OBJECTIVES: The aim of this study was to assess the hypothesis that alcohol consumption is associated with onset of atrial fibrillation (AF) and/or heart failure (HF).

BACKGROUND: The connection between ethanol intake and AF or HF remains controversial.

METHODS: The study population was 22,824 AF- or HF-free subjects (48% men, age >/=35 years) randomly recruited from the general population included in the Moli-sani study, for whom complete data on HF, AF, and alcohol consumption were available. The cohort was followed up to December 31, 2015, for a median of 8.2 years (183,912 person-years). Incident cases were identified through linkage to the Molise regional archive of hospital discharges. Hazard ratios were calculated using Cox proportional hazard models and cubic spline regression.

RESULTS: A total of 943 incident cases of HF and 554 of AF were identified. In comparison with never drinkers, both former and occasional drinkers showed comparable risk for developing HF. Drinking alcohol in the range of 1 to 4 drinks/day was associated with a lower risk for HF, with a 22% maximum risk reduction at 20 g/day, independent of common confounders. In contrast, no association of alcohol consumption with onset of AF was observed. Very similar results were obtained after restriction of the analyses to regular or only wine drinkers or according to sex, age, social status, or adherence to the Mediterranean diet.

CONCLUSIONS: Consumption of alcohol in moderation was associated with a lower incidence of HF but not with development of AF.

Published in Cardiovascular System
BACKGROUND: Compelling evidence suggests that excessive alcohol consumption increases the risk of atrial fibrillation (AF), but the effect of light-moderate alcohol consumption is less certain. We investigated the association between alcohol consumption within recommended limits and AF risk in a light-drinking population. METHODS AND RESULTS: Among 47 002 participants with information on alcohol consumption in a population-based cohort study in Norway, conducted from October 2006 to June 2008, 1697 validated AF diagnoses were registered during the 8 years of follow-up. We used Cox proportional hazard models with fractional polynomials to analyze the association between alcohol intake and AF. Population attributable risk for drinking within the recommended limit (ie, at most 1 drink per day for women and 2 drinks per day for men without risky drinking) compared with nondrinking was also calculated. The average alcohol intake was 3.8+/-4.8 g/d. The adjusted hazard ratio for AF was 1.38 (95% confidence interval, 1.06-1.80) when we compared participants consuming >7 drinks per week with abstainers. When we modeled the quantity of alcohol intake as a continuous variable, the risk increased in a curvilinear manner. It was higher with heavier alcohol intake, but there was virtually no association at <1 drink per day for women and <2 drinks per day for men in the absence of risky drinking. The population attributable risk among nonrisky drinkers was 0.07% (95% confidence interval, -0.01% to 0.13%). CONCLUSIONS: Although alcohol consumption was associated with a curvilinearly increasing risk of AF in general, the attributable risk of alcohol consumption within recommended limits among participants without binge or problem drinking was negligible in this population
Published in Cardiovascular System

INTRODUCTION: The benefits of alcohol consumption for cardiovascular and metabolic health may have been overstated due to inappropriate comparisons with abstainers and inadequate control for confounding factors including physical activity and mental health. We examined alcohol consumption and cardio-metabolic health in a cohort of young Australian adults overcoming these limitations.

METHODS: Cross-sectional data of a cohort of 2200 participants (age range 25-36 years) from the 2004-06 Childhood Determinants of Adult Health were used. Alcohol consumption was assessed from questionnaire and cardio-metabolic risk factors were measured in clinics. Linear and log binomial regression were used to examine total alcohol consumption (categories: none 0 g/day; light >0-10 g/day [reference]; moderate >10-20 g/day; heavy >20-30 g/day; very heavy >30 g/day) against dichotomous metabolic syndrome and its components: waist circumference, triglycerides, high-density lipoprotein cholesterol, blood pressure and glucose. Covariates included socio-demographics, smoking, diet, physical activity, fitness, depression and anxiety.

RESULTS: Of the 2220 participants (48% males, mean (standard deviation) age 29.5 (2.5) years), most were classified in the 'light drinking' group (54.2%), less were in the 'non-drinking' (13.2%), 'heavy' (5.2%) or 'very heavy' (5.5%) drinking groups. Only moderate drinking was associated with a significantly lower prevalence of metabolic syndrome (prevalence ratio = 0.64, p < 0.05) compared with light drinking. Higher levels of alcohol consumption were associated with higher high-density lipoprotein cholesterol (beta = 0.05, ptrend < 0.001). Very heavy compared to light drinkers had higher systolic (beta = 3.01 mm Hg, p < 0.01) and diastolic (beta = 2.07 mm Hg, p < 0.05) blood pressure.

CONCLUSION: Moderate alcohol consumption was associated with a lower prevalence of MetS, and more favourable levels of lipids but not glucose or blood pressure even when compared to light consumption and with account for a range of confounding factors.

Published in Cardiovascular System

BACKGROUND: Observational studies show moderate alcohol use negatively associated with ischemic heart disease (IHD) and cardiovascular disease (CVD). However, healthier attributes among moderate users compared to never users may confound the apparent association. A potentially less biased way to examine the association is Mendelian randomization, using alcohol metabolizing genes which influence alcohol use.

METHODS: We used instrumental variable analysis with aldehyde dehydrogenase 2 (ALDH2) genotypes (AA/GA/GG) as instrumental variables for alcohol use to examine the association of alcohol use (10 g ethanol/day) with CVD risk factors (blood pressure, lipids and glucose) and morbidity (self-reported IHD and CVD) among men in the Guangzhou Biobank Cohort Study.

RESULTS: ALDH2 genotypes were a credible instrument for alcohol use (F-statistic 74.6). Alcohol was positively associated with HDL-cholesterol (0.05 mmol/L per alcohol unit, 95% confidence interval (CI) 0.02 to 0.08) and diastolic blood pressure (1.15 mmHg, 95% CI 0.23 to 2.07) but not with systolic blood pressure (1.00 mmHg, 95% CI -0.74 to 2.74), LDL-cholesterol (0.03 mmol/L, 95% CI -0.03 to 0.08), log transformed triglycerides (0.03 mmol/L, 95% CI -0.01 to 0.08) or log transformed fasting glucose (0.01 mmol/L, 95% CI -0.006 to 0.03), self-reported CVD (odds ratio (OR) 0.98, 95% CI 0.76 to 1.27) or self-reported IHD (OR 1.10, 95% CI 0.83 to 1.45).

CONCLUSION: Low to moderate alcohol use among men had the expected effects on most CVD risk factors but not fasting glucose. Larger studies are needed to confirm the null associations with IHD, CVD and fasting glucose.

Published in Cardiovascular System

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