22 June 2017 In General Health

Alcohol consumption is a complex trait determined by both genetic and environmental factors, and is correlated with the risk of alcohol use disorders. Although a small number of genetic loci have been reported to be associated with variation in alcohol consumption, genetic factors are estimated to explain about half of the variance in alcohol consumption, suggesting that additional loci remain to be discovered. We conducted a genome-wide association study (GWAS) of alcohol consumption in the large Genetic Epidemiology Research in Adult Health and Aging (GERA) cohort, in four race/ethnicity groups: non-Hispanic whites, Hispanic/Latinos, East Asians and African Americans. We examined two statistically independent phenotypes reflecting subjects' alcohol consumption during the past year, based on self-reported information: any alcohol intake (drinker/non-drinker status) and the regular quantity of drinks consumed per week (drinks/week) among drinkers. We assessed these two alcohol consumption phenotypes in each race/ethnicity group, and in a combined trans-ethnic meta-analysis comprising a total of 86 627 individuals. We observed the strongest association between the previously reported single nucleotide polymorphism (SNP) rs671 in ALDH2 and alcohol drinker status (odd ratio (OR)=0.40, P=2.28 x 10-72) in East Asians, and also an effect on drinks/week (beta=-0.17, P=5.42 x 10-4) in the same group. We also observed a genome-wide significant association in non-Hispanic whites between the previously reported SNP rs1229984 in ADH1B and both alcohol consumption phenotypes (OR=0.79, P=2.47 x 10-20 for drinker status and beta=-0.19, P=1.91 x 10-35 for drinks/week), which replicated in Hispanic/Latinos (OR=0.72, P=4.35 x 10-7 and beta=-0.21, P=2.58 x 10-6, respectively). Although prior studies reported effects of ADH1B and ALDH2 on lifetime measures, such as risk of alcohol dependence, our study adds further evidence of the effect of the same genes on a cross-sectional measure of average drinking. Our trans-ethnic meta-analysis confirmed recent findings implicating the KLB and GCKR loci in alcohol consumption, with strongest associations observed for rs7686419 (beta=-0.04, P=3.41 x 10-10 for drinks/week and OR=0.96, P=4.08 x 10-5 for drinker status), and rs4665985 (beta=0.04, P=2.26 x 10-8 for drinks/week and OR=1.04, P=5 x 10-4 for drinker status), respectively. Finally, we also obtained confirmatory results extending previous findings implicating AUTS2, SGOL1 and SERPINC1 genes in alcohol consumption traits in non-Hispanic whites.Molecular Psychiatry advance online publication, 9 May 2017; doi:10.1038/mp.2017.101

01 February 2017 In Social and Cultural Aspects

BACKGROUND: Alcohol consumption is influenced by a complex causal system of interconnected psychological, behavioural, social, economic, legal and environmental factors. These factors are shaped by governments (eg, licensing laws and taxation), by consumers (eg, patterns of alcohol consumption drive demand) and by alcohol industry practices, such as advertising. The marketing and advertising of alcoholic products contributes to an 'alcogenic environment' and is a modifiable influence on alcohol consumption and harm. The public health perspective is that there is sufficient evidence that alcohol advertising influences consumption. The alcohol industry disputes this, asserting that advertising only aims to help consumers choose between brands.

METHODS: We review the evidence from recent systematic reviews, including their theoretical and methodological assumptions, to help understand what conclusions can be drawn about the relationships between alcohol advertising, advertising restrictions and alcohol consumption.

CONCLUSIONS: A wide evidence base needs to be drawn on to provide a system-level overview of the relationship between alcohol advertising, advertising restrictions and consumption. Advertising aims to influence not just consumption, but also to influence awareness, attitudes and social norms; this is because advertising is a system-level intervention with multiple objectives. Given this, assessments of the effects of advertising restrictions which focus only on sales or consumption are insufficient and may be misleading. For this reason, previous systematic reviews, such as the 2014 Cochrane review on advertising restrictions (Siegfried et al) contribute important, but incomplete representations of 'the evidence' needed to inform the public health case for policy decisions on alcohol advertising. We conclude that an unintended consequence of narrow, linear framings of complex system-level issues is that they can produce misleading answers. Systems problems require systems perspectives.

21 September 2016 In Cancer

PURPOSE: Alcohol intake may be associated with cancer risk, but epidemiologic evidence for prostate cancer is inconsistent. We aimed to prospectively investigate the association between midlife alcohol intake and drinking patterns with future prostate cancer risk and mortality in a population-based cohort of Finnish twins.

METHODS: Data were drawn from the Older Finnish Twin Cohort and included 11,372 twins followed from 1981 to 2012. Alcohol consumption was assessed by questionnaires administered at two time points over follow-up. Over the study period, 601 incident cases of prostate cancer and 110 deaths from prostate cancer occurred. Cox regression was used to evaluate associations between weekly alcohol intake and binge drinking patterns with prostate cancer risk and prostate cancer-specific mortality. Within-pair co-twin analyses were performed to control for potential confounding by shared genetic and early environmental factors.

RESULTS: Compared to light drinkers (14 drinks/week) were at a 1.46-fold higher risk (HR 1.46; 95 % CI 1.12, 1.91) of prostate cancer, adjusting for important confounders. Among current drinkers, binge drinkers were at a significantly increased risk of prostate cancer (HR 1.28; 95 % CI 1.06, 1.55) compared to non-binge drinkers. Abstainers were at a 1.90-fold higher risk (HR 1.90; 95 % CI 1.04, 3.47) of prostate cancer-specific mortality compared to light drinkers, but no other significant associations for mortality were found. Co-twin analyses suggested that alcohol consumption may be associated with prostate cancer risk independent of early environmental and genetic factors.

CONCLUSION: Heavy regular alcohol consumption and binge drinking patterns may be associated with increased prostate cancer risk, while abstinence may be associated with increased risk of prostate cancer-specific mortality compared to light alcohol consumption.

27 January 2016 In Cancer

PURPOSE: Alcohol is an established breast cancer risk factor, but there is little evidence on whether the association differs between African Americans and whites.

METHODS: Invasive breast cancers (n = 1,795; 1,014 white, 781 African American) and age- and race-matched controls (n = 1,558; 844 white, 714 African American) from the Carolina Breast Cancer Study (Phases I-II) were used to estimate odds ratios (ORs) and 95 % confidence interval (CI) for pre-diagnosis drinks per week and breast cancer risk.

RESULTS: African American controls reported lower alcohol intake than white controls across all age groups. Light drinking (0 to 7 drinks per week had an elevated risk compared to light drinkers [adjusted OR, 95% CI 1.62 (1.03-2.54)]. A weaker association was observed among whites [adjusted OR, 95% CI 1.20 (0.87-1.67)]. The association of >7 drinks per week with estrogen receptor-negative [adjusted OR, 95% CI 2.17 (1.25-3.75)] and triple-negative [adjusted OR, 95% CI 2.12 (1.12-4.04)] breast cancers was significant for African American, but not white women. We observed significantly elevated ORs for heavy intake at ages 50 years of age for African American women only. We found no evidence of statistical interaction between alcohol intake and oral contraceptive use or smoking.

CONCLUSIONS: Drinking more than seven alcoholic beverages per week increased invasive breast cancer risk among white and African American women, with significant increases only among African American women. Genetic or environmental factors that differ by race may mediate the alcohol-breast cancer risk association.

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