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(Circulation. 2000;102:2347.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Alcohol Consumption Raises HDL Cholesterol Levels by Increasing the Transport Rate of Apolipoproteins A-I and A-II
From The Rockefeller University (E.R. De O. e S., C.E.S., J.D.S., J.L.B.), New York, NY; University of Washington (D.F.) (Seattle); Hunter College (M.M.H.), City University of New York; and Carl T. Hayden VA Medical Center (E.A.B.), Phoenix, Ariz.
Correspondence to Jan L. Breslow, Laboratory of Biochemical Genetics and Metabolism, Box 179, The Rockefeller University, 1230 York Ave, New York, NY 10021-6399. E-mail breslow{at}rockvax.rockefeller.edu
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Abstract |
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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.
Key Words: alcohol • lipoproteins • cholesterol • apolipoproteins • metabolism
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Introduction |
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HDL cholesterol (HDL-C) concentrations are well established as a major protective factor against coronary heart disease.1 Moderate alcohol intake has been associated with protection against coronary heart disease in observational studies, an effect that appears to be mediated in large part by alcohol-induced increases in HDL-C concentrations.2 3 4 5 6 7 8 Despite the potential importance of the association between alcohol consumption and increased HDL-C concentrations, the mechanism of this effect has not been established. Two previous turnover studies in human subjects had contradictory conclusions, perhaps because study subjects were few in number and were in a state of caloric excess while on alcohol.9 10
The present study tested the hypothesis that the increase in HDL-C concentrations with moderate alcohol intake results from increased transport rate (TR) of the major HDL apolipoproteins apoA-I and -II. We measured the in vivo turnover of apoA-I and -II in paired HDL turnover studies in healthy men and women without and with alcohol consumption. We found that the increase in plasma HDL-C with moderate alcohol consumption is associated with an increase in the TR of apoA-I and -II, without a significant change in the fractional catabolic rate (FCR).
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Methods |
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Study Population
Five women and nine men were recruited from the clinic of the Laboratory of Biochemical Genetics and Metabolism and via posted advertisements. Eligibility was confined to subjects
21 years
old who consumed alcohol on a regular basis and had no personal or
family history of alcoholism. Subjects were also excluded for
significant systemic disease by history, physical examination, and
laboratory screening and for use of tobacco or medications known to
alter lipid concentrations, including birth control pills. Although
there were no exclusions based on race or ethnic background, all
subjects were white.
Experimental Protocol
All subjects underwent 2 study periods each of 4 weeks’
duration; the first 2 weeks served as an equilibration phase, and the
turnover study was carried out during the second 2 weeks. Each subject
consumed both a Western-type diet (control) and the same diet plus
ethanol (EtOH), in varied order. The subjects were studied at the
inpatient unit of The Rockefeller University Clinical Research Center
and were encouraged to continue their usual physical activity. The
Rockefeller University Institutional Review Board approved the study,
and informed consent was obtained from each subject.
Diets
The control diet was designed with use of the US Department of
Agriculture Nutrient Data Base11 to conform to a high-fat
diet often consumed in Western societies. The diet contained 15%
protein, 43% carbohydrate, and 42% fat at a P/S ratio of 0.1, with
215 mg cholesterol/1000 Kcal consumed. The EtOH diet was
identical to the control diet except that alcohol (as vodka) was
substituted for carbohydrate in an isocaloric manner. The EtOH dose
reflected the subject’s reported usual intake up to 1 mL ·
kg-1 · d-1. The
EtOH was given in a single or divided dose according to the subject’s
usual intake pattern and was consumed at the end of meals. The diets
consisted of whole foods from common ingredients of known
composition.11
Kinetic Studies
Both apoA-I and -II were prepared and radioiodinated
as previously described.12 After the injection of labeled
apolipoprotein, blood samples of 7 to 20 mL each were drawn at 10
minutes; 4, 12, 24, 36, and 48 hours; and then daily through day 14.
Plasma was prepared, and 1-mL aliquots were used for the determination
of the remaining 125I-apoA-I and
131I-apoA-II radioactivity. The plasma apoA-I and
-II decay curves were normalized to the 10-minute sample and
analyzed with the Matthews model.13 The model,
fitted to each decay curve with SAAM II software,14 was
used to estimate the FCR. The TR of each apolipoprotein was calculated
as the product of its plasma concentration, its FCR, and the plasma
volume (assumed to be 4.5% of the body weight), all divided by the
body weight.
