Alcohol drinking and all cancer mortality: a meta-analysis

BackgroundEpidemiological studies have suggested an inconsistent relationship between alcohol drinking and risk of all cancer mortality. As far as we know, no meta-analysis has been conducted to explore this issue.Patients and methodsWe carried out a PubMed search to find relevant articles published before April 2012 in English. Categorical and dose–response meta-analyses were conducted to identify the impact of alcohol drinking on all cancer mortality. Potential sources of heterogeneity were detected by meta-regression and stratification analyses. Sensitivity and cumulative meta-analyses were also carried out.ResultsEighteen independent cohort studies met the inclusion criteria. Compared with non/occasional drinkers, the pooled relative risks (RRs) were 0.91 [95% confidence interval (CI) 0.89–0.94] for light, 1.02 (95% CI 0.99–1.06) for moderate, and 1.31 (95% CI 1.23–1.39) for heavy drinkers. Former drinkers presented a higher risk (RR = 1.32, 95% CI 1.15–1.50) than current drinkers (RR = 1.06, 95% CI 0.98–1.16). There was a J-shaped relationship between all cancer mortality and alcohol consumption in males but not in females.ConclusionsThis meta-analysis confirms the health hazards of heavy drinking (≥50 g/day) and benefits of light drinking (≤12.5 g/day). Large-sample, well-designed, prospective epidemiological studies, especially on heavy drinking among women, should be developed in future.     

Alcohol drinking and non-Hodgkin lymphoma risk: a systematic review and a meta-analysis

BackgroundWhether an association between alcohol drinking and non-Hodgkin lymphoma (NHL) risk exists is an open question. In order to provide quantification of the issue, we carried out a meta-analysis of published data.MethodsWe identified 21 case–control and 8 cohort studies, including a total of 18 759 NHL cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates.ResultsThe overall relative risk (RR) of NHL for drinkers versus non-drinkers was 0.85 [95% confidence interval (CI) 0.79–0.91]. Compared with non-drinkers, the pooled RRs were 0.88 for light (≤1 drink per day), 0.87 for moderate (1 to <4 drinks per day), and 0.84 for heavy (≥4 drinks per day) alcohol drinking. There was no association for light drinkers in cohort studies, whereas for moderate and heavy drinkers, the RRs were similar in case–control (0.85 for moderate, 0.92 for heavy) and cohort (0.89 for moderate, 0.79 for heavy) studies. The inverse relation with alcohol consumption (drinkers versus non-drinkers) was similar in men (RR = 0.83) and women (RR = 0.86), but apparently stronger in studies from Asia (RR = 0.69) than other world areas (RR = 0.88).ConclusionThis meta-analysis provides quantitative evidence of a favourable role of alcohol drinking on NHL risk, though the lack of a biological explanation suggests caution in the interpretation of results.     

Wine drinking and epithelial ovarian cancer risk: a meta-analysis

Objective

Wine has been the focus in the prevention of epithelial ovarian cancer (EOC) development because resveratrol abundant in wine has anti-carcinogenic properties. However, epidemiologic results have been heterogenous in the chemopreventive effect of wine on the development of EOC. Thus, we performed a meta-analysis for comparing EOC risk between wine and never drinkers using previous related studies.

Methods

After extensive search of the literature between January 1986 and December 2008, we analyzed 10 studies (3 cohort and 7 case control studies) with 135,871 women, who included 65,578 of wine and 70,293 of never drinkers.

Results

In all studies, there was no significant difference in EOC risk between wine and never drinkers (odds ratio [OR], 1.13; 95% confidence interval [CI], 0.92 to 1.38; random effects). When we performed re-analysis according to the study design, 3 cohort and 7 case control studies showed that there were also no significant differences in EOC risk between wine and never drinkers, respectively (OR, 1.44 and 1.04; 95% CI, 0.74 and 2.82 and 0.88 to 1.22; random effects). In sub-analyses using 2 case-control studies, EOC risk was not different between former and never drinkers (OR, 1.12; 95% CI, 0.87 to 1.44; fixed effect), and between current and former drinkers (OR, 0.74; 95% CI, 0.41 to 1.34; random effects).

