Abstract

Plasma lipoprotein changes during a 2-week period of abstinence were followed in 6 male, chronic alcoholics without evidence of severe liver disease and with initial HDL cholesterol (HDL-CH) > 60 mg/dl. Fasting blood samples were obtained on days 1, 3, 7 and 14 of the study. Reference data were obtained from healthy non-alcoholic normolipidemic men who had abstained from alcohol for 10 days. At day 1, plasma- and HDL-CH (by the heparin-Mn2+ technique) were 17 and 69% higher, respectively, than those of controls. During abstinence, VLDL-CH increased 52% whereas HDL-CH decreased 30% compared to day 1 values. (IDL + LDL)-CH increased during abstinence to levels 33% higher than that of controls. Plasma, SF > 400, VLDL- and d > 1.006 g/ml-triglycerides (TG) were not significantly different from those of the control group. Only the d > 1.006 g/ml-TG showed a significant effect of abstinence, increasing by 37%. Initial plasma and d > 1.006 g/ml-phospholipid (PL) concentrations were 17 and 31% higher, respectively, than those of controls; and the latter was the only fraction to change significantly with abstinence, decreasing by 13%. Density gradient ultracentrifugation was employed to further resolve the d > 1.006 g/ml fraction into IDL, LDL, HDL and VHDL subfractions. Initial levels of IDL- and LDL-CH and -PL in the alcoholic group did not differ from those of controls. IDL-CH and -PL were invariant during abstinence, whereas LDL-CH and -PL levels increased 38 and 28%, during this period. Apo A-I, CH and PL contained in the ‘lighter’ density HDL region of the gradient (d = 1.063-1.125 g/ml) were 70–108% increased over the corresponding parameters for controls; and with abstinence decreased 30–40% between days 1 and 14. CH and PL in the `heavier' density HDL region (d = 1.125-1.21 g/ml) were 30% increased over those of controls, while apo A-I levels were similar to controls. During abstinence, ‘heavy’ HDL-CH, -PL and -apo A-I decreased 25% compared to day 1 values. Inspection of ‘difference’ density gradient plots indicated that the dominant decrease in HDL occurred in the ‘light’ HDL subspecies in only one-half of the subjects. Other investigators have reported a preferential decrease in ‘light’ HDL subspecies during abstinence in chronic alcoholics, and have related the decrease to decreased TG turnover. We conclude that additional mechanisms related to the synthesis and/or catabolism of HDL may need to be considered in explaining decreases in HDL subspecies in alcoholics during abstinence.

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