Lipid and Lipoprotein Measurements
Plasma samples anticoagulated with EDTA were obtained after a
12-hour overnight fast on days 1, 3, 7, 10, and 14 after isotope
injection for the determination of lipid and lipoprotein
concentrations. No temporal trends were observed, so the mean of all 5
determinations was used in the data analysis. Lipid and
lipoprotein measurements were made with fresh specimens, and
apolipoprotein determinations were made with aliquots of plasma stored
at -70°C. Total cholesterol and triglyceride
concentrations were determined with enzymatic methods with reagents
from Boehringer-Mannheim. Lipoprotein cholesterol
concentrations were determined after serial
ultracentrifugation.15 Total and HDL-C
values were standardized by the Lipid Standardization Program of the
Centers for Disease Control and Prevention, supported by the National
Heart, Lung, and Blood Institute.16 The apoA-I
concentrations were measured with enzyme-linked immunosorbent
assay.12 The apoA-II concentrations were determined in the
Northwest Lipids Research Clinics laboratories based on a radial
immunodiffusion assay.17
Postheparin Lipase Activity
On day 11 of each metabolic diet and 3 days before
isotope injection, an intravenous bolus injection of
heparin was administered at a dose of 60 U/kg body wt. Blood was drawn
exactly 15 minutes later, and postheparin plasma was
obtained and stored at -70° until assay for hepatic lipase (HL) and
lipoprotein lipase (LPL) activity. The activity of LPL was determined
with radioactive triolein in a glycerol-based assay.12 The
activity of HL was measured in triplicate with a commercially available
fluorometric assay (Progen)18 and adapted to a 96-well
microtiter plate format. Lipase activities were expressed as
µmol free fatty acids released ·
h-1 · mL postheparin
plasma-1.
Lipoprotein Size Determinations
The average sizes of HDL, LDL, and VLDL were determined with
proton NMR spectroscopy by Dr James Otvos (University of North Carolina
[Raleigh]).19
Statistical Analysis
The present study was a standard 2-treatment, 2-period
crossover trial. We compared mean differences between the 2 diets with
a Wilcoxon signed-rank test. The null hypothesis for this test
is that there is no difference between the 2 diets. The correlations
between the dose of EtOH and the EtOH diet–induced changes in HDL and
related parameters were examined with Pearson’s
correlation, as were the correlations between changes in HDL-C and the
changes in HDL turnover parameters. A similar
analysis with Spearman’s rank order correlations gave similar
results. The statistical software package S-Plus 3.4 for Windows was
used for data analysis.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Baseline characteristics, EtOH intake, and plasma lipid and lipoprotein values during the control and EtOH diets are shown for each subject in Table 1
. The subjects
varied in age from 21 to 70 years (mean±SD 53.3±15.9 years), in
weight from 51.4 to 97.5 kg (75.7±14.6 kg), and in body mass index
from 18.9 to 35.0 kg/m2 (25.6±4.2
kg/m2), and they consumed alcohol in an amount
ranging from 0.20 to 0.81 g · kg-1
· d-1 (0.45±0.19 g ·
kg-1 · d-1). There
was no significant change in weight or physical activity during and
between the 2 turnover studies.
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As expected, HDL-C concentrations were 18% higher on the EtOH diet than on the control diet (P=0.002). HDL particle size did not change (P=0.23), suggesting that all size subspecies increased equally. There were no significant changes in total cholesterol (P=0.30), triglyceride (P=0.93), VLDL-C (P=0.14), or LDL-C (P=0.25) concentrations with alcohol consumption.
The results of the paired HDL turnover studies with the control and
EtOH diets are shown in Table 2. The
apoA-I concentrations were 10% higher (P=0.048) with the
EtOH compared with the control diet, associated with a 21% increase in
apoA-I TR (P=0.041) but no significant change in apoA-I FCR
(P=0.12). Similarly, apoA-II concentrations were 17% higher
(P=0.005) with the EtOH compared with the control diet, with
a 19% increase in apoA-II TR (P=0.016) but no significant
change in apoA-II FCR (P=0.92). Thus, alcohol intake appears
to increase HDL-C concentrations via an increase in the TR of the 2
major HDL apolipoproteins apoA-I and -II.