Conclusion

Although resveratrol, abundantly found in wine, is a promising naturally occurring compound with chemopreventive properties on EOC in preclinical studies, this meta-analysis suggests the epidemiologic evidence shows no association between wine drinking and EOC risk.     

Alcohol drinking and risk of renal cell carcinoma: results of a meta-analysis

BackgroundThe role of alcohol consumption in relation with renal cell carcinoma is still unclear; a few studies have reported a beneficial effect of moderate levels of alcohol consumption, whereas it remains still under debate whether there is a dose–response association.Materials and methodsTwenty observational studies (4 cohort, 1 pooled and 15 case–control) reporting results on at least three levels of alcohol consumption were selected through a combined search with PubMed and EMBASE of articles published before November 2010. Overall relative risks (RRs) and 95% confidence intervals (CIs) were estimated using random-effects models, and both second-order fractional polynomials and random effect meta-regression models were implemented for the study of dose–risk relation.ResultsThe estimated RRs were 0.85 (95% CI: 0.80–0.92) for any alcohol drinking, 0.90 (95% CI: 0.83–0.97) for light drinking (0.01–12.49 g/day), 0.79 (95% CI: 0.71–0.88) for moderate drinking (12.5–49.9 g/day) and 0.89 (95% CI: 0.58–1.39) for heavy drinking (≥50 g/day), respectively.ConclusionOur meta-analysis supports the hypothesis of a negative effect of moderate alcohol consumption on the risk of renal cell cancer.     

Alcohol intake and renal cell cancer risk: a meta-analysis

Background:

An inverse association between alcoholic beverage intake and risk of renal cell cancer has been suggested in recent studies.

Methods:

We examined the association between alcoholic beverages and renal cell cancer risk in a meta-analysis. We identified relevant studies by searching the database of PubMed, EMBASE, and MEDLINE published through August 2011. We combined the study-specific relative risks (RRs) using a random-effects model.

Results:

A total of 20 case–control studies, 3 cohort studies, and 1 pooled analysis of cohort studies were included in the meta-analysis. We observed that alcoholic beverage intake was associated with a lower risk of renal cell cancer in combined analysis of case–control and cohort studies; for total alcoholic beverage intake, combined RRs (95% confidence intervals) comparing top with bottom categories were 0.76 (0.68–0.85) in case–control studies, and 0.71 (0.63–0.78) in cohort studies (P for difference by study design=0.02). The inverse associations were observed for both men and women and for each specific type alcoholic beverage (beer, wine, and liquor). Also, we found that one drink per day of alcoholic beverage conferred the reduction in renal cell cancer risk, but further drinking above that level did not add benefit.

Conclusion:

The findings from our meta-analysis support the hypothesis that alcoholic beverage intake is inversely associated with a lower risk of renal cell cancer, with moderate consumption conferring the protection and higher consumption conferring no additional benefits.     

Coffee drinking and risk of bladder cancer

The relationship between coffee drinking and risk of bladder cancer was assessed with the use of data from a case-control study of bladder cancer. Incident cases (2,982) and general population controls (5,782) were interviewed. Overall, the relative risk (RR) of bladder cancer for subjects who had ever drunk coffee was estimated as 1.4 (95% confidence interval = 1.1-1.8). There was no consistent relation between the RR estimate and the current consumption level. Among men who drank coffee, those who drank more than 49 cupfuls of coffee per week had an apparent excess in risk, but women who drank that much had an apparent deficit in risk.     

