Changes in serum apolipoprotein and lipoprotein profile induced by chronic alcohol consumption and withdrawal: determinant effect on heart disease?
The effects of alcohol consumption on serum concentrations of apolipoproteins (apo) A-I, C-III, B, and E and of lipoproteins (Lp) A-I, A-I:A-II, C-III, C-III:B, and (a) were studied in 132 healthy subjects, including 55 low drinkers of alcohol (<20 g/day), 36 moderate drinkers (20-50 g/day), and 41 heavy drinkers (>50 g/day), and in 97 hospitalized alcoholic patients (> 100 g/day) without severe liver disease (especially functional insufficiency), before and after 21 days of withdrawal treatment. Serum concentrations of apo A-I, LpA-I, LpA-I:A-II, apo C-III, and LpC-III significantly (P </= 0.01) increased with alcohol intake (mean +/- SE in low drinkers vs in alcoholics)--1.45 +/- 0.03 vs 1.78 +/- 0.05 g/L; 0.45 +/- 0.02 vs 0.56 +/- 0.02 g/L; 0.99 +/- 0.02 vs 1.22 +/- 0.04 g/L; 27.6 +/- 1.5 vs 39.7 +/- 1.7 mg/L; and 8.4 +/- 0.9 vs 24.7 +/- 1.7 mg/L, respectively-whereas apo B and LpC-III:B concentrations tended to decrease--1.20 +/- 0.04 vs 1.06 +/- 0.04 g/L and 19.3 +/- 1.2 vs 14.9 +/- 1.0 mg/L, respectively. No significant difference between these four types of alcohol consumption was noticed for cholesterol, triglycerides, apo E, and Lp(a). After withdrawal, the concentrations of serum apo A-I, apo C-III, LpA-I, LpA-I:A-II, and LpC-III decreased significantly (P </= 0.01), reaching values comparable with those in low drinkers; concentrations of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol concentration was unaffected. In multiple regression analysis, after adjustment for serum concentrations of albumin, aspartate aminotransferase, and gamma-glutamyltransferase and for the Quetelet index, alcohol consumption remained positively correlated to apo A-I, LpA-I:A-II, apo C-III, and LpC-III concentrations. Study of other determinants of serum apo and lipoprotein concentrations suggests that alcohol-related variations in some of them, especially apo A-I, might depend on the metabolic ability of the liver to synthesize proteins and on induction phenomena. Finally, although the increase of antiatherogenic apo- and lipoproteins and the decrease of those known to be atherogenic were generally marked in alcoholics, alcohol-related modifications of these markers were very limited in our sample of French healthy men. We conclude, therefore, that moderate alcohol consumption (20-50 g/day) is unlikely to protect against ischemic heart disease through an effect on the proteins measured in this study.
Lecomte
E
E
Laboratoire du Centre de Médecine Pr'eventive, Vandoeuvre-lés-Nancy, France.
Herbeth
B
B
Paille
F
F
Steinmetz
J
J
Artur
Y
Y
Siest
G
G
D000328:Adult; D000437:Alcoholism / Q000097:blood*; D016632:Apolipoprotein A-I / Q000378:metabolism; D053305:Apolipoprotein C-III; D001053:Apolipoproteins / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood; D001056:Apolipoproteins C / Q000097:blood; D001057:Apolipoproteins E / Q000097:blood; D001161:Arteriosclerosis / Q000097:blood*; D000431:Ethanol / Q000008:administration & dosage*; D006801:Humans; D017270:Lipoprotein(a) / Q000031:analogs & derivatives / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D013375:Substance Withdrawal Syndrome / Q000097:blood*; D014280:Triglycerides / Q000097:blood
D016632:Apolipoprotein A-I; D053305:Apolipoprotein C-III; D001053:Apolipoproteins; D001055:Apolipoproteins B; D001056:Apolipoproteins C; D001057:Apolipoproteins E; D017270:Lipoprotein(a); D008074:Lipoproteins; D014280:Triglycerides; D000431:Ethanol; C078260:lipoprotein A-I