27 July 2018 In Cancer

BACKGROUND: Individual participant data pooled analyses allow access to non-published data and statistical reanalyses based on more homogeneous criteria than meta-analyses based on systematic reviews. We quantified the impact of publication-related biases and heterogeneity in data analysis and presentation in summary estimates of the association between alcohol drinking and gastric cancer.

METHODS: We compared estimates obtained from conventional meta-analyses, using only data available in published reports from studies that take part in the Stomach Cancer Pooling (StoP) Project, with individual participant data pooled analyses including the same studies.

RESULTS: A total of 22 studies from the StoP Project assessed the relation between alcohol intake and gastric cancer, 19 had specific data for levels of consumption and 18 according to cancer location; published reports addressing these associations were available from 18, 5 and 5 studies, respectively. The summary odds ratios [OR, (95%CI)] estimate obtained with published data for drinkers vs. non-drinkers was 10% higher than the one obtained with individual StoP data [18 vs. 22 studies: 1.21 (1.07-1.36) vs. 1.10 (0.99-1.23)] and more heterogeneous (I(2): 63.6% vs 54.4%). In general, published data yielded less precise summary estimates (standard errors up to 2.6 times higher). Funnel plot analysis suggested publication bias.

CONCLUSION: Meta-analyses of the association between alcohol drinking and gastric cancer tended to overestimate the magnitude of the effects, possibly due to publication bias. Additionally, individual participant data pooled analyses yielded more precise estimates for different levels of exposure or cancer subtypes.

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.

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.

22 March 2016 In Cardiovascular System

OBJECTIVES: To investigate and quantify the potential dose-response association between alcohol consumption and risk of coronary artery disease (CAD).

METHODS: We searched the PubMed database from inception to March 2015 and reviewed the reference list of relevant articles to identify prospective studies assessing the association between alcohol consumption and risk of CAD. Study-specific relative risk (RR) estimates were combined using a random-effects model. Publication bias was estimated using Begg's funnel plot and Egger's regression asymmetry test. The meta-analysis included 18 prospective studies, with a total of 214 340 participants and 7756 CAD cases. The pooled adjusted RRs were 0.62 (95% confidence interval [CI] 0.56-0.68) for highest alcohol consumption amount versus lowest amount. Begg's and Egger's regression tests provided no evidence of substantial publication bias (P = 0.762 for Begg's test and 0.172 for Egger's test).

RESULTS: In a dose response analysis, we observed a nonlinear association between alcohol consumption and risk of CAD (P for nonlinearity <0.00). Compared with non-drinkers, the RRs (95% CI) of CAD across levels of alcohol consumption were 0.75 (0.70-0.80) for 12 g/d, 0.70 (0.66-0.75) for 24 g/d, 0.69 (0.64-0.75) for 36 g/d, 0.70 (0.64-0.77) for 60 g/d, 0.74 (0.67-0.83) for 90 g/d, and 0.83 (0.67-1.04) for 135 g/d.

CONCLUSIONS: Alcohol consumption in moderation is associated with a reduced risk of CAD with 36 grams/d of alcohol conferring a lower risk than other levels.

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