Alcohol consumption and lung cancer risk in never smokers: a meta-analysis

BackgroundThe role of alcohol consumption as an independent risk factor for lung cancer is controversial. Since drinking and smoking are strongly associated, residual confounding by smoking may bias the estimation of alcohol consumption and lung cancer risk relation. Therefore, we undertook a meta-analysis to quantitatively assess the association between alcohol and risk of lung cancer in never smokers.MethodsAfter a literature search in Medline, we included all case–control and cohort studies published up to January 2010 that reported an estimate of the association between alcohol intake and lung cancer risk in never smokers.ResultsWe selected 10 articles, including 1913 never smoker lung cancer cases. The random-effects pooled relative risk (RR) for drinkers versus nondrinkers was 1.21 [95% confidence interval (CI) 0.95–1.55]. The same figure was 1.05 (95% CI 0.89–1.23) after the exclusion of one outlier study. At the dose–response analysis, RR for an increase in alcohol intake of 10 g/day was 1.01 (95% CI 0.92–1.10).ConclusionsAlcohol consumption was not associated with lung cancer risk in never smokers. Even if the synergistic effect of smoking and alcohol cannot be ruled out, our results suggest that alcohol does not play an independent role in lung cancer etiology.     

Alcohol intake and endometrial cancer risk: a meta-analysis of prospective studies

Background:

Studies on alcohol intake in relation to endometrial cancer risk have produced inconsistent results.

Methods:

For a meta-analysis, we identified cohort studies of alcohol and endometrial cancer by a literature search of Pub-Med and Embase up to 1 March 2010 and by searching the reference lists of relevant articles.

Results:

Seven cohort studies, including 1 511 661 participants and 6086 endometrial cancer cases, were included in the dose–response random-effect meta-regression model. Compared with non-drinkers, women drinking less than 1 drink of alcohol (13 g of ethanol) per day had a lower risk for endometrial cancer; this risk was lower by 4% (95% confidence interval (95% CI): 0.93–1.00) for consumption up to 0.5 drink per day and by 7% (95% CI: 0.85–1.02) for consumption up to 1 drink. However, we found evidence of an increased risk for endometrial cancer for intakes higher than two alcoholic drinks per day: compared with non-drinkers, the risk was higher by 14% (95% CI: 0.95–1.36) for 2–2.5 drinks per day and by 25% (95% CI: 0.98–1.58) for >2.5 drinks per day.

Conclusion:

Our meta-analysis indicates a possible J-shaped relationship between alcohol intake and endometrial cancer risk.     

Alcohol consumption and prostate cancer risk: a meta-analysis of the dose-risk relation

Inconsistent results on the relationship between alcohol drinking and prostate cancer have been found. In order to provide a definite quantification of the dose-risk relation, we investigated the risk of prostate cancer at different levels of alcohol consumption, by conducting a meta-analysis of epidemiological studies. We performed a literature search using PubMed of all case-control and cohort studies published as original articles in English up to December 2010. We identified 50 case-control and 22 cohort studies, including a total of 52 899 prostate cancer cases. We derived pooled meta-analytic estimates using random-effects models, taking into account the correlation between estimates. We performed a dose-risk analysis using nonlinear random-effects meta-regression models. The overall relative risk for any alcohol drinking compared with non/occasional drinking was 1.06 [95% confidence interval (CI), 1.01-1.10]. The relative risks were 1.05 (95% CI, 1.02-1.08), 1.06 (95% CI, 1.01-1.11), and 1.08 (95% CI, 0.97-1.20) for light (≤1 drink/day), moderate (>1 to <4 drinks/day), and heavy alcohol drinking (≥4 drinks/day), respectively. This comprehensive meta-analysis provided no evidence of a material association between alcohol drinking and prostate cancer, even at high doses.     

