title: A controlled trial of the effects of pattern of alcohol intake on serum lipid levels in regular drinkers.
abstract: To determine whether the effects of drinking pattern (predominantly weekend versus daily drinking) have differential effects on serum lipids, 55 healthy male drinkers were recruited on the basis of a regular alcohol intake, 210-500 ml absolute alcohol/week (approximately 3-6 standard drinks/day), with more than 60% consumed as beer. Fourteen subjects were categorised as predominantly weekend drinkers, while 41 subjects regularly drank on a daily basis. After maintenance of their drinking pattern during a 4-week familiarisation, subjects were randomised to either consume low alcohol beer (0.9%, v/v) only, or to maintain their usual drinking habit consuming full-strength beer (5%, v/v) for the next 4 weeks. They then switched to full-strength or low alcohol beer, respectively, for a further 4 weeks. Their drinking pattern remained constant during the study. In both weekend and daily drinkers, a reduction in alcohol intake (i.e. from 387 ml/week to 88 ml/week for weekend drinkers and from 418 ml/week to 95 ml/week for daily drinkers, respectively, P < 0.001) resulted in a similar 0.12 mmol/l fall in HDL-C (P < 0.01) with a concomitant significant fall in both apolipoproteins A-I and A-II. In daily drinkers total cholesterol fell by 0.28 mmol/l (P < 0.001) and triglyceride by 0.22 mmol/l (P < 0.01) with a reduction in alcohol intake, but no change in LDL-C was seen. In contrast, weekend drinkers total cholesterol was unchanged while triglyceride decreased by 0.26 mmol/l (P < 0.05) and LDL-C increased by 0.25 mmol/l (P < 0.01). Lp(a) increased with a reduction in alcohol intake in both daily (9.1 U/l, P < 0.05) and weekend drinkers (27.6 U/l, P = 0.07). Previous reports of a more atherogenic lipid profile with episodic versus regular daily drinking were not confirmed in this study and potentially favourable effects of alcohol to increase HDL-C and decrease Lp(a) were shown to be independent of drinking pattern in these moderate to heavy drinkers.
authors.affiliation: The University Department of Medicine (Royal Perth Hospital) and the West Australian Heart Research Institute, Australia. vrakic@cyllene.uwa.edu.au
authors.forename: V
authors.initials: V
authors.lastname: Rakic
authors.forename: I B
authors.initials: IB
authors.lastname: Puddey
authors.forename: S B
authors.initials: SB
authors.lastname: Dimmitt
authors.forename: V
authors.initials: V
authors.lastname: Burke
authors.forename: L J
authors.initials: LJ
authors.lastname: Beilin
mesh_terms: D000328:Adult; D000368:Aged; D000428:Alcohol Drinking / Q000097:blood*; D016632:Apolipoprotein A-I / Q000097:blood / Q000187:drug effects; D016633:Apolipoprotein A-II / Q000097:blood / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D000431:Ethanol / Q000008:administration & dosage; D006801:Humans; D008019:Life Style; D008055:Lipids / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D011795:Surveys and Questionnaires; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids; D017270:Lipoprotein(a); D014280:Triglycerides; D000431:Ethanol; D002784:Cholesterol