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

BACKGROUND: Alcohol is a possible risk factor for abdominal aortic aneurysm (AAA), but evidence from individual studies is weak and inconsistent. Existing narrative reviews suggest the possibility of non-linear associations. The aim here was to quantify any association using a systematic literature review, followed by dose-response meta-analysis of prospective studies.

METHODS: MEDLINE, Embase and Web of Science were searched systematically to January 2017 for relevant prospective studies of alcohol consumption and AAA risk. Summary estimates of highest versus lowest levels of consumption, and linear and non-linear dose-response curves were quantified using random-effects models.

RESULTS: Eleven relevant cohorts were identified describing results from 3580 individuals with among 473 092 participants. Data were extracted from ten cohorts for meta-analyses of high versus low levels of alcohol consumption (risk ratio for AAA 0.93, 95 per cent c.i. 0.78 to 1.11; P = 0.4, I2 = 47 per cent). The linear dose-response risk ratio for AAA, derived from 11 cohorts, was 1.00 (0.97 to 1.04) per 8 g alcohol per day (P = 0.9, I2 = 73 per cent). Non-linear dose-response results showed a tick-shaped curve with lower risk up to 2 units/day, but increasing risk beyond that (P = 0.05). The increase in risk beyond 2 units/day was stronger in men than in women.

CONCLUSION: Although the linear dose-response analysis revealed little evidence of an association between alcohol consumption and AAA risk, a tick-shaped trend in the association was observed. This non-linear dose-response analysis revealed reduced risks for alcohol consumption below 2 units/day, masking increased risks for 2 or more units/day.

Published in Cardiovascular System

BACKGROUND: Whilst high levels of alcohol consumption are known to be associated with atrial fibrillation (AF), it is unclear if any level of alcohol consumption can be recommended to prevent the onset of the condition. The aim of this review is to characterise the association between chronic alcohol intake and incident AF.

METHODS AND RESULTS: Electronic literature searches were undertaken using PubMed and Embase databases up to 1 February 2016 to identify studies examining the impact of alcohol on the risk of incident AF. Prospective studies reporting on at least three levels of alcohol intake and published in English were eligible for inclusion. Studies of a retrospective or case control design were excluded. The primary study outcome was development of incident AF. Consistent with previous studies, high levels of alcohol intake were associated with an increased incident AF risk (HR 1.34, 95% CI 1.20-1.49, p<0.001). Moderate levels of alcohol intake were associated with a heightened AF risk in males (HR 1.26, 95% CI 1.04-1.54, p=0.02) but not females (HR 1.03, 95% CI 0.86-1.25, p=0.74). Low alcohol intake, of up to 1 standard drink (SD) per day, was not associated with AF development (HR 0.95, 95% CI 0.85-1.06, p=0.37).

CONCLUSIONS: Low levels of alcohol intake are not associated with the development of AF. Gender differences exist in the association between moderate alcohol intake and AF with males demonstrating greater increases in risk, whilst high alcohol intake is associated with a heightened AF risk across both genders.

Published in Cardiovascular System

BACKGROUND: Racial disparities in the incidence of major cancers may be attributed to differences in the prevalence of established, modifiable risk factors such as obesity, smoking, physical activity and diet.

METHODS: Data from a prospective cohort of 566,398 adults aged 50-71 years, 19,677 African-American and 450,623 Whites, was analyzed. Baseline data on cancer-related risk factors such as smoking, alcohol, physical activity and dietary patterns were used to create an individual adherence score. Differences in adherence by race, gender and geographic region were assessed using descriptive statistics, and Cox proportional hazards models were used to determine the association between adherence and cancer incidence.

RESULTS: Only 1.5% of study participants were adherent to all five cancer-related risk factor guidelines, with marked race-, gender- and regional differences in adherence overall. Compared with participants who were fully adherent to all five cancer risk factor criteria, those adherent to one or less had a 76% increased risk of any cancer incidence (HR: 1.76, 95% CI: 1.70 - 1.82), 38% increased risk of breast cancer (HR: 1.38, 95% CI: 1.25 - 1.52), and doubled the risk of colorectal cancer (HR: 2.06, 95% CI: 1.84 - 2.29). However, risk of prostate cancer was lower among participants adherent to one or less compared with those who were fully adherent (HR: 0.79, 95% CI: 0.75 - 0.85). The proportion of cancer incident cases attributable to low adherence was higher among African-Americans compared with Whites for all cancers (21% vs. 19%), and highest for colorectal cancer (25%) regardless of race.

CONCLUSION: Racial differences in the proportion of cancer incidence attributable to low adherence suggests unique opportunities for targeted cancer prevention strategies that may help eliminate racial disparities in cancer burden among older US adults.

Published in Cancer

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