Objective: To estimate the prevalence of alcohol consumption during pregnancy among the general population of Latin America and the Caribbean, by country, in 2012.

Methods: Three steps were taken: a comprehensive, systematic literature search; meta-analyses, assuming a random-effects model for countries with published studies; and regression modelling (data prediction) for countries with either no published studies or too few to obtain an estimate.

Results: Based on 24 existing studies, the pooled prevalence of alcohol consumption during pregnancy among the general population was estimated for Brazil (15.2%; 95% confidence interval [95%CI]: 10.4%-20.8%) and Mexico (1.2%; 95%CI: 0.0%-2.7%). The prevalence of alcohol consumption during pregnancy among the general population was predicted for 31 countries and ranged from 4.8% (95%CI: 4.2%-5.4%) in Cuba to 23.3% (95%CI: 20.1%-26.5%) in Grenada.

Conclusions: Greater prevention efforts and measures are needed in the countries of Latin America and the Caribbean to prevent pregnant women from consuming alcohol during pregnancy and decrease the rates of Fetal Alcohol Spectrum Disorder. Additional high quality studies on the prevalence of alcohol consumption during pregnancy in Latin America and the Caribbean are also needed.

Published in Pregnant Women

We performed this meta-analysis to explore the precise quantification relationship between alcohol consumption and gastric cancer and to provide evidence for preventing gastric cancer. We searched PubMed, Embase, and Web of Science for articles published up to December 2016, and identified 23 cohort studies that included a total population of 5,886,792 subjects. We derived meta-analytic estimates using random-effects models, taking into account correlations between estimates. We also investigated the dose-response relationship between gastric cancer risk and alcohol consumption. We found that alcohol consumption increased gastric cancer risk, where the summary risk ratio was 1.17 (95% confidence interval (CI): 1.00-1.34; I2 = 79.6%, p < 0.05. The dose-response analysis showed that every 10 g/d increment in alcohol consumption was associated with 7% increased gastric cancer risk (95% CI 1.02-1.12; I2 = 28.9%, p = 0.002). This meta-analysis provides evidence that alcohol consumption is an important risk factor of the incidence of gastric cancer.

Published in Cancer

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

Published in General Health

BACKGROUND & AIMS: Controversy exists on the association between alcohol consumption and risk of heart failure (HF). We carried out a meta-analysis to summarize available prospective data on alcohol consumption and HF.

METHODS: We searched PubMed for relevant studies published until January 1, 2017. Relative risk (RR) estimates from individual studies were pooled in a random-effects meta-analysis.

RESULTS: A total of 13 prospective studies, with 13,738 HF cases and 355,804 participants, were included in the meta-analysis. Light alcohol drinking (0.1-7 drinks/week) was inversely associated with risk of HF (RR, 0.86; 95% confidence interval, 0.81-0.90). There was no statistically significant association between moderate (7.1-14 drinks/week), high (14.1-28 drinks/week), or heavy (>28 drinks/week) alcohol consumption and HF risk. Former drinking was associated with an increased risk of HF compared with never or occasional drinking (RR, 1.22; 95% confidence interval, 1.11-1.33).

CONCLUSIONS: This meta-analysis found that light alcohol drinking was associated with a lower risk of HF. Former drinking was associated with a higher risk of HF.

Published in Cardiovascular System
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