BACKGROUND: Previous studies have revealed inconsistent findings regarding the association of light to moderate alcohol consumption with cardiovascular disease (CVD) and cancer mortality.

OBJECTIVES: The aim of this study was to examine the association between alcohol consumption and risk of mortality from all causes, cancer, and CVD in U.S. adults. METHODS: Data were obtained by linking 13 waves of the National Health Interview Surveys (1997 to 2009) to the National Death Index records through December 31, 2011. A total of 333,247 participants >/=18 years of age were included. Self-reported alcohol consumption patterns were categorized into 6 groups: lifetime abstainers; lifetime infrequent drinkers; former drinkers; and current light, moderate, or heavy drinkers. Secondary exposure included participants' binge-drinking status. The main outcome was all-cause, cancer, or CVD mortality.

RESULTS: After a median follow-up of 8.2 years (2.7 million person-years), 34,754 participants died of all causes (including 8,947 CVD deaths and 8,427 cancer deaths). Compared with lifetime abstainers, those who were light or moderate alcohol consumers were at a reduced risk of mortality for all causes (light-hazard ratio [HR]: 0.79; 95% confidence interval [CI]: 0.76 to 0.82; moderate-HR: 0.78; 95% CI: 0.74 to 0.82) and CVD (light-HR: 0.74; 95% CI: 0.69 to 0.80; moderate-HR: 0.71; 95% CI: 0.64 to 0.78), respectively. In contrast, there was a significantly increased risk of mortality for all causes (HR: 1.11; 95% CI: 1.04 to 1.19) and cancer (HR: 1.27; 95% CI: 1.13 to 1.42) in adults with heavy alcohol consumption. Binge drinking >/=1 d/week was also associated with an increased risk of mortality for all causes (HR: 1.13; 95% CI: 1.04 to 1.23) and cancer (HR: 1.22; 95% CI: 1.05 to 1.41).

CONCLUSIONS: Light and moderate alcohol intake might have a protective effect on all-cause and CVD-specific mortality in U.S. adults. Heavy or binge drinking was associated with increased risk of all-cause and cancer-specific mortality.

Published in General Health

BACKGROUND: Previous studies have revealed inconsistent findings regarding the association of light to moderate alcohol consumption with cardiovascular disease (CVD) and cancer mortality.

OBJECTIVES: The aim of this study was to examine the association between alcohol consumption and risk of mortality from all causes, cancer, and CVD in U.S. adults.

METHODS: Data were obtained by linking 13 waves of the National Health Interview Surveys (1997 to 2009) to the National Death Index records through December 31, 2011. A total of 333,247 participants >/=18 years of age were included. Self-reported alcohol consumption patterns were categorized into 6 groups: lifetime abstainers; lifetime infrequent drinkers; former drinkers; and current light, moderate, or heavy drinkers. Secondary exposure included participants' binge-drinking status. The main outcome was all-cause, cancer, or CVD mortality.

RESULTS: After a median follow-up of 8.2 years (2.7 million person-years), 34,754 participants died of all causes (including 8,947 CVD deaths and 8,427 cancer deaths). Compared with lifetime abstainers, those who were light or moderate alcohol consumers were at a reduced risk of mortality for all causes (light-hazard ratio [HR]: 0.79; 95% confidence interval [CI]: 0.76 to 0.82; moderate-HR: 0.78; 95% CI: 0.74 to 0.82) and CVD (light-HR: 0.74; 95% CI: 0.69 to 0.80; moderate-HR: 0.71; 95% CI: 0.64 to 0.78), respectively. In contrast, there was a significantly increased risk of mortality for all causes (HR: 1.11; 95% CI: 1.04 to 1.19) and cancer (HR: 1.27; 95% CI: 1.13 to 1.42) in adults with heavy alcohol consumption. Binge drinking >/=1 d/week was also associated with an increased risk of mortality for all causes (HR: 1.13; 95% CI: 1.04 to 1.23) and cancer (HR: 1.22; 95% CI: 1.05 to 1.41).

CONCLUSIONS: Light and moderate alcohol intake might have a protective effect on all-cause and CVD-specific mortality in U.S. adults. Heavy or binge drinking was associated with increased risk of all-cause and cancer-specific mortality.

Published in Cancer

The quantity and frequency of alcohol consumption are crucial both in risk assessment as well as epidemiological and clinical research. Using the Munich Composite International Diagnostic Interview (M-CIDI), drinking amounts have been assessed in numerous large-scale studies. However, the accuracy of this assessment has rarely been evaluated. This study evaluates the relevance of drink categories and pouring sizes, and the factors used to convert actual drinks into standard drinks. We compare the M-CIDI to alternative drink assessment instruments and empirically validate drink categories using a general population sample (n = 3165 from Germany), primary care samples (n = 322 from Italy, n = 1189 from Germany), and a non-representative set of k = 22503 alcoholic beverages sold in Germany in 2010-2016. The M-CIDI supplement sheet displays more categories than other instruments (AUDIT, TLFB, WHO-CIDI). Beer, wine, and spirits represent the most prevalent categories in the samples. The suggested standard drink conversion factors were inconsistent for different pouring sizes of the same drink and, to a smaller extent, across drink categories. For the use in Germany and Italy, we propose the limiting of drink categories and pouring sizes, and a revision of the proposed standard drinks. We further suggest corresponding examinations and revisions in other cultures.

Published in Drinking Patterns

Humans are cumulatively exposed to acetaldehyde from various sources including alcoholic beverages, tobacco smoke, foods and beverages. The genetic-epidemiologic and biochemical evidence in ALDH2-deficient humans provides strong evidence for the causal relationship between acetaldehyde-exposure due to alcohol consumption and cancer of the upper digestive tract. The risk assessment has so far relied on thresholds based on animal toxicology with lower one-sided confidence limit of the benchmark dose values (BMDL) typically ranging between 11 and 63 mg/kg bodyweight (bw)/day dependent on species and endpoint. The animal data is problematic for regulatory toxicology for various reasons (lack in study quality, problems in animal models and appropriateness of endpoints - especially cancer - for transfer to humans). In this study, data from genetic epidemiologic and biochemical studies are reviewed. The increase in the daily exposure dose to acetaldehyde in alcohol-consuming ALDH2-deficients vs. ALDH2-actives was about twofold. The acetaldehyde increase due to ALDH2 inactivity was calculated to be 6.7 mug/kg bw/day for heavy drinkers, which is associated with odds ratios of up to 7 for head and neck as well as oesophageal cancer. Previous animal toxicology based risk assessments may have underestimated the risk of acetaldehyde. Risk assessments of acetaldehyde need to be revised using this updated evidence.

Published in Cancer
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The authors have taken reasonable care in ensuring the accuracy of the information herein at the time of publication and are not responsible for any errors or omissions. Read more on our disclaimer.