Light alcohol drinking and cancer: a meta-analysis

BackgroundThere is convincing evidence that alcohol consumption increases the risk of cancer of the colorectum, breast, larynx, liver, esophagus, oral cavity and pharynx. Most of the data derive from studies that focused on the effect of moderate/high alcohol intakes, while little is known about light alcohol drinking (up to 1 drink/day).Patients and methodsWe evaluated the association between light drinking and cancer of the colorectum, breast, larynx, liver, esophagus, oral cavity and pharynx, through a meta-analytic approach. We searched epidemiological studies using PubMed, ISI Web of Science and EMBASE, published before December 2010.ResultsWe included 222 articles comprising ∼92 000 light drinkers and 60 000 non-drinkers with cancer. Light drinking was associated with the risk of oropharyngeal cancer [relative risk, RR = 1.17; 95% confidence interval (CI) 1.06–1.29], esophageal squamous cell carcinoma (SCC) (RR = 1.30; 95% CI 1.09–1.56) and female breast cancer (RR = 1.05; 95% CI 1.02–1.08). We estimated that ∼5000 deaths from oropharyngeal cancer, 24 000 from esophageal SCC and 5000 from breast cancer were attributable to light drinking in 2004 worldwide. No association was found for colorectum, liver and larynx tumors.ConclusionsLight drinking increases the risk of cancer of oral cavity and pharynx, esophagus and female breast.     

A meta-analysis on alcohol drinking and gastric cancer risk

BackgroundWhether an association between alcohol drinking and gastric cancer risk exists is an open question. In order to provide a definite quantification of the association between alcohol drinking and gastric cancer risk, we conducted a meta-analysis of available data.Patients and methods:We carried out a PubMed search of articles published up to June 2010 and identified 44 case–control and 15 cohort studies, including a total of 34 557 gastric cancer cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates. We carried out a dose–risk analysis using nonlinear random-effects meta-regression models.ResultsCompared with nondrinkers, the pooled relative risk (RR) was 1.07 [95% confidence interval (CI) 1.01–1.13] for alcohol drinkers and 1.20 (95% CI 1.01–1.44) for heavy alcohol drinkers (≥4 drinks per day). The pooled estimates were apparently higher for gastric noncardia (RR for heavy drinkers = 1.17, 95% CI 0.78–1.75) than for gastric cardia (RR = 0.99, 95% CI 0.67–1.47) adenocarcinoma. The dose–risk model estimated a RR of 0.95 (95% CI 0.91–0.99) for 10 g/day and 1.14 (95% CI 1.08–1.21) for 50 g/day.ConclusionsThis meta-analysis provides definite evidence of a lack of association between moderate alcohol drinking and gastric cancer risk. There was, however, a positive association with heavy alcohol drinking.     

A meta-analysis of alcohol drinking and cancer risk.

To evaluate the strength of the evidence provided by the epidemiological literature on the association between alcohol consumption and the risk of 18 neoplasms, we performed a search of the epidemiological literature from 1966 to 2000 using several bibliographic databases. Meta-regression models were fitted considering linear and non-linear effects of alcohol intake. The effects of characteristics of the studies, of selected covariates (tobacco) and of the gender of individuals included in the studies, were also investigated as putative sources of heterogeneity of the estimates. A total of 235 studies including over 117 000 cases were considered. Strong trends in risk were observed for cancers of the oral cavity and pharynx, oesophagus and larynx. Less strong direct relations were observed for cancers of the stomach, colon and rectum, liver, breast and ovary. For all these diseases, significant increased risks were found also for ethanol intake of 25 g per day. No significant nor consistent relation was observed for cancers of the pancreas, lung, prostate or bladder. Allowance for tobacco appreciably modified the relations with laryngeal, lung and bladder cancers, but not those with oral, oesophageal or colorectal cancers. This meta-analysis showed no evidence of a threshold effect for most alcohol-related neoplasms. The inference is limited by absence of distinction between lifelong abstainers and former drinkers in several studies, and the possible selective inclusion of relevant sites only in cohort studies.     

