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.

15 December 2016 In Drinking & Eating Patterns

PURPOSE: We seek answers to three questions about adolescent risk of starting to drink alcoholic beverages: (1) in new United States (US) data, can we reproduce a recently discovered female excess risk? (2) has a female excess risk emerged in European countries? and (3) might the size of country-level female-male differences (FMD) be influenced by macro-level gender equality and development processes?

METHODS: Estimates are from US and European surveys of adolescents, 2010-2014. For US estimates, newly incident drinking refers to consuming the first full drink during the 12-month interval just prior to assessment. For all countries, lifetime cumulative incidence of drinking refers to any drinking before assessment of the sampled 15-16 years.

RESULTS: Cumulative meta-analysis summary estimates from the US show a highly reproducible female excess in newly incident drinking among 12-17 years (final estimated female-male difference in risk, FMD = 2.1%; 95% confidence interval = 1.5%, 2.7%). Several European countries show female excess risk, estimated as lifetime cumulative incidence of drinking onsets before age 17 years. At the country level, the observed magnitude of FMD in risk is positively associated with the Gender Development Index (especially facets related to education and life expectancy of females relative to males), and with residence in a higher income European country.

CONCLUSIONS: New FMD estimates support reproducibility of a female excess risk in the US. In Europe, evidence of a female excess is modest. Educational attainment, life expectancies, and income merit attention in future FMD research on suspected macro-level processes that influence drinking onsets.

15 December 2016 In Cardiovascular System

BACKGROUND: Whether light-to-moderate alcohol consumption is protective against stroke, and whether any association differs by stroke type, is controversial. We conducted a meta-analysis to summarize the evidence from prospective studies on alcohol drinking and stroke types.

METHODS: Studies were identified by searching PubMed to September 1, 2016, and reference lists of retrieved articles. Additional data from 73,587 Swedish adults in two prospective studies were included. Study-specific results were combined in a random-effects model.

RESULTS: The meta-analysis included 27 prospective studies with data on ischemic stroke (25 studies), intracerebral hemorrhage (11 studies), and/or subarachnoid hemorrhage (11 studies). Light and moderate alcohol consumption was associated with a lower risk of ischemic stroke, whereas high and heavy drinking was associated with an increased risk; the overall RRs were 0.90 (95 % CI, 0.85-0.95) for less than 1 drink/day, 0.92 (95 % CI, 0.87-0.97) for 1-2 drinks/day, 1.08 (95 % CI, 1.01-1.15) for more than 2-4 drinks/day, and 1.14 (95 % CI, 1.02-1.28) for more than 4 drinks/day. Light and moderate alcohol drinking was not associated with any hemorrhagic stroke subtype. High alcohol consumption (>2-4 drinks/day) was associated with a non-significant increased risk of both hemorrhagic stroke subtypes, and the relative risk for heavy drinking (>4 drinks/day) were 1.67 (95 % CI, 1.25-2.23) for intracerebral hemorrhage and 1.82 (95 % CI, 1.18-2.82) for subarachnoid hemorrhage.

CONCLUSION: Light and moderate alcohol consumption was inversely associated only with ischemic stroke, whereas heavy drinking was associated with increased risk of all stroke types with a stronger association for hemorrhagic strokes.

27 October 2016 In Cardiovascular System

The association between alcohol consumption and the risk of subarachnoid hemorrhage (SAH) is inconsistent. Thus, meta- and a dose-response analyses are presented with the purpose of assessing their associations. A systematic literature search was performed using Pubmed and Embase electronic databases for pertinent observational studies. Random-effects or fixed-effect models were employed to combine the estimates of the relative risks (RRs) with corresponding 95% confidence intervals (CIs). A dose-response pattern was conducted for further analysis. The current meta-analysis includes 14 observational studies reporting data on 483,553 individuals and 2,556 patients. The combined RRs of light alcohol consumption (30 g/day) when compared with no alcohol consumption, as demonstrated by a result of 1.78 (95% CI: 1.46, 2.17). Dose-response analysis showed evidence of a linear association (P=0.0125) between alcohol consumption and SAH. The risk of SAH increased by 12.1% when alcohol consumption was increased by 10 g/day. Therefore, heavy alcohol consumption was found to be associated with an increased risk of SAH. Furthermore, the association between SAH and alcohol consumption has clinical relevance with regard to risk factor modification and the primary and secondary prevention of SAH.

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