01 February 2017 In Cardiovascular System
BACKGROUND: Many studies suggest that mild alcohol consumption can help avert cardiovascular disease (CVD). This study investigated the association between alcohol consumption and CVD incidence, and assessed whether this differed by reference group classification. As alcohol consumption amounts may change over time, the results of simple and time-dependent analyses were compared. METHODS: Data were from a community-based cohort study on 40- to 69-year-old Koreans recruited in 2001 to 2002. A total of 8,330 participants were followed up for 10 years and classed as nondrinkers (0 g/d), drinker group 1 (/=15 g/d). The risk of CVD, including myocardial infarction and coronary artery disease, was compared among groups using simple and time-dependent Cox analysis. Occasional drinkers (
01 February 2017 In Cancer

Genome-wide association studies (GWAS) have identified many genetic susceptibility loci for colorectal cancer (CRC). However, variants in these loci explain only a small proportion of familial aggregation, and there are likely additional variants that are associated with CRC susceptibility. Genome-wide studies of gene-environment interactions may identify variants that are not detected in GWAS of marginal gene effects. To study this, we conducted a genome-wide analysis for interaction between genetic variants and alcohol consumption and cigarette smoking using data from the Colon Cancer Family Registry (CCFR) and the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Interactions were tested using logistic regression. We identified interaction between CRC risk and alcohol consumption and variants in the 9q22.32/HIATL1 (Pinteraction = 1.76x10-8; permuted p-value 3.51x10-8) region. Compared to non-/occasional drinking light to moderate alcohol consumption was associated with a lower risk of colorectal cancer among individuals with rs9409565 CT genotype (OR, 0.82 [95% CI, 0.74-0.91]; P = 2.1x10-4) and TT genotypes (OR,0.62 [95% CI, 0.51-0.75]; P = 1.3x10-6) but not associated among those with the CC genotype (p = 0.059). No genome-wide statistically significant interactions were observed for smoking. If replicated our suggestive finding of a genome-wide significant interaction between genetic variants and alcohol consumption might contribute to understanding colorectal cancer etiology and identifying subpopulations with differential susceptibility to the effect of alcohol on CRC risk.

01 February 2017 In Cancer

It is still inconclusive whether alcohol consumption affects the risk of thyroid cancer. We conducted a meta-analysis of available epidemiological data to address this issue. Compared with nondrinkers, the pooled relative risks (RRs) and corresponding 95% confidential intervals (CIs) of thyroid cancer were 0.80 (95% CI 0.71-0.90) for any drinkers, 0.81 (95% CI 0.70-0.93) for light and 0.71 (95% CI 0.63-0.79) for moderate drinkers. The dose-response analysis suggested that there is no evidence of a dose-risk relationship between alcohol intaking and thyroid cancer risk (P = 0.112). Eligible studies were identified by searching PubMed and EMbase databases. A total of 24 studies, included 9,990 cases with thyroid cancer, were included in this meta-analysis. We defined light alcohol intake as one drink/day. The summary risk estimates were calculated by the random effects model. A dose-response analysis was also conducted for modeling the dose-risk relation. This meta-analysis confirmed an inverse association between alcohol consumption and thyroid cancer risk. Further studies are needed to better understand the potential mechanisms underlying this association.

01 February 2017 In Cancer

BACKGROUND We sought to determine by meta-analysis the relationship between drinking alcohol and the risk of gastric cancer.

MATERIAL AND METHODS A systematic Medline search was performed to identify all published reports of drinking alcohol and the associated risk of gastric cancer. Initially we retrieved 2,494 studies, but after applying inclusion and exclusion criteria, only ten studies were found to be eligible for our meta-analysis.

RESULTS Our meta-analysis showed that alcohol consumption elevated the risk of gastric cancer with an odds ratio (OR) of 1.39 (95% CI 1.20-1.61). Additionally, subgroup analysis showed that only a nested case-control report from Sweden did not support this observation. Subgroup analysis of moderate drinking and heavy drinking also confirmed that drinking alcohol increased the risk of gastric cancer. Publication bias analysis (Begg's and Egger's tests) showed p values were more than 0.05, suggesting that the 10 articles included in our analysis did not have a publication bias.

CONCLUSIONS The results from this meta-analysis support the hypothesis that alcohol consumption can increase the risk of gastric cancer; suggesting that effective moderation of alcohol drinking may reduce the risk of gastric cancer.

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