DNA repair gene XRCC3 polymorphisms and bladder cancer risk: a meta-analysis

The X-ray repair cross-complementing group 3 (XRCC3) in homologous recombination repair (HRR) pathway plays a vital role in DNA double-strand break repair (DSBR). Variants in the XRCC3 gene might result in altered protein structure or function which may influence DSBR efficiency and lead to cancer. Numerous epidemiological studies have been conducted to evaluate the association between XRCC3 polymorphisms and bladder cancer risk. However, the results of these previous studies have been inconsistent. To derive a more precise estimation of the association, we performed a meta-analysis of all available studies relating XRCC3 polymorphisms and bladder cancer. All studies published up to April 2013 on the association between XRCC3 polymorphisms and bladder cancer risk were identified by searching electronic databases PubMed, EMBASE, and Chinese Biomedical Literature databases. The association between the XRCC3 polymorphisms and bladder cancer risk was assessed by odds ratios (ORs) together with their 95 % confidence intervals (CIs). A total of 16 case–control studies met the inclusion criteria and were selected. With respect to C18067T polymorphism, significant increased bladder cancer risk was found when all eligible studies were pooled into the meta-analysis (TT vs. CC: OR?=?1.174, 95%CI?=?1.033–1.335, P?=?0.014 and recessive model TT vs. TC?+?CC: OR?=?1.147, 95 %CI?=?1.020–1.290, P?=?0.022, respectively). The results were still significant after excluding the Hardy–Weinberg equilibrium violation studies (TT vs. CC: OR?=?1.178, 95 %CI?=?1.036–1.339, P?=?0.013 and recessive model TT vs. TC?+?CC: OR?=?1.144, 95 %CI?=?1.017–1.287, P?=?0.025, respectively). In subgroup analysis by ethnicity, significant elevated risk was found among Asians (dominant model TT?+?TC vs. CC: OR?=?1.285, 95 %CI?=?1.012–1.631). In the subgroup analyses according to smoking status, no significant association was detected in all genetic comparison models. With respect to A17893G and A4541G polymorphisms, no significant association with bladder cancer risk was observed in the overall and subgroup analyses. This meta-analysis suggests that the XRCC3 C18067T polymorphism was associated with increased bladder cancer risk especially among Asians. However, the XRCC3 A17893G and A4541G polymorphisms may not play important roles in bladder carcinogenesis. Further studies with larger sample sizes are needed to validate our finds.     

XRCC1 polymorphisms increase bladder cancer risk in Asians: a meta-analysis

X-ray cross complementing group 1 (XRCC1) polymorphisms and bladder cancer risk has been investigated for years, but the result in Asian population is till inconclusive. Thus, we performed this meta-analysis to determine the association of XRCC1 Arg194Trp, Arg280His, and Arg399Gln polymorphisms with bladder cancer risk in the Asian population. PubMed, EMBASE, and China National Knowledge Infrastructure were searched up to January 2013 to identify eligible studies. The association strength was measured with odd ratios (ORs) and 95 % confidence intervals (95 % CIs). A total of nine eligible studies, including 1,931 bladder cancer patients and 2,192 controls, were identified. Significant increased risk of bladder cancer was observed for Arg194Trp polymorphism (allele comparison OR?=?1.20, 95 % CI: 1.06–1.36, P_{heterogeneity}?=?0.11; dominant model OR?=?1.20, 95 % CI: 1.02–1.41, P_{heterogeneity}?=?0.37) and Arg280His polymorphism (heterozygote comparison OR?=?1.87, 95 % CI: 1.21–2.90, P_{heterogeneity}?=?0.01; dominant model OR?=?1.75, 95 % CI: 1.05–2.90, P_{heterogeneity}?=?0.01); however, Arg399Gln was not associated with susceptibility to bladder cancer. No evidence of publication bias was detected. Our meta-analysis results suggest that XRCC1 Arg194Trp and Arg280His polymorphisms are associated with significantly increased risk of bladder cancer in Asians.     

