Abstract
Over the last 2 decades, observational evidence largely supports an association between light to moderate alcohol consumption (up to 1 drink per day in women and up to 2 drinks per day in men) and a lower risk of cardiovascular disease (CVD), largely driven by a reduction in coronary heart disease. Most studies suggest a nadir in risk in the light to moderate range of alcohol intake, which is then countered by an increase in cardiomyopathy, sudden death, and hemorrhagic stroke at higher drinking levels that offsets potential benefits. The mechanisms of cardioprotective effects of alcohol are complex and there are multiple pathways by which moderate alcohol consumption reduces the risk of CVD. Recent evidence continues to emerge on the physiologic and genetic mechanisms through which alcohol may reduce the risk of developing CVD. Ongoing debate also lingers whether there are important differences in cardiovascular effects according to alcoholic beverage type (beer vs red wine vs liquor). Another emerging area of interest is the role of alcohol consumption on the development of intermediate cardiovascular endpoints such as hypertension and diabetes that lead to the development of CVD as well as other important cardiovascular sequelae. Alcohol consumption has also been shown to impact the risk of other CVD endpoints including congestive heart failure, alcoholic cardiomyopathy, atrial fibrillation, and peripheral artery disease. Overall, alcohol still carries significant public health implications given its plausible benefits on CVD along with its well-documented adverse effects, warranting continued caution and a discussion with one's primary care provider regarding intake.