26 April 2017 In General Health

BACKGROUND: In cross-sectional studies and short-term clinical trials, it has been suggested that there is a positive dose-response relation between alcohol consumption and HDL concentrations. However, prospective data have been limited.

OBJECTIVE: We sought to determine the association between total alcohol intake, the type of alcohol-containing beverage, and the 6-y (2006-2012) longitudinal change in HDL-cholesterol concentrations in a community-based cohort.

DESIGN: A total of 71,379 Chinese adults (mean age: 50 y) who were free of cardiovascular diseases and cancer and did not use cholesterol-lowering agents during follow-up were included in the study. Alcohol intake was assessed via a questionnaire in 2006 (baseline), and participants were classified into the following categories of alcohol consumption: never, past, light (women: 0-0.4 servings/d; men: 0-0.9 servings/d), moderate (women: 0.5-1.0 servings/d; men: 1-2 servings/d), and heavy (women: >1.0 servings/d; men: >2 servings/d). HDL-cholesterol concentrations were measured in 2006, 2008, 2010, and 2012. We used generalized estimating equation models to examine the associations between baseline alcohol intake and the change in HDL-cholesterol concentrations with adjustment for age, sex, smoking, physical activity, obesity, hypertension, diabetes, liver function, and C-reactive protein concentrations.

RESULTS: An umbrella-shaped association was observed between total alcohol consumption and changes in HDL-cholesterol concentrations. Compared with never drinkers, past, light, moderate, and heavy drinkers experienced slower decreases in HDL cholesterol of 0.012 mmol . L-1 . y-1 (95% CI: 0.008, 0.016 mmol . L-1 . y-1), 0.013 mmol . L-1 . y-1 (95% CI: 0.010, 0.016 mmol . L-1 . y-1), 0.017 mmol . L-1 . y-1 (95% CI: 0.009, 0.025 mmol . L-1 . y-1), and 0.008 mmol . L-1 . y-1 (95% CI: 0.005, 0.011 mmol . L-1 . y-1), respectively (P < 0.0001 for all), after adjustment for potential confounders. Moderate alcohol consumption was associated with the slowest increase in total-cholesterol:HDL-cholesterol and triglyceride: HDL-cholesterol ratios. We observed a similar association between hard-liquor consumption and the HDL-cholesterol change. In contrast, greater beer consumption was associated with slower HDL-cholesterol decreases in a dose-response manner.

CONCLUSION: Moderate alcohol consumption was associated with slower HDL-cholesterol decreases; however, the type of alcoholic beverage had differential effects on the change in the HDL-cholesterol concentration.

26 April 2017 In Cardiovascular System

BACKGROUND: The potential cardioprotective effect of light-to-moderate alcohol consumption is disputed, and the association between heavy drinking and heart failure (HF) risk is unclear. We examined the association between alcohol consumption and risk of myocardial infarction (MI) and HF in two prospective cohorts.

METHODS: We analyzed data from the Cohort of Swedish Men (40,590 men) and the Swedish Mammography Cohort (34,022 women). Participants were free of ischemic heart disease and HF at baseline. MI and HF cases were ascertained by linkage with the Swedish National Patient Register. Cox proportional hazards regression model was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs).

RESULTS: During follow-up (1998-2010), we ascertained 3678 and 1905 cases of MI and HF, respectively, in men and 1500 and 1328 cases of MI and HF, respectively, in women. Alcohol consumption was inversely associated with MI in both men and women (P trend <0.001); compared with light drinkers, the multivariable HRs were 0.70 (95% CI, 0.56-0.87) in men who consumed >28 drinks/week and 0.32 (95% CI, 0.15-0.67) in women who consumed 15-21 drinks/week. Alcohol consumption was not inversely associated with HF risk. However, in men, the risk of HF was higher in never, former, and heavy drinkers (>28 drinks/week; HR=1.45; 95% CI, 1.09-1.93) compared with light drinkers.

CONCLUSIONS: Alcohol consumption has divergent associations with MI and HF, with an inverse association observed for MI but not HF. Heavy drinking was associated with an increased HF risk in men.

27 February 2017 In Cancer

It is not clear whether alcohol consumption is associated with lung cancer risk. The relationship is likely confounded by smoking, complicating the interpretation of previous studies. We examined the association of alcohol consumption and lung cancer risk in a large pooled international sample, minimizing potential confounding of tobacco consumption by restricting analyses to never smokers. Our study included 22 case-control and cohort studies with a total of 2548 never-smoking lung cancer patients and 9362 never-smoking controls from North America, Europe and Asia within the International Lung Cancer Consortium (ILCCO) and SYNERGY Consortium. Alcohol consumption was categorized into amounts consumed (grams per day) and also modelled as a continuous variable using restricted cubic splines for potential non-linearity. Analyses by histologic sub-type were included. Associations by type of alcohol consumed (wine, beer and liquor) were also investigated. Alcohol consumption was inversely associated with lung cancer risk with evidence most strongly supporting lower risk for light and moderate drinkers relative to non-drinkers (>0-4.9g per day: OR=0.80, 95% CI=0.70-0.90; 5-9.9g per day: OR=0.82, 95% CI=0.69-0.99; 10-19.9g per day: OR=0.79, 95% CI=0.65-0.96). Inverse associations were found for consumption of wine and liquor, but not beer. The results indicate that alcohol consumption is inversely associated with lung cancer risk, particularly among subjects with low to moderate consumption levels, and among wine and liquor drinkers, but not beer drinkers. Although our results should have no relevant bias from the confounding effect of smoking we cannot preclude that confounding by other factors contributed to the observed associations. Confounding in relation to the non-drinker reference category may be of particular importance.

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01 February 2017 In Liver Disease

BACKGROUND: Previous epidemiological studies suggest that patients diagnosed with nonalcoholic fatty liver disease (NAFLD) who drink light to moderate amounts of alcohol (up to ~30 g per day) have less severe histological lesions compared with nondrinkers. However, while the cross-sectional nature of current evidence precludes assessment of causality, cumulative lifetime-exposure of moderate alcohol consumption on histological outcomes has never been evaluated.

AIM: To overcome these limitations, a Mendelian randomisation study was performed using a validated genetic variant (rs1229984 A;G) in the alcohol dehydrogenase (ADH1B) gene as a proxy of long-term alcohol exposure.

METHODS: We first assessed whether the instrumental variant (rs1229984) was associated with the amount of alcohol consumption in our cohort. We further explored the association between the variant and histological outcomes; a sample of 466 individuals, including 266 patients with NAFLD confirmed by liver biopsy, was studied.

RESULTS: We found that carriers of the A-allele consumed significantly lower amounts of alcohol compared with noncarriers (2.3 +/- 5.3 vs. 8.18 +/- 21 g per day, mean +/- s.d., P = 0.03). The analysis of association with the disease severity showed that carriers of the A-allele had lower degree of histological steatosis (1.76 +/- 0.83 vs. 2.19 +/- 0.78, P = 0.03) and lower scores of lobular inflammation (0.54 +/- 0.65 vs. 0.95 +/- 0.92, P = 0.02) and NAFLD-Activity Score (2.9 +/- 1.4 vs. 3.7 +/- 1.4, P = 0.015) compared with noncarriers.

CONCLUSION: Mendelian randomisation analysis suggests no beneficial effect of moderate alcohol consumption on NAFLD disease severity.

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