Alcohol consumption and plasma concentration of C-reactive protein

Moderate alcohol intake has been associated with lower cardiovascular mortality. However, data evaluating the relationship between C-reactive protein (CRP), a predictor of cardiovascular risk, and alcohol consumption are sparse.

The relationship between alcohol consumption and CRP was evaluated in a cross-sectional survey and over time among 1732 men and 1101 women participating in the Pravastatin Inflammation/CRP Evaluation Study. CRP levels were lower in those with moderate alcohol intake versus light or occasional intake: in 5 categories of alcohol intake (no alcohol or <1 drink monthly, 1 to 3 drinks monthly, 1 to 4 drinks weekly, 5 to 7 drinks weekly, and > or =2 drinks daily), median CRP levels were 2.60 mg/L (interquartile range (IQR), 1.20 to 5.30 mg/L), 2.20 mg/L (IQR, 1.00 to 4.40 mg/L), 1.70 mg/L (IQR, 0.80 to 3.80 mg/L), 1.60 mg/L (IQR, 0.80 to 3.30 mg/L), and 1.80 mg/L (IQR, 0.80 to 2.90 mg/L), respectively. This relationship was present among men, women not taking hormone replacement therapy, nonsmokers, and those individuals with and without a history of cardiovascular disease (all P<0.001). In multivariate analysis, the relationship between alcohol consumption and CRP remained significant after controlling for multiple traditional cardiovascular risk factors. Alcohol consumption did not significantly affect the change in CRP or lipid levels associated with statin use.

Moderate alcohol consumption was associated with lower CRP concentrations than no or occasional alcohol intake, an effect that was independent of alcohol-related effects on lipids. Alcohol may attenuate cardiovascular mortality in part through an anti-inflammatory mechanism.