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 apolipop roteins (ape) 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, inc luding 55 lon drinkers of alcohol (< 20 g/day), 36 moderate drinkers ( 20-50 g/day), and 41 heavy drinkers (> 50 g/day), and in 97 hospitaliz ed alcoholic patients (> 100 g/day) without severe liver disease (espe cially functional insufficiency), before and after 21 days of withdraw al treatment. Serum concentrations of apo A-I, LpA-I, LpA-I:A-II, apo C-III, and LpC-III significantly (P less than or equal to 0.01) increa sed 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 a nd 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 si gnificant difference between these four types of alcohol consumption w as noticed for cholesterol, triglycerides, apo E, and Lp(a). After wit hdrawal, the concentrations of serum apo A-I, apo C-III, LpA-I, LpA-I: A-II, and LpC-III decreased significantly (P less than or equal to 0.0 1), reaching values comparable with those in low drinkers; concentrati ons of triglycerides, apo B, apo E, and Lp(a) rose; and cholesterol co ncentration was unaffected. In multiple regression analysis, after adj ustment for serum concentrations of albumin, aspartate aminotransferas e, and gamma-glutamyltransferase and for the Quetelet index, alcohol c onsumption 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 vari ations in some of them, especially apo A-I, might depend on the metabo lic ability of the liver to synthesize proteins and on induction pheno mena. Finally, although the increase of antiatherogenic apo- and lipop roteins and the decrease of those known to be atherogenic were general ly marked in alcoholics, alcohol-related modifications of these marker s 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 pr oteins measured in this study.