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Alcohol intake altered the activity of both endothelial lipases in directions believed to lower atherosclerosis risk. HL concentrations were 8% lower (P=0.01) on the EtOH diet, whereas LPL concentrations were 23% higher (P=0.001).
The variability in alcohol consumption among subjects provided the
opportunity to test for a dose-response relationship between alcohol
intake and HDL changes. The dose of EtOH correlated positively with the
increase in HDL-C (r=0.66, P=0.01), and the 2
subjects (subjects 5 and 6) with the lowest alcohol intake (0.2 g
EtOH · kg-1 ·
d-1) had no increase in HDL-C concentrations
(Figure 1). The EtOH dose also correlated
positively with the change in apoA-I (r=0.74,
P=0.003) and apoA-II (r=0.58, P=0.03)
concentrations. EtOH dose predicted the increase in apoA-I TR (Figure 1, r=0.57, P=0.03) but not in apoA-II TR
(r=0.44, P=0.11). In conjunction with the lack of
net change in FCR with alcohol consumption, EtOH dose failed to
correlate with the change in apoA-I FCR (r=0.26,
P=0.38) or apoA-II FCR (r=0.08,
P=0.78).
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The changes in HDL-C correlated with changes in some of the HDL
turnover parameters (Figure 2). The change in HDL-C concentrations
correlated strongly with the change in apoA-I TR (r=0.61,
P=0.02) but not with the change in apoA-I FCR
(r=0.43, P=0.12). Despite the fact that the
changes in HDL-C correlated more strongly with changes in apoA-II
concentrations (r=0.60, P=0.02) than with changes
in apoA-I concentrations (r=0.51, P=0.06), the
correlation between changes in HDL-C and changes in apoA-II TR failed
to reach statistical significance (r=0.43,
P=0.12), and there was no correlation with apoA-II FCR
(r=0.08, P=0.76). Although the changes in either
of the lipases was of a direction that might have contributed to the
increase in HDL-C with EtOH use, HDL-C changes did not correlate with
the changes in HL (r=0.01, P=0.98) or LPL
(r=-0.34, P=0.25).
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Discussion |
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Several observational studies suggest that moderate alcohol intake reduces the risk of atherosclerosis, and the major mechanism appears to be the well known ability of alcohol to raise HDL-C concentrations.5 20 21 22 23 24 Despite this, the metabolic pathway or pathways by which alcohol increases HDL-C concentrations are not well understood. Because the liver is reported to be the major site of apoA-I synthesis25 and because alcohol increases apoA-I production in transformed human hepatocytes,26 27 28 we hypothesized that alcohol raises HDL-C primarily by raising the TR of apoA-I and -II. In paired metabolic HDL apolipoprotein turnover studies, we found that dietary alcohol increases the TR of both apoA-I and -II, roughly to the same degree as the increase in their concentrations and in the HDL-C concentration. We also found that the amount of alcohol consumed predicted the degree of increase in the TR and that both correlated with the increase in HDL-C. These results suggest that the increase in TR is the major mechanism by which alcohol consumption raises HDL-C.
Our results in part confirm and in part contradict the results of the only 2 published studies of which we are aware that explore the effects of alcohol consumption on HDL turnover in human subjects.9 10 Malmendier and Delcroix9 studied apoA-I metabolism in 7 healthy nonobese men before and during a 4-week intake of 60 to 70 g EtOH/d and found a 49% increase in the TR and a 30% increase in the FCR of apoA-I. Thus, we confirm their finding that a prominent effect of alcohol on HDL turnover is an increase in apoA-I TR. The fact that the degree of increase in apoA-I TR in their study was more than double that seen in the present study may be due to their use of twice as much alcohol (60 to 70 g/d versus 33 g/d mean in our study), especially given our evidence for a dose-response effect in the range of 13 to 51 g/d. Surprisingly, they saw no increase in HDL-C (2% rise, NS), which is inconsistent with almost all other human studies and perhaps due to confounding from the small number of subjects and the relative lack of dietary control. It might also reflect a counterbalancing of the increase in apoA-I TR by a significant 30% increase in the apoA-I FCR, although they did report a statistically significant 12% increase in plasma apoA-I concentrations. In a second, smaller study by Gottrand et al,10 5 normolipemic men received 50 g/d EtOH as red wine added to a metabolic diet, apparently without any compensating reduction in other caloric intake. Alcohol induced a 14% increase in HDL-C accompanied by 20% and 60% increases in apoA-I and -II concentrations, respectively. They reported no change in the TR of either apoA-I or apoA-II; although a trend to increased TR was observed (11% and 18%, respectively). They did not find a significant change in apoA-I FCR, which is in agreement with our result but not with those of Malmendier and Delcroix,9 whereas the 21% decrease in apoA-II FCR reported by Gottrand et al10 was found by neither Malmendier and Delcroix9 nor us. These apparent discrepancies may be explained by the very small numbers of subjects in the prior studies, their lesser dietary control, and, in the case of the study by Gottrand et al,10 the intake of the many nonalcoholic components of wine.
