Alcohol consumption and gastric cancer risk—A pooled analysis within the StoP project consortium

An association between heavy alcohol drinking and gastric cancer risk has been recently reported, but the issue is still open to discussion and quantification. We investigated the role of alcohol drinking on gastric cancer risk in the “Stomach cancer Pooling (StoP) Project,” a consortium of epidemiological studies. A total of 9,669 cases and 25,336 controls from 20 studies from Europe, Asia and North America were included. We estimated summary odds‐ratios (ORs) and the corresponding 95% confidence intervals (CIs) by pooling study‐specific ORs using random‐effects meta‐regression models. Compared with abstainers, drinkers of up to 4 drinks/day of alcohol had no increase in gastric cancer risk, while the ORs were 1.26 (95% CI, 1.08–1.48) for heavy (>4 to 6 drinks/day) and 1.48 (95% CI 1.29–1.70) for very heavy (>6 drinks/day) drinkers. The risk for drinkers of >4 drinks/day was higher in never smokers (OR 1.87, 95% CI 1.35–2.58) as compared with current smokers (OR 1.14, 95% CI 0.93–1.40). Somewhat stronger associations emerged with heavy drinking in cardia (OR 1.61, 95% CI 1.11–2.34) than in non‐cardia (OR 1.28, 95% CI 1.13–1.45) gastric cancers, and in intestinal‐type (OR 1.54, 95% CI 1.20–1.97) than in diffuse‐type (OR 1.29, 95% CI 1.05–1.58) cancers. The association was similar in strata of H. pylori infected (OR = 1.52, 95% CI 1.16–2.00) and noninfected subjects (OR = 1.69, 95% CI 0.95–3.01). Our collaborative pooled‐analysis provides definite, more precise quantitative evidence than previously available of an association between heavy alcohol drinking and gastric cancer risk.     

Alcohol drinking and colorectal cancer risk: an overall and dose–response meta-analysis of published studies

BackgroundThe International Agency for Research on Cancer (IARC) concluded that alcohol consumption is related to colorectal cancer (CRC). However, several issues remain unresolved, including quantification of the association for light (≤1 drink/day) and moderate (2–3 drinks/day) alcohol drinking, investigation of the dose–response relationship, and potential heterogeneity of effects by sex, colorectal site, and geographical region.MethodsTwenty-seven cohort and 34 case–control studies presenting results for at least three categories of alcohol intake were identified from a PubMed search of articles published before May 2010. The summary relative risks (RRs) were estimated by the random effects model. Second-order fractional polynomials and random effects meta-regression models were used for modeling the dose–risk relation.ResultsThe RRs were 1.21 [95% confidence interval (CI) 1.13–1.28] for moderate and 1.52 (95% CI 1.27–1.81) for heavy (≥4 drinks/day) alcohol drinking. The RR for moderate drinkers, compared with non-/occasional drinkers, was stronger for men (RR = 1.24, 95% CI 1.13–1.37) than for women (RR = 1.08, 95% CI 1.03–1.13; P_{heterogeneity} = 0.02). For heavy drinkers, the association was stronger in Asian studies (RR = 1.81, 95% CI 1.33–2.46; P_{heterogeneity} = 0.04). The dose–risk analysis estimated RRs of 1.07 (95% CI 1.04–1.10), 1.38 (95% CI 1.28–1.50), and 1.82 (95% CI 1.41–2.35) for 10, 50, and 100 g/day of alcohol, respectively.ConclusionsThis meta-analysis provides strong evidence for an association between alcohol drinking of >1 drink/day and colorectal cancer risk.     

Coffee consumption and the risk of colorectal cancer by anatomical subsite in Japan: Results from the HERPACC studies

