Red meat intake and the risk of endometrial cancer:Metaanalysis of observational studies

AIM:To evaluate whether red meat intake is related to the risk of endometrial cancer(EC) using meta-analysis.METHODS:We searched Pub Med,EMBASE,and the Cochrane Library up to June 2013,using common keywords related to red meat and EC.Case-control studies and cohort studies comparing the risk of endometrial cancer among categories by the amount of intake were included.Eleven case-control studies and five cohort studies met our criteria.We performed a conventional and a dose-response meta-analysis of case-control studies using the Der Simonian-Laird method for random-effects.For cohort studies we performed a conventional meta-analysis.Publication bias was evaluated using Egger's test.RESULTS:In the meta-analysis of 11 case-control studies including 5419 cases and 12654 controls,higher red meat consumption was associated with an increased risk of EC [summary relative risk(SRR) = 1.43,95%CI:1.15-1.79;I2 = 73.3% comparing extreme intake categories).In a dose-response analysis,for red meat intake of 100 g/d,SRR was 1.84(95%CI:1.64-2.05).In contrast,in the meta-analysis of five prospective studies including a total of 2549 cases among 247746 participants,no significant association between red meat intake and EC risk(SRR = 0.97,95%CI:0.85-1.11;I2 = 4.9% comparing extreme intake categories) was observed.CONCLUSION:Our meta-analysis found a significantlinear association between red meat intake and EC risk based on case-control studies but this was not confirmed in prospective studies.

Systematic review with meta-analysis of the epidemiological evidence relating smoking to type 2 diabetes

BACKGROUND Evidence relating tobacco smoking to type 2 diabetes has accumulated rapidly in the last few years,rendering earlier reviews considerably incomplete.AIM To review and meta-analyse evidence from prospective studies of the relationship between smoking and the onset of type 2 diabetes.METHODS Prospective studies were selected if the population was free of type 2 diabetes at baseline and evidence was available relating smoking to onset of the disease.Papers were identified from previous reviews,searches on Medline and Embase and reference lists.Data were extracted on a range of study characteristics and relative risks(RRs)were extracted comparing current,ever or former smokers with never smokers,and current smokers with non-current smokers,as well as by amount currently smoked and duration of quitting.Fixed-and random-effects estimates summarized RRs for each index of smoking overall and by various subdivisions of the data:Sex;continent;publication year;method of diagnosis;nature of the baseline population(inclusion/exclusion of pre-diabetes);number of adjustment factors;cohort size;number of type 2 diabetes cases;age;length of follow-up;definition of smoking;and whether or not various factors were adjusted for.Tests of heterogeneity and publication bias were also conducted.RESULTS The literature searches identified 157 relevant publications providing results from 145 studies.Fifty-three studies were conducted in Asia and 53 in Europe,with 32 in North America,and seven elsewhere.Twenty-four were in males,10 in females and the rest in both sexes.Fifteen diagnosed type 2 diabetes from selfreport by the individuals,79 on medical records,and 51 on both.Studies varied widely in size of the cohort,number of cases,length of follow-up,and age.Overall,random-effects estimates of the RR were 1.33[95%confidence interval(CI):1.28-1.38]for current vs never smoking,1.28(95%CI:1.24-1.32)for current vs non-smoking,1.13(95%CI:1.11-1.16)for former vs never smoking,and 1.25(95%CI:1.21-1.28)for ever vs never smoking based on,respectively,99,156,100 and 100 individual risk estimates.Risk estimates were generally elevated in each subdivision of the data by the various factors considered(exceptions being where numbers of estimates in the subsets were very low),though there was significant(P<0.05)evidence of variation by level for some factors.Dose-response analysis showed a clear trend of increasing risk with increasing amount smoked by current smokers and of decreasing risk with increasing time quit.There was limited evidence of publication bias.CONCLUSION The analyses confirmed earlier reports of a modest dose-related association of current smoking and a weaker dose-related association of former smoking with type 2 diabetes risk.

Efficacy and Safety of Aspirin for Prevention of Hepatocellular Carcinoma:An Updated Meta-analysis

Background and Aims:Previous meta-analyses have shown that aspirin use may reduce the risk of hepatocellular carcinoma(HCC).However,the optimal dose,frequency,and duration of aspirin use or the safety and efficacy of aspirin in target populations for HCC prevention remain unclear.The study aim was to investigate the efficacy and safety of aspirin for prevention of HCC.Methods:Publications were retrieved by a comprehensive literature research of several databases.Based on a random-effects model,hazard ratios(HRs)and the corresponding 95%confidence intervals(CIs)were used to assess the pooled risk.The dose-response relationship between aspirin use and HCC risk was assessed with a restricted cubic spline model.Results:Twenty-two studies were included in the metaanalysis.Aspirin use was associated with a reduced risk of HCC(HR=0.64,95%CI:0.56–0.75).The effect was robust across sex and age;however,women and the non-elderly had the greatest benefit from aspirin use.The preventive effect was well reproduced in those with comorbidities.Daily use and long-term use of aspirin appeared to offer greater benefits.Aspirin 100 mg/d was associated with maximum reduction of HCC risk.Aspirin use did slightly increase the risk of bleeding(HR=1.14,95%CI:1.02–1.27).Conclusions:Our meta-analysis confirmed that use of aspirin significantly reduced the incident risk of HCC.Regular and long-term aspirin use offers a greater advantage.Aspirin use was associated with an increased risk of bleeding.We recommend 100 mg/d aspirin as a feasible dose for further research on primary prevention of HCC in a broad at-risk population.