title: An expanding knowledge of the mechanisms and effects of alcohol consumption on cardiovascular disease.
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.
authors.affiliation: Division of Aging, Department of Medicine, Brigham and Women's Hospital (Drs Matsumoto, Miedema, Ofman, Gaziano, and Sesso), Harvard Medical School (Drs Matsumoto, Miedema, Ofman, Gaziano, and Sesso), Boston Veterans Affairs Healthcare System (Drs Miedema, Ofman, and Gaziano), and Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, (Drs Gaziano and Sesso), Boston, Massachusetts.
authors.forename: Chisa
authors.initials: C
authors.lastname: Matsumoto
authors.forename: Michael D
authors.initials: MD
authors.lastname: Miedema
authors.forename: Peter
authors.initials: P
authors.lastname: Ofman
authors.forename: J Michael
authors.initials: JM
authors.lastname: Gaziano
authors.forename: Howard D
authors.initials: HD
authors.lastname: Sesso
mesh_terms: D000367:Age Factors; D000426:Alcohol Dehydrogenase / Q000235:genetics; D000428:Alcohol Drinking / Q000009:adverse effects; D000445:Aldehyde Oxidoreductases / Q000235:genetics; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000517:prevention & control*; D002492:Central Nervous System Depressants / Q000008:administration & dosage / Q000009:adverse effects / Q000032:analysis*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015986:Confounding Factors, Epidemiologic; D003376:Counseling; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000008:administration & dosage / Q000009:adverse effects / Q000032:analysis*; D020022:Genetic Predisposition to Disease; D006801:Humans; D007333:Insulin Resistance; D008019:Life Style; D011634:Public Health; D018570:Risk Assessment; D012737:Sex Factors; D020521:Stroke / Q000139:chemically induced / Q000517:prevention & control; D013345:Subarachnoid Hemorrhage / Q000139:chemically induced
chemical_list: D002492:Central Nervous System Depressants; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000431:Ethanol; D000426:Alcohol Dehydrogenase; D000445:Aldehyde Oxidoreductases; C018699:aldehyde dehydrogenase (NAD(P)+)