Consumption of coffee, a popular beverage worldwide, has been associated with lower colorectal cancer (CRC) risk. Although CRC exhibits different biological characteristics by anatomical subsite, the possibly heterogeneous impact of coffee on CRC by anatomical subsite has remained unclear. Here, we conducted two case‐control studies to examine the association between coffee consumption and CRC risk as well as risk by anatomic subsite among Japanese using data from the Hospital‐based Epidemiological Research Program at Aichi Cancer Center I and II (HERPACC‐I and II). Subjects were enrolled in HERPACC‐I between 1988 and 2000 and in HERPACC‐II between 2001 and 2005. Coffee consumption was measured with a self‐administered questionnaire. A conditional logistic regression model was used to calculate odds ratios (ORs) of CRC with coffee consumption, adjusted for potential confounders of age, smoking, alcohol drinking, red meat intake, BMI, exercise, family history of CRC, and diabetes mellitus history. We estimated summary ORs by pooling study‐specific ORs with a fixed effects model. In total, 2,696 CRC cases and 13,480 non‐cancer outpatients as controls were included. Overall, compared to non‐drinkers, ORs of less than 1 cup/day, 1–2 cups/day and 3 or more cups/day for CRC were 0.88 (95% CI: 0.77–1.00), 0.90 (95% CI: 0.80–1.01) and 0.78 (95% CI: 0.65–0.92), respectively (trend‐p = 0.009). Subsite‐specific analysis revealed a significant inverse linear trend between coffee consumption and distal colon cancer (p‐trend = 0.048), and a tendency toward a lower risk of rectal cancer (p‐trend = 0.068). These findings suggest that coffee consumption might impact the prevention of CRC, especially distal colon cancer.     

Alcohol drinking and pancreatic cancer risk: a meta‐analysis of the dose‐risk relation

In order to provide a more precise quantification of the association between alcohol consumption and pancreatic cancer risk, we performed a meta‐analysis of relevant dose‐risk results. We conducted a PubMed search of all case‐control (N=21) and cohort (N=11) studies published up to March 2009. We computed summary relative risk (RR) estimates using either fixed‐ or, in the presence of heterogeneity, random‐effects models. The pooled RR was 0.92 (95% confidence interval, 95% CI, 0.86–0.97) for <3 drinks/day and 1.22 (95% CI, 1.12–1.34) for ≥3 drinks/day. The increased risk for heavy drinking was similar in women and men, but apparently stronger in cohort studies (RR=1.29), in studies with high quality index (RR=1.30), and did not appear to be explained by residual confounding by either history of pancreatitis or tobacco smoking. This meta‐analysis provides strong evidence for the absence of a role of moderate drinking in pancreatic carcinogenesis, coupled to an increased risk for heavy alcohol drinking. Given the moderate increase in risk and the low prevalence of heavy drinkers in most populations, alcohol appears to be responsible only for a small fraction of all pancreatic cancers.     

Alcohol Consumption and Breast Cancer among Black and White Women in North Carolina (United States)

Objective: The purpose of this study was to investigate the effects of alcohol consumption on breast cancer risk in black and white women. Methods: We used data from the Carolina Breast Cancer Study, a population-based, case-control study of black and white women in North Carolina. Interviews were conducted with 890 cases and 841 controls frequency-matched on age and race. Results: Overall, the prevalence of moderate to high levels of alcohol consumption was low. Compared with abstainers, the multivariate odds ratio for recent intake of one or two drinks per day was 1.4 (95% CI = 0.9 2.1) and two or more drinks a day was 1.0 (95% CI = 0.6–1.6); increasing consumption was not associated with risk (p for trend = 0.6). The associations were similar, but somewhat weaker, for average lifetime consumption. Among women who consumed 91 g/week or more of alcohol, a nonsignificant increased risk of breast cancer was observed for women reporting binge drinking (OR = 1.5; 95% CI = 0.9–2.3), but not for those who consumed less than 91 g/week reporting binge drinking (OR = 1.0; 95% CI = 0.6–1.5). Odds ratios did not differ meaningfully by race, age, menopausal status, exogenous hormone use, or body mass index. Conclusions: These data provide little evidence for an association between alcohol consumption and risk of breas cancer among either black or white women.     

Risk of pancreatic cancer by alcohol dose,duration, and pattern of consumption,including binge drinking: a population-based study

Alcohol consumption is postulated to be a risk factor for pancreatic cancer (PCA), but clarification of degree of risk related to consumption characteristics is lacking. We examined the association between alcohol consumption and PCA in a population-based case–control study (532 cases, 1,701 controls) in the San Francisco Bay Area. Population-based controls were frequency-matched by sex, age within 5-year categories and county of residence to cases identified by the cancer registry’s rapid case ascertainment. Detailed alcohol consumption data, including binge drinking (≥5 drinks/day), were collected during in-person interviews. Odds ratios (OR) and 95% confidence intervals (95% CI) were computed using adjusted unconditional logistic regression. Depending on dose, duration, and pattern of drinking, ORs were increased 1.5- to 6-fold among men but not women. In men, ORs increased with increasing overall alcohol consumption (22–35 drinks/week OR = 2.2, 95% CI = 1.1–4.0; ≥35 drinks/week OR = 2.6, 95% CI = 1.3–5.1, p-trend = 0.04). Most notable were effects with a history of binge drinking (OR = 3.5, 95% CI = 1.6–7.5) including increased number of drinks per day (p-trend = 0.002), and increased years of binge drinking (p-trend = 0.0006). In fully adjusted models that included smoking and other confounders, ORs for binge drinking in men were somewhat higher than in age-adjusted models. Results from our detailed analyses provide support for heavy alcohol consumption (including binge drinking) as a risk factor for PCA in men.     