The effect of alcohol intake on HDL turnover has also been studied in nonhuman primates.29 In squirrel monkeys, high-dose alcohol intake increased HDL-C and apoA-I concentrations.29 However, this was associated with a decrease in apoA-I FCR and no change in apoA-I TR. The possible reasons for the differences between the present results and those reported in squirrel monkeys cannot be assessed given the lack of information in this model about the effects of alcohol on lipase activities, HDL size, apoA-II turnover, and hepatocyte metabolism.
The effect of alcohol consumption on the major HDL particle size or density subfractions, HDL2 and HDL3, is inconsistent among studies. Haskell et al21 found an increase in HDL-C and HDL3 mass, but not HDL2, on resumption of moderate drinking. In contrast, Contaldo et al30 reported that the increase in HDL-C after short-term alcohol intake was primarily an increase in HDL2. Two other studies have indicated that alcohol consumption is associated with increased concentrations of both HDL2 and HDL3.5 24 In agreement with these latter 2 studies and with a more detailed assessment of HDL size than in prior published studies, we found no significant change in HDL particle size distribution. Although some reports suggest that larger HDL subfractions may be more strongly related to low atherosclerosis risk, others have found that large and small HDL particles may be equally associated with decreased risks of myocardial infarction.5 Interestingly, the only study that simultaneously measured HDL size, alcohol intake, and atherosclerosis event rates found that increases in both large and small HDL particles contribute to the reduced risk of events with alcohol consumption.5
We found that moderate alcohol consumption causes an increase in LPL and a decrease in HL activity, both of which would be expected to cause an increase in HDL particle size. The fact that there was no such increase is surprising and suggests the interesting possibility of a counterbalancing increase of smaller particles, which may have resulted from the increase in HDL apolipoprotein TR. Our previous work demonstrated that LPL and HL strongly predict apolipoprotein HDL FCR (inversely and positively, respectively).31 On this basis, we would have predicted that the alcohol-induced changes in LPL and HL both should have caused a reduction in HDL apolipoprotein FCR. Thus, the observed lack of change in FCR appears paradoxical, until one considers the lack of change in HDL particle size distribution. If HDL apolipoprotein FCR is primarily a function of HDL particle size rather than a direct function of LPL or HL activity, the observed lack of change in FCR would be expected as a result of the lack of change in HDL size.
The major mechanism of the alcohol-induced increase in HDL
apolipoprotein TR is likely an increase in hepatic production,
because the liver is estimated to be the site of synthesis of 
90%
of plasma apoA-I in humans.25 Although on the basis of our
studies we cannot rule out an effect of alcohol on intestinal apoA-I
production, this is unlikely, because alcohol intake is
associated with increased postprandial lipemia32 and
decreased HDL2 concentrations.33
Studies of HepG2 cells, a transformed human hepatocyte cell
line, have shown that alcohol increases the synthesis and secretion of
apoA-I, causing an increase in cholesterol efflux
ability.26 Furthermore, the increase with chronic exposure
to alcohol appears to be specific for apoA-I compared with some other
apolipoproteins,27 although apoA-II data were not
reported. Interestingly, this in vitro effect is dose dependent (0.05%
to 0.5%),28 reminiscent of our finding of dose-dependency
of the TR effects. The molecular mechanism of the increased
apolipoprotein synthesis is not known and cannot be readily addressed
in humans in vivo. In hepatocyte culture, this effect
appears to involve the microsomal EtOH-oxidizing system27
and is speculated to be due to intracellular increases in phospholipid
and cholesterol.28
In conclusion, we demonstrated that moderate alcohol consumption results in dose-dependent increases in plasma concentrations of the major HDL components (HDL-C, apoA-I and -II) through an increase in the HDL apolipoprotein TR, without a change in FCR or HDL particle size distribution.
