Editor—We agree with Paassilta et al that there may be a relation between moderate alcohol consumption and lower Lp(a) lipoprotein concentrations.1 The relation between alcohol consumption and cardiovascular mortality is U shaped, with the lowest mortality at an alcohol consumption of 2-4 units (16-32 g) a day.2 Several mechanisms contribute to this cardioprotective effect including beneficial increases in high density lipoprotein cholesterol3 and inhibition of platelet aggregation.4 However, other factors may be involved. Lp(a) lipoprotein is a recognised independent risk factor for the development of atherosclerosis and, as stated by Paassilta et al, little attention has been directed to the effects of alcohol on Lp(a) lipoprotein.
In 1995 we reported a significant reduction in Lp(a) lipoprotein concentration in a prospective study of 20 healthy volunteers (men and women) given 21 g of alcohol daily for 10 days in the form of red wine (median (range) 186 (15-1420) mg/l v 132 (10-1210) mg/l, P<0.001).5 This reduction was not repeated when the same subjects were given white wine, raising the issue of potential differences between various alcoholic drinks. Interestingly, we found no changes in high density lipoprotein cholesterol concentrations.
We have conducted a larger unpublished crossover trial in 50 men comparing the effects of 3 units (24 g) of alcohol a day as red wine or vodka for 14 days on Lp(a) lipoprotein concentrations. Each period of alcohol consumption was preceded by two weeks’ abstinence. Both drinks produced a 10-12% decrease in Lp(a) concentration (geometric mean 153 mg/100 ml v 135 mg/l after vodka, P<0.001; 151 mg/l v 136 mg/l after red wine, P<0.01). These results suggest that moderate alcohol consumption results in changes in Lp(a) lipoprotein which are independent of the type of alcoholic drink consumed. In conclusion, we agree with Paassilta et al that lower Lp(a) concentrations may be one factor conferring lower mortality and cardiovascular benefit in social drinkers.
References
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