Alcohol consumption,variability in alcohol dehydrogenase genes and risk of renal cell carcinoma

Alcohol consumption has been associated inversely with renal cell carcinoma (RCC) risk; however, no study has examined effect modification by germline variation in alcohol‐metabolizing genes. We investigated whether the association between alcohol intake and RCC risk is modulated by germline variants in alcohol dehydrogenase genes in a large case–control study. Data from 652 RCC cases and 1,366 non‐cancer controls were analyzed. Alcohol intake was assessed using a standardized risk factor questionnaire. Three previously genotyped polymorphisms in ADH6 and ADH7 with the TaqMan assay were examined. Odds ratios (ORs) and 95% confidence interval (CI) were calculated using logistic regression, adjusting for covariates. Compared to non‐drinkers, ever consumption of alcohol was associated with lower RCC risk (OR = 0.52, 95% CI = 0.42–0.65). Analysis with cubic spline regression curve showed a “J‐shaped” relationship between alcohol drinks/day and RCC risk, such that there was no added benefit against RCC for consumption of more than two drinks/day. We observed effect modification by variation in rs1154454 (ADH7) (p_interaction = 0.007); a per unit increase in alcohol drink/day was associated with 35% lower RCC risk among non‐minor allele carriers, a 27% lower risk among those who carry one copy of the minor allele, but no association was observed among those with two copies of the minor allele. These findings indicate that alcohol consumption is associated with lower RCC risk. Consuming more than two drinks a day does not confer additional protection against RCC. The association between alcohol intake and RCC risk appears to be modulated by inter‐individual germline variation in alcohol‐metabolizing genes.     

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.     

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.     

Alcohol consumption, type of alcoholic beverage and risk of colorectal cancer at specific subsites

Within the Netherlands Cohort Study on diet and cancer, we investigated associations between total alcohol consumption, specific alcoholic beverage consumption and risk of colorectal cancer (CRC) according to anatomical subsite. Hazard Ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models. Analyses were performed on 2,323 CRC cases, available after 13.3 years of follow-up. Compared to abstaining, alcohol consumption of >/=30.0 g/day ( approximately 3 alcoholic drinks) was positively associated with the risk of CRC (HR: 1.32, 95% CI: 1.06-1.65). Analyses restricted to subjects who reported to have consumed equal amounts of alcohol 5 years before baseline compared to baseline, showed elevated risk estimates for consumers of >/=30.0 g of total alcohol per day as well (HR: 1.53, 95% CI: 1.16-2.01). Suggestive of a subsite-specific effect, cancer risk seemed to increase from proximal colon through rectum; HR: 1.29, 95% CI: 0.85-1.96 for proximal colon cancer, HR: 1.41, 95% CI: 0.94-2.11 for distal colon cancer, HR: 2.07, 95% CI: 1.03-4.18 for rectosigmoid cancer and HR: 1.69, 95% CI: 1.08-2.64 for rectal cancer. No associations were observed between consumption of alcoholic beverages and CRC risk when compared with the nondrinkers of the specific beverage and after adjustment for total alcohol intake. No evidence was found for sex-specific effects of alcohol and alcoholic beverages. In conclusion, our data showed a positive association between alcohol consumption and risk of CRC, which seemed to be mainly explained by the alcoholic content of alcoholic beverages, rather than other constituents. Also, cancer risk may vary according to anatomical subsite.     