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Acknowledgments |
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This work was supported by General Clinical Research Center grant M01-RR-00102 from the National Center for Research Resources, a Clinical Investigator Award (HL-02034) from the National Institutes of Health, and a Merit Review Award from the Department of Veterans’ Affairs (to Dr Brinton). We thank the nutrition research and nursing services of the General Clinical Research Center of the Rockefeller University Hospital. We thank Katie Tsang for technical assistance and all study participants for their cooperation.
Received April 20, 2000; revision received June 13, 2000; accepted June 27, 2000.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Gordon DJ, Probstfield JL, Garrison RJ, et al. High-density lipoprotein cholesterol and cardiovascular disease: four prospective American studies. Circulation. 1989;79:8–15.
2. Gaziano JM, Manson JE. Diet and heart disease: the role of fat, alcohol, and antioxidants. Cardiol Clin. 1996;14:69–83.[Medline] [Order article via Infotrieve]
3. Stampfer MJ, Colditz GA, Willett WC, et al. A prospective study of moderate alcohol consumption and the risk of coronary disease and stroke in women. N Engl J Med. 1988;319:267–273.[Abstract]
4. Rimm EB, Giovannucci EL, Willett WC, et al. Prospective study of alcohol consumption and risk of coronary disease in men. Lancet. 1991;338:464–468.[Medline] [Order article via Infotrieve]
5.
Gaziano JM, Buring JE, Breslow JL, et al. Moderate
alcohol intake, increased levels of high-density lipoprotein and its
subfractions, and decreased risk of myocardial infarction. N
Engl J Med. 1993;329:1829–1834.
6.
Pearson TA. Alcohol and heart disease.
Circulation. 1996;94:3023–3025.
7. Suh I, Shaten BJ, Cutler JA, et al. Alcohol use and mortality from coronary heart disease: the role of high-density lipoprotein cholesterol: the Multiple Risk Factor Intervention Trial Research Group. Ann Intern Med. 1992;116:881–887.
8. Schaefer EJ, Lamon-Fava S, Ordovas JM, et al. Factors associated with low and elevated plasma high density lipoprotein cholesterol and apolipoprotein A-I levels in the Framingham Offspring Study. J Lipid Res. 1994;35:871–882.[Abstract]
9. Malmendier CL, Delcroix C. Effect of alcohol intake on high and low density lipoprotein metabolism in health volunteers. Clin Chim Acta. 1985;152;281–288:.
10. Gottrand F, Beghin L, Duhal N, et al. Moderate red wine consumption in healthy volunteers reduced plasma clearance of apolipoprotein A-II. Eur J Clin Invest. 1999;29:387–394.[Medline] [Order article via Infotrieve]
11. United States Department of Agriculture, Agricultural Research Service. USDA Nutrient Data Base for Standard Reference, Release 9. Hyattsville, Md: United States Department of Agriculture, Agricultural Research Service; 1990.
12. Brinton EA, Eisenberg S, Breslow JL. Elevated high density lipoprotein cholesterol levels correlate with decreased apolipoprotein A-I and A-II fractional catabolic rate in women. J Clin Invest. 1989;84:262–269.
13. Matthews CME. The theory of tracer experiments with 131-I labelled plasma proteins. Physics Med Biol. 1957;2:36–53.[Medline] [Order article via Infotrieve]
14. SAAM Institute. SAAM II User Guide 1998. Seattle, Wash: SAAM Institute, Inc; 1998.
15.
Warnick GR, Benderson J, Albers JJ. Dextran
sulfate-Mg2+ precipitation procedure for
quantitation of high-density-lipoprotein cholesterol.
Clin Chem. 1982;28:1379–1388.
