SAGE-Hindawi Access to Research Journal of Aging Research Volume 2011, Article ID 805062, 10 pages doi:10.4061/2011/805062 Research Article Alcohol Consumption and Risk of All-Cause and Cardiovascular Disease Mortality in Men Erin K. Howie,1 Xuemei Sui,1 Duck-chul Lee,1 Steven P. Hooker,1, 2 James R. He´ bert,3 and Steven N. Blair1, 3 1 Department of Exercise Science, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA 2 Prevention Research Center, University of South Carolina, Columbia, SC, USA 3 Cancer Prevention and Control Program and Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA Correspondence should be addressed to Erin K. Howie, howieek@email.sc.edu Received 26 January 2011; Accepted 9 May 2011 Academic Editor: Leonard W. Poon Copyright © 2011 Erin K. Howie et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This study examined the association between consumption of alcoholic beverages and all-cause and cardiovascular disease (CVD) mortality in a cohort of men (n = 31,367). In the Cox proportional hazards model adjusted for age, year of examination, body mass index (BMI), smoking, family history of CVD, and aerobic ﬁtness, there were no signiﬁcant diﬀerences in risk of all-cause mortality across alcohol intake groups. Risk of CVD mortality was reduced 29% in quartile 1 (HR = 0.71, 95% conﬁdence interval (CI): 0.53, 0.95) and 25% in quartile 2 (HR = 0.75, 95% CI: 0.58, 0.98). The amount of alcohol consumed to achieve this risk reduction was <6 drinks/week; less than the amount currently recommended. The addition of other potential confounders and eﬀect modiﬁers including blood pressure, insulin sensitivity, lipid levels, and psychological variables did not aﬀect the magnitude of association. Future research is needed to validate the current public health recommendations for alcohol consumption. 1. Introduction Light-to-moderate alcohol consumption has been shown in several prospective studies to reduce the risk of all-cause mortality and several cardiac outcomes, including cardio- vascular disease (CVD) mortality in men [1–10]. Several hypotheses exist for the mechanism of this protective eﬀect including increased exposure to antioxidants, improved lipid proﬁles, reduced insulin resistance, decreased blood coagulation, and modiﬁed inﬂammation pathways [11, 12]. Despite a large number of studies examining alcohol consumption and mortality, questions remain about the nature of this relationship. Three primary concerns include the inﬂuence of confounding factors, appropriate public health recommendations, and diﬀerential eﬀects between types of alcohol [13, 14]. Selection bias is a particular concern when comparing nondrinkers to drinkers. Non- drinkers may abstain from alcohol because of an initial health condition and be more likely to have other conditions that might confound the relationship including obesity, physical inactivity, and overall health problems [14]. In addition, moderate alcohol consumption has been associated with positive psychosocial outcomes including sociability and stress reduction, which may further confound the association with mortality [15, 16]. Confounding is a limitation of nonexperimental studies, yet it is unethical and impractical to conduct long-term randomized controlled trials of alcohol consumption. In an attempt to address this challenge, investigators have used statistical methods to control for possible confounders that may increase the risk of mortality independent of alcohol consumption, but that may be diﬀerentially distributed in those who drink alcohol versus those who do not, such as smoking or physical inactivity. Several problems have hampered the ability to construct an appropriate public health message about alcohol con- sumption. Methodological variation has led to inconsistent estimates of protective amounts of alcohol and, thus, an inability to quantify safe recommendations [17]. In addition, any protective eﬀect must simultaneously be weighed against