title: Alcohol consumption and hemostatic factors: analysis of the Framingham Offspring cohort.
abstract: BACKGROUND
  Moderate alcohol consumers have lower rates of cardiovascular disease than abstainers. One proposed mechanism is a beneficial effect on hemostatic parameters, but previous studies have provided conflicting results.
  
  
  RESULTS
  We measured levels of fibrinogen, plasma viscosity, von Willebrand factor, factor VII, plasminogen activator inhibitor antigen-1, and tissue plasminogen activator antigen in a cross-sectional analysis of 3223 adults free of cardiovascular disease enrolled in the Framingham Offspring Study. We assessed their alcohol consumption with a standardized questionnaire. Light-to-moderate alcohol consumption was associated with lower levels of fibrinogen, plasma viscosity, von Willebrand factor, and factor VII. This association was most pronounced for consumers of 3 to 7 drinks weekly for viscosity and 7 to 21 drinks weekly for the other hemostatic measures. Alcohol intake of 7 to 21 drinks weekly or more was associated with impaired fibrinolytic potential, reflected by higher levels of plasminogen activator inhibitor antigen-1 and tissue plasminogen activator antigen. Wine drinkers had lower plasminogen activator inhibitor antigen-1 levels than other drinkers, particularly at 3 to 21 drinks weekly, but beverage type did not otherwise consistently affect the results.
  
  
  CONCLUSIONS
  Light-to-moderate alcohol consumption is associated with lower levels of coagulatory factors, but higher intake is associated with impaired fibrinolytic potential. These findings are consistent with the hypothesis that a balance between hemostatic and fibrinolytic activity may contribute to the complex relation of alcohol use with coronary heart disease.
authors.affiliation: Division of General Medicine and Primary Care, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. kmukamal@caregroup.harvard.edu
authors.forename: K J
authors.initials: KJ
authors.lastname: Mukamal
authors.forename: P P
authors.initials: PP
authors.lastname: Jadhav
authors.forename: R B
authors.initials: RB
authors.lastname: D'Agostino
authors.forename: J M
authors.initials: JM
authors.lastname: Massaro
authors.forename: M A
authors.initials: MA
authors.lastname: Mittleman
authors.forename: I
authors.initials: I
authors.lastname: Lipinska
authors.forename: P A
authors.initials: PA
authors.lastname: Sutherland
authors.forename: T
authors.initials: T
authors.lastname: Matheney
authors.forename: D
authors.initials: D
authors.lastname: Levy
authors.forename: P W
authors.initials: PW
authors.lastname: Wilson
authors.forename: R C
authors.initials: RC
authors.lastname: Ellison
authors.forename: H
authors.initials: H
authors.lastname: Silbershatz
authors.forename: J E
authors.initials: JE
authors.lastname: Muller
authors.forename: G H
authors.initials: GH
authors.lastname: Tofler
mesh_terms: D000428:Alcohol Drinking / Q000453:epidemiology* / Q000378:metabolism*; D000434:Alcoholic Beverages / Q000145:classification; D001809:Blood Viscosity / Q000502:physiology; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D003710:Demography; D005167:Factor VII / Q000032:analysis; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis / Q000502:physiology; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D008297:Male; D008404:Massachusetts / Q000453:epidemiology; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011795:Surveys and Questionnaires; D010959:Tissue Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D005167:Factor VII; D005340:Fibrinogen; D010959:Tissue Plasminogen Activator