Alcohol consumption, particularly white wine and liquor, was associated with decreased platelet reactivity (β -0.042; 95% CI -0.07 to -0.02 for white wine), though effects were smaller than aspirin.
Cross-Sectional (n=3,427)
Does alcohol consumption decrease platelet reactivity in a general population sample?
Alcohol consumption, particularly white wine and liquor, is associated with modestly decreased platelet reactivity, though the inhibitory effect is substantially smaller than that of aspirin.
Effect estimate: β -0.042 (95% CI -0.07, -0.02)
p-value: p=2.6E-3
BACKGROUND: Alcohol consumption is linked to decreased platelet function. Whether this link is dependent on sex or type of beverage remains unclear. METHODS: Cross-sectional data were obtained from the Framingham Heart Study (N = 3427). Alcohol consumption was assessed by using standardized medical history and Harvard semi-quantitative food frequency questionnaires. Five bioassays measured 120 platelet reactivity traits across agonists in whole-blood and platelet-rich plasma samples. Linear mixed-effects models adjusted for age, sex and aspirin use, hypertension, body mass index, cholesterol, high-density lipoprotein, triglycerides, smoking and diabetes evaluated associations between platelet reactivity and alcohol consumption. Beta effects, the regression coefficients that estimate the amount of change in each unit of the predictor variable whereas all other predictor variables remain fixed, for heavy alcohol consumption were compared with effects of aspirin use. RESULTS: Alcohol consumption was associated with decreased platelet reactivity, with more associations among wine and liquor compared with beer. Many platelet-alcohol associations in the full sample (86%, P < 0.01) had larger effect sizes in females. Lower light transmission aggregometry adenosine diphosphate (1.82 µM) maximum aggregation (P = 2.6E-3, 95% CI = -0.07, -0.02, β = -0.042) and area under the curve (P = 7.7E-3, 95% CI = -0.07, -0.01, β = -0.039) were associated with white wine consumption; however, red wine had no associations with platelet reactivity. The effect of aspirin use was on average 11.3 (±4.0) times greater than that of heavy drinking in our full sample. CONCLUSIONS: We confirm associations between alcohol consumption and decreased platelet reactivity. Effects appeared larger for liquor and wine intake and in our female cohort. Red wine consumption is not associated with lower platelet function, contrasting with prior population studies. Although we report an inhibitory relationship between alcohol intake and platelet function, these effects appear much smaller than that of aspirin use.
Pashek et al. (Tue,) conducted a cross-sectional in General population (n=3,427). Alcohol consumption vs. Aspirin use (for effect size comparison) was evaluated on Light transmission aggregometry adenosine diphosphate (1.82 µM) maximum aggregation (β -0.042, 95% CI -0.07, -0.02, p=2.6E-3). Alcohol consumption, particularly white wine and liquor, was associated with decreased platelet reactivity (β -0.042; 95% CI -0.07 to -0.02 for white wine), though effects were smaller than aspirin.