Alcohol intake and colorectal cancer risk: a dose-response meta-analysis of published cohort studies

The epidemiologic evidence support that alcohol intake might be associated with increased colorectal cancer risk. However, the results by anatomic site in the large bowel are inconsistent. We conducted a meta-analysis of prospective cohort studies published between 1990 and June 2005 on the relationship between alcohol intake and colon and rectal cancer. We quantified associations with colon and rectal cancer using meta-analysis of relative risk (RR) associated to the highest versus the lowest category of alcohol intake and meta-analysis of study-specific dose-response slopes using fixed or random effect models depending on the heterogeneity of effects among studies. Sixteen prospective cohort studies including more than 6,300 patients with colorectal cancer were eligible for inclusion. High alcohol intake was significantly associated with increased risk of colon (RR = 1.50; 95% CI = 1.25, 1.79) and rectal cancer (RR = 1.63; 95% CI = 1.35, 1.97) when comparing the highest with the lowest category of alcohol intake, equivalent to a 15% increase of risk of colon or rectal cancer for an increase of 100 g of alcohol intake per week. The relationship did not differ significantly by anatomical site (colon, rectum). Using meta-regression analysis, we identified geographical area where the study was conducted as a possible source of between-study heterogeneity of effects among studies. Lifestyle recommendations for prevention of colorectal cancer should consider limiting alcohol intake.     

Alcohol drinking and one-carbon metabolism-related gene polymorphisms on pancreatic cancer risk

Effect of alcohol consumption on pancreatic cancer risk has been investigated in many studies, but results have been inconsistent. We conducted a case-control study to assess the effect of alcohol on pancreatic cancer in conjunction with polymorphisms in one-carbon metabolism enzymes, methylenetetrahydrofolate reductase (MTHFR C677T), methionine synthase (MTR A2756G), methionine synthase reductase (MTRR A66G), and thymidylate synthase (TS) variable number of tandem repeat. A total of 157 pancreatic cancer patients and 785 age- and sex- matched control subjects were genotyped for polymorphisms. Odds ratios (OR) with 95% confidence intervals (95% CI) were estimated using unconditional logistic models adjusted for potential confounders. Heavy alcohol drinking was marginally associated with an increased risk of pancreatic cancer (OR, 1.90; 95% CI, 1.00-3.62). None of the polymorphisms showed any significant effect on pancreatic cancer risk by genotype alone. In stratified analysis, effect of alcohol consumption on pancreatic cancer was observed in individuals with the MTHFR 667 CC, MTR 2756 AA, or MTRR 66 G allele. OR (95% CI) of pancreatic cancer for heavy drinkers compared with never drinkers was 4.50 (1.44-14.05) in the MTHFR 667 CC genotype, 2.65 (1.17-6.00) in the MTR 2756 AA genotype, and 3.35 (1.34-8.36) in the MTRR 66 G allele carriers. These results suggest that the folate-related enzyme polymorphism modifies the association between drinking habit and pancreatic cancer risk.     

饮酒与膀胱癌关系的全人群病例对照研究

目的探讨饮酒与膀胱癌发生的关系。方法采用全人群为基础的病例对照研究,共调查1996年1月1日~1998年12月31日期间确诊的上海市区膀胱癌新发病例608例,健康人群对照607例。采用非条件logistic回归分析,调整吸烟等可能的混杂因素,以估计饮酒对膀胱癌发生的危险度及其95%可信区间。结果与不饮酒者相比,男、女性饮酒者患膀胱癌相对危险度分别是1.22(95%CI0.94~1.59)、0.50(95%CI0.13~1.90)。男性随总酒精摄入量增加患膀胱癌的危险有增加趋势,OR值分别为1.10(1~80g/d)和1.56(>80g/d)(趋势检验P=0.043)。男性总酒精摄入量与饮酒年限的联合作用分析表明,与不饮酒者相比,总酒精摄入量超过80g/d、饮酒年限超过40年者患膀胱癌危险度为2.11(95%CI1.11~4.01)。将饮酒分3层、吸烟分4层进行男性饮酒与吸烟的联合作用分析,结果显示总酒精摄入量>80g/d且吸烟≥35包年者的OR值为2.78(95%CI1.46~5.28)。未发现各饮酒种类与男性膀胱癌有显著关联。在不吸烟男性组中的分析显示,饮酒习惯的OR值均没有统计学意义。结论饮酒可能与男性膀胱癌有一定联系,但作用较弱,似乎主要表现为对吸烟男性的作用。