased risk of IHD, an apparent discrepancy named the French paradox. It has been suggested, but never tested prospectively, that regular use of alcohol might explain this low risk. We investigated the interplay between use of alcohol, LDL and risk of IHD in a prospective study controlling for a number of relevant confounders including other lipid fraction, including 2,826 males aged 53-74 years without overt IHD. The incidence of IHD during a six year follow-up period was registered. One hundred and seventy-two men (6.1%) had a first IHD event. There was an overall inverse association between alcohol intake and risk of IHD. The association was highly dependent on LDL. In men with a high LDL (> or = 5.25 mmol/l), cumulative incidence rates of IHD were 16.4% for abstainers, 8.7% for those who drank 1-21 beverages/week and 4.4% for those who drank 22+. Using abstainers as reference, adjusted for confounders, corresponding relative risks (95% CI) were 0.4 (0.2-1.0), p < 0.05, and 0.2 (0.1-0.8), p < 0.01. In men with a low LDL (< 3.63 mmol/l) use of alcohol was not associated with risk. The attributable risk (AR) of IHD among men with LDL > or = 3.63 mmol/l who abstained from drinking alcohol was calculated; AR with 95% confidence limits was 43% (10-64%). To conclude, in middleaged and elderly men the inverse association between alcohol consumption and risk of IHD was highly dependent on the level of LDL. These results support the suggestion that alcohol intake may at least in part explain the French paradox.

Alcohol drinking determines the effect of the APOE locus on LDL-cholesterol concentrations in men: the Framingham Offspring Study
Corella, D., K. Tucker, et al. (2001), Am J Clin Nutr 73(4): 736-45.
Abstract: BACKGROUND: The effect of alcohol drinking on LDL-cholesterol concentrations is unclear. The reported variability may be due to interactions between genetic factors and alcohol intake. OBJECTIVE: The purpose of the study was to examine whether variation at the apolipoprotein E gene (APOE) locus modulates the association between alcohol drinking and LDL cholesterol. DESIGN: We used a cross-sectional design in a healthy population-based sample of 1014 men and 1133 women from the Framingham Offspring Study. RESULTS: In male nondrinkers (n = 197), LDL cholesterol was not significantly different across APOE allele groups APOE*E2 (E2), APOE*E3 (E3), and APOE*E4 (E4). However, in male drinkers (n = 817), differences were observed (P: < 0.001); those with the E2 allele had the lowest concentrations. LDL cholesterol in men with the E2 allele was significantly lower in drinkers than in nondrinkers but was significantly higher in drinkers than in nondrinkers in men with the E4 allele. This APOE-alcohol interaction remained significant (P < 0.001) after age, body mass index, smoking status, and fat and energy intakes were controlled for. In women, the expected effect of APOE alleles on LDL cholesterol occurred in both drinkers (n = 791; P < 0.001) and nondrinkers (n = 342; P < 0.001). Multiple linear regression models showed a negative association (P < 0.05) between alcohol and LDL cholesterol in men with the E2 allele but a positive association in men with the E4 allele. No significant associations were observed in men or women with the E3 allele. CONCLUSION: In men, the effects of alcohol intake on LDL cholesterol are modulated in part by variability at the APOE locus.

Alcohol increases plasma levels of cholesterol diet-induced atherogenic lipoproteins and aortic atherosclerosis in rabbits
Shaish, A., M. Pape, et al. (1997), Arterioscler Thromb Vasc Biol 17(6): 1091-7.
Abstract: The purpose of the present study was to reexamine the relationship between alcohol and atherosclerosis. Two experiments were performed: The first contained three groups of New Zealand White (NZW) female rabbits. The control group was fed a cholesterol-containing liquid diet and the other two groups were fed the same diet with either 20% or 30% of the calories supplied by alcohol. The second experiment had two treatments: one control group and another group fed a 10% alcohol diet. In experiment 1, alcohol at the 20% and 30% levels increased VLDL and LDL but not HDL compared with levels in control rabbits. Hepatic mRNA levels of apolipoprotein (apo) A-I, apoB, and 7 alpha-hydroxylase were not affected by alcohol. However, the LDL-receptor mRNA was decreased to half of control values by either 20% or 30% alcohol. Lesion areas and aortic cholesterols were significantly increased in the 20% and 30% alcohol-treated groups. Also, significant correlations were found between plasma cholesterol levels and total lesion area or lesion cholesterol contents. In experiment 2, the 10% alcohol-treated rabbits showed no differences in circulating lipoproteins, LDL-receptor mRNA, or lesion formation above that observed in controls. These experiments suggest that alcohol substituted at 20% or 30% of the dietary calories induces hypercholesterolemia and more aortic atherosclerotic lesions. The alcohol-induced accumulation of VLDL and LDL was accompanied by low hepatic LDL-receptor mRNA levels, suggesting that alcohol may affect LDL-receptor expression and rates of lipoprotein clearance, but more experiments are needed to evaluate this possibility.

Alcohol intake and high density lipoprotein-cholesterol: comparison of food frequency questionnaire and diet record in a general population sample
Muller, E., T. Sturmer, et al. (2001), J Epidemiol Biostat 6(3): 297-303.
Abstract: BACKGROUND: Moderate alcohol consumption is known to affect several cardiovascular risk factors, including high density lipoprotein-cholesterol (HDL-C). Accurate measurement of alcohol intake in epidemiological studies is crucial for valid estimation of alcohol-related effects. METHODS: We compared two widely used alcohol-intake assessment methods, a food frequency questionnaire (FFQ) and a 7-day diet record (DR) regarding the association between alcohol intake and HDL-C in the general population. RESULTS: In a representative sample (842 men, 1103 women) of the population of former West Germany (VERA study), 75.6% of the participants reported drinking alcoholic beverages in the FFQ, whereas the percentage was 84.9% according to the DR. The median daily alcohol intake of consumers was 10.3 and 12.1 g, as assessed by the FFQ and the DR, respectively. There was moderate agreement between reported consumption levels ranked by quintiles according to FFQ and DR (kappa = 0.49). With both approaches alcohol intake showed a strong positive association with HDL-C in linear regression models. The estimated increases in HDL-C (mg dL(-1)) per gram alcohol per day from the FFQ and DR were 0.15 95% confidence interval (CI): 0.12-0.18 and 0.14 (95% CI: 0.11-0.17), respectively. When participants with different classification of the amount of alcohol consumed by FFQ and DR were excluded from the analysis, the association between alcohol intake and HDL-C was more pronounced. DISCUSSION: Our analyses suggest that both FFQ and DR lead to similar results regarding the alcohol-HDL-C association in the general population, despite major differences in the recorded prevalence of drinking and amount of alcohol consumed. Both methods may tend to under-estimate the true alcohol-HDL-C association.

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