18 May 2018 In Cancer

Objective: To investigate the impact of moderate wine consumption on the risk of prostate cancer (PCa). We focused on the differential effect of moderate consumption of red versus white wine.

Design: This study was a meta-analysis that includes data from case-control and cohort studies.

Materials and methods: A systematic search of Web of Science, Medline/PubMed, and Cochrane library was performed on December 1, 2017. Studies were deemed eligible if they assessed the risk of PCa due to red, white, or any wine using multivariable logistic regression analysis. We performed a formal meta-analysis for the risk of PCa according to moderate wine and wine type consumption (white or red). Heterogeneity between studies was assessed using Cochrane's Q test and I(2) statistics. Publication bias was assessed using Egger's regression test.

Results: A total of 930 abstracts and titles were initially identified. After removal of duplicates, reviews, and conference abstracts, 83 full-text original articles were screened. Seventeen studies (611,169 subjects) were included for final evaluation and fulfilled the inclusion criteria. In the case of moderate wine consumption: the pooled risk ratio (RR) for the risk of PCa was 0.98 (95% CI 0.92-1.05, p=0.57) in the multivariable analysis. Moderate white wine consumption increased the risk of PCa with a pooled RR of 1.26 (95% CI 1.10-1.43, p=0.001) in the multi-variable analysis. Meanwhile, moderate red wine consumption had a protective role reducing the risk by 12% (RR 0.88, 95% CI 0.78-0.999, p=0.047) in the multivariable analysis that comprised 222,447 subjects.

Conclusions: In this meta-analysis, moderate wine consumption did not impact the risk of PCa. Interestingly, regarding the type of wine, moderate consumption of white wine increased the risk of PCa, whereas moderate consumption of red wine had a protective effect. Further analyses are needed to assess the differential molecular effect of white and red wine conferring their impact on PCa risk.

04 August 2017 In Pregnant Women

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.

04 August 2017 In Cancer

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.

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

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