16. Clinical Chemistry Standardization Section. Lipid Standardization Programs of the Centers for Disease Control. Atlanta, Ga: Center for Environmental Health, Centers for Disease Control, Department of Health and Human Services; December 1985.
17. Cheung MC, Albers JJ. The measurement of apolipoprotein A-I and A-II levels in men and women by immunoassay. J Clin Invest. 1977;60:43–50.
18.
De Oliveira e Silva ER, Kong M, Han Z, et al.
Metabolic and genetic determinants of HDL
metabolism, and hepatic lipase activity in a
metabolic ward study of normolipidemic females. J
Lipid Res. 1999;40:1211–1221.
19.
Otvos JD, Jeyarajah EJ, Bennett DW, et al. Development
of a proton nuclear magnetic resonance spectroscopic method for
determining plasma lipoprotein concentrations and subspecies
distributions from a single, rapid measurement. Clin Chem. 1992;38:1632–1638.
20. Fraser GE, Anderson JT, Foster N, et al. The effect of alcohol on serum high density lipoprotein (HDL): a controlled experiment. Atherosclerosis. 1983;46:275–286.[Medline] [Order article via Infotrieve]
21. Haskell WL, Camargo C Jr, Williams PT, et al. The effect of cessation and resumption of moderate alcohol intake on serum high-density-lipoprotein subfractions: a controlled study. N Engl J Med. 1984;310:805–810.[Abstract]
22. Crouse JR, Grundy SM. Effects of alcohol on plasma lipoproteins and cholesterol and triglyceride metabolism in man. J Lipid Res. 1984;25:486–496.[Abstract]
23. Taskinen MR, Nikkila EA, Valimaki M, et al. Alcohol-induced changes in serum lipoproteins and in their metabolism. Am Heart J. 1987;113(2 pt 2):458–464.
24.
Clevidence BA, Reichman ME, Judd JT, et al. Effects of
alcohol consumption on lipoproteins of premenopausal women: a
controlled diet study. Arterioscler Thromb Vasc Biol. 1995;15:179–184.
25.
Ikewaki K, Zech LA, Kindt M, et al. Apolipoprotein A-II
production rate is a major factor regulating the distribution
of apolipoprotein A-I among HDL subclasses Lp A-I and A-II in
normolipidemic humans. Arterioscler Thromb Vasc Biol. 1995;15:306–312.
26. Amarasuriya RN, Gupta AK, Civen M, et al. Ethanol stimulates apolipoprotein A-I secretion by human hepatocytes: implications for a mechanism for atherosclerosis protection. Metabolism. 1992;41:827–832.[Medline] [Order article via Infotrieve]
27. Tam S-P. Effect of ethanol on lipoprotein secretion in two human hepatoma cell lines, HepG2 and Hep 3B. Alcohol Clin Exp Res. 1992;16:1021–1028.[Medline] [Order article via Infotrieve]
28. Dashti N, Franklin FA, Abrahamson DR. Effect of ethanol on the synthesis and secretion of apo A-I and apo B-containing lipoproteins in HepG2 cells. J Lipid Res. 1996;37:810–824.[Abstract]
29. Hojnacki JL, Cluette-Brown JE, Dawson M, et al. Alcohol delays clearance of lipoproteins from the circulation. Metabolism. 1992;41:1151–1153.[Medline] [Order article via Infotrieve]
30. Contaldo F, D’Arrigo E, Carandente V, et al. Short-term effects of moderate alcohol consumption on lipid metabolism and energy balance in normal men. Metabolism. 1989;38:166–171.[Medline] [Order article via Infotrieve]
31.
Brinton EA, Eisenberg S, Breslow JL. Human HDL
cholesterol levels are determined by apoA-I fractional
catabolic rate, which correlates inversely with estimates of HDL
particle size: effects of gender, hepatic and lipoprotein lipases,
triglyceride and insulin levels, and body fat distribution.
Arterioscler Thromb. 1994;14:707–720.
32. Wilson DE, Schreibman PH, Brewster AC, et al. The enhancement of alimentary lipemia by ethanol in man. J Lab Clin Med. 1970;75;264–274.
33. Patsch JR, Karlin JB, Scott LW, et al. Inverse relationship between blood levels of high density lipoprotein subfraction 2 and magnitude of postprandial lipemia. Proc Natl Acad Sci U S A.1983;80:1449–1453.
