title: Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction.
abstract: BACKGROUND
  Previous studies have suggested that moderate alcohol intake exerts a protective effect against coronary heart disease. Alterations in plasma lipoprotein levels represent one plausible mechanism of this apparent protective effect.
  
  
  METHODS
  We therefore examined the interrelation among alcohol consumption, plasma lipoprotein levels, and the risk of myocardial infarction in 340 patients who had had myocardial infarctions and an equal number of age- and sex-matched controls. The case patients were men or women less than 76 years of age with no history of coronary disease who were discharged from one of six hospitals in the Boston area with a diagnosis of a confirmed myocardial infarction. Alcohol consumption was estimated by means of a food-frequency questionnaire.
  
  
  RESULTS
  We observed a significant inverse association between alcohol consumption and the risk of myocardial infarction (P for trend, < 0.001 after control for known coronary risk factors). In multivariate analyses, the relative risk for the highest intake category (subjects who consumed three or more drinks per day) as compared with the lowest (those who had less than one drink a month) was 0.45 (95 percent confidence interval, 0.26 to 0.80). The levels of total high-density lipoprotein cholesterol (HDL) and its HDL2 and HDL3 subfractions were strongly associated with alcohol consumption (P for trend, < 0.001 for each). The addition of HDL or either of its subfractions to the multivariate model substantially reduced the inverse association between alcohol intake and myocardial infarction, whereas the addition of the other plasma lipid measurements did not materially alter the relation.
  
  
  CONCLUSIONS
  These data confirm the inverse association of moderate alcohol intake with the risk of myocardial infarction and support the view that the effect is mediated, in large part, by increases in both HDL2 and HDL3.
authors.affiliation: Division of Preventive Medicine, Channing Laboratory, Boston, MA.
authors.forename: J M
authors.initials: JM
authors.lastname: Gaziano
authors.forename: J E
authors.initials: JE
authors.lastname: Buring
authors.forename: J L
authors.initials: JL
authors.lastname: Breslow
authors.forename: S Z
authors.initials: SZ
authors.lastname: Goldhaber
authors.forename: B
authors.initials: B
authors.lastname: Rosner
authors.forename: M
authors.initials: M
authors.lastname: VanDenburgh
authors.forename: W
authors.initials: W
authors.lastname: Willett
authors.forename: C H
authors.initials: CH
authors.lastname: Hennekens
mesh_terms: D000368:Aged; D000428:Alcohol Drinking; D001053:Apolipoproteins / Q000032:analysis; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology*; D012306:Risk; D014280:Triglycerides / Q000097:blood
chemical_list: D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D002784:Cholesterol