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 M. L Eigenbrodt, F. D Fuchs, D. J Couper, D. C Goff Jr, C. P. Sanford, R. G Hutchinson, and Z. Bursac Changing drinking pattern does not influence health perception: a longitudinal study of the atherosclerosis risk in communities study. J Epidemiol Community Health, April 1, 2006; 60(4): 345 - 350. [Abstract] [Full Text] [PDF]
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 E. Ruttmann, L. J. Brant, H. Concin, G. Diem, K. Rapp, H. Ulmer, and the Vorarlberg Health Monitoring and Promotion Pro {gamma}-Glutamyltransferase as a Risk Factor for Cardiovascular Disease Mortality: An Epidemiological Investigation in a Cohort of 163 944 Austrian Adults Circulation, October 4, 2005; 112(14): 2130 - 2137. [Abstract] [Full Text] [PDF]
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 P. E. Szmitko and S. Verma Antiatherogenic potential of red wine: clinician update Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2023 - H2030. [Abstract] [Full Text] [PDF]
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 A. M. Gotto Jr and E. A. Brinton Assessing low levels of high-density lipoprotein cholesterol as a risk factor in coronary heart disease: A working group report and update J. Am. Coll. Cardiol., March 3, 2004; 43(5): 717 - 724. [Abstract] [Full Text] [PDF]
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 M. Averina, O. Nilssen, T. Brenn, J. Brox, V. L. Arkhipovsky, and A. G. Kalinin Factors behind the Increase in Cardiovascular Mortality in Russia: Apolipoprotein AI and B Distribution in the Arkhangelsk Study 2000 Clin. Chem., February 1, 2004; 50(2): 346 - 354. [Abstract] [Full Text] [PDF]
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 M. Bohm, S. Rosenkranz, and U. Laufs Alcohol and red wine: impact on cardiovascular risk Nephrol. Dial. Transplant., January 1, 2004; 19(1): 11 - 16. [Full Text] [PDF]
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R. A. Vogel Vintners and vasodilators: are French red wines more cardioprotective? J. Am. Coll. Cardiol., February 5, 2003; 41(3): 479 - 481. [Full Text] [PDF]
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 O. I Bermudez, W. Velez-Carrasco, E. J Schaefer, and K. L Tucker Dietary and plasma lipid, lipoprotein, and apolipoprotein profiles among elderly Hispanics and non-Hispanics and their association with diabetes Am. J. Clinical Nutrition, December 1, 2002; 76(6): 1214 - 1221. [Abstract] [Full Text] [PDF]
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D. P. Agarwal CARDIOPROTECTIVE EFFECTS OF LIGHT-MODERATE CONSUMPTION OF ALCOHOL: A REVIEW OF PUTATIVE MECHANISMS Alcohol Alcohol., September 1, 2002; 37(5): 409 - 415. [Abstract] [Full Text] [PDF]
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S. Lussier-Cacan, A. Bolduc, M. Xhignesse, T. Niyonsenga, and C. F. Sing Impact of Alcohol Intake on Measures of Lipid Metabolism Depends on Context Defined by Gender, Body Mass Index, Cigarette Smoking, and Apolipoprotein E Genotype Arterioscler Thromb Vasc Biol, May 1, 2002; 22(5): 824 - 831. [Abstract] [Full Text] [PDF]
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D. J Baer, J. T Judd, B. A Clevidence, R. A Muesing, W. S Campbell, E. D Brown, and P. R Taylor Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet Am. J. Clinical Nutrition, March 1, 2002; 75(3): 593 - 599. [Abstract] [Full Text] [PDF]
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M. S. van der Gaag, A. van Tol, S. H. F. Vermunt, L. M. Scheek, G. Schaafsma, and H. F. J. Hendriks Alcohol consumption stimulates early steps in reverse cholesterol transport J. Lipid Res., December 1, 2001; 42(12): 2077 - 2083. [Abstract] [Full Text] [PDF]
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F. Blanco-Vaca, J. C. Escola-Gil, J. M. Martin-Campos, and J. Julve Role of apoA-II in lipid metabolism and atherosclerosis: advances in the study of an enigmatic protein J. Lipid Res., November 1, 2001; 42(11): 1727 - 1739. [Abstract] [Full Text] [PDF]
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