Alcohol and liver cancer: a systematic review and meta-analysis of prospective studies

Despite several studies support a positive association between heavy alcohol consumption and liver cancer risk, a consistent dose–risk relationship has not yet been established. We carried out a systematic review and a meta-analysis of the association between alcohol intake and liver cancer occurrence, following the Meta-analysis Of Observational Studies in Epidemiology guidelines. We searched for cohort and nested case–control studies on the general population published before April 2013, using PubMed and EMBASE. Summary meta-analytic relative risks (RRs) were estimated using random-effect models. We included 16 articles (19 cohorts) for a total of 4445 incident cases and 5550 deaths from liver cancer. Compared with non-drinking, the pooled RRs were 0.91 (95% confidence interval, CI, 0.81–1.02) for moderate drinking (<3 drinks per day) and 1.16 (95% CI, 1.01–1.34) for heavy drinking (≥3 drinks per day), with significant heterogeneity among studies. The dose–risk curve suggested a linear relationship with increasing alcohol intake in drinkers, with estimated excess risk of 46% for 50 g of ethanol per day and 66% for 100 g per day. This systematic review suggests a moderate detrimental role of consumption of 3 or more alcoholic drinks per day on liver cancer, and a lack of association with moderate drinking. Our results have to be taken with due caution on account of the possible limitations of the original studies included in the meta-analysis.     

A meta-analysis on alcohol drinking and esophageal and gastric cardia adenocarcinoma risk

BackgroundIn order to provide a precise quantification of the association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, we conducted a meta-analysis of available data.Patients and methodsWe identified 20 case–control and 4 cohort studies, including a total of 5500 cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates, and we carried out a dose–risk analysis using nonlinear random-effects meta-regression models.ResultsThe relative risk (RR) for drinkers versus nondrinkers was 0.96 [95% confidence interval (CI) 0.85–1.09] overall, 0.87 (95% CI 0.74–1.01) for esophageal adenocarcinoma and 0.89 (95% CI 0.76–1.03) for gastric cardia adenocarcinoma. Compared with nondrinkers, the pooled RRs were 0.86 for light (≤1 drink per day), 0.90 for moderate (1 to <4 drinks per day), and 1.16 for heavy (≥4 drinks per day) alcohol drinking. The dose–risk model found a minimum at 25 g/day, and the curve was <1 up to 70 g/day.ConclusionsThis meta-analysis provides definite evidence of an absence of association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, even at higher doses of consumption.     

Tobacco smoking,alcohol consumption and pancreatic cancer risk: A case-control study in Italy

In Italy, pancreatic cancer accounts for approximately 5% of cancer-related deaths. Tobacco smoking is the major established risk factor for this cancer, whereas the role of alcohol consumption is open to debate.Between 1991 and 2008, we conducted a hospital-based case-control study on pancreatic cancer in northern Italy. Cases were 326 patients (median age 63 years) with incident pancreatic cancer admitted to major general hospitals. Controls were 652 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospital network of cases. Multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI).Pancreatic cancer was associated to current smoking (OR = 1.68; 95% CI: 1.13–2.48), and the risk rose with increasing number of cigarettes/day (OR = 2.04; 95% CI: 1.14–3.66 for ?20 cigarettes/day). No association emerged for former smokers (OR = 0.98; 95% CI: 0.66–1.45). Alcohol consumption was associated to increased pancreatic cancer risk, but ORs were significant only among heavy drinkers (ORs: 2.03 and 3.42 for 21–34 and ?35 drinks/week, respectively). Pancreatic cancer risk was 4.3-fold higher in heavy smokers (?20 cigarettes/day) and heavy drinkers (?21 drinks/week) in comparison with never smokers who drunk <7 drinks/week, which is compatible with an additive effect of these exposures.In conclusion, we found that tobacco smoking and alcohol drinking are two independent risk factors for pancreatic cancer which may be responsible for approximately one third of these cancers in our population.     

Green tea drinking,high tea temperature and esophageal cancer in high‐ and low‐risk areas of Jiangsu Province,China: A population‐based case–control study

Epidemiological studies suggested drinking green tea is inversely associated with esophageal cancer but results remain inconclusive. Moreover, inconsistent observations found high temperature drinks are associated with esophageal cancer. A population‐based case–control study was conducted in a high‐risk area (Dafeng) and a low‐risk area (Ganyu) of esophageal cancer in Jiangsu province China from 2003 to 2007. It aimed to explore green tea drinking and tea temperature with the risk of esophageal cancer, and to compare the difference between different risk regions. Using identical protocols, 1,520 cases and 3,879 healthy controls were recruited as study subjects in 2 regions. Detailed information was collected to assess green tea drinking habits. Unconditional logistic regression was used to obtain OR and 95% CI. Results showed that ever drinking green tea elevated OR in both counties (Dafeng OR = 1.2, 95% CI = 0.9–1.5; Ganyu: OR = 1.9, 95% CI = 1.4–2.4). Drinking tea at high temperature was found to increase cancer risk in both areas (Dafeng: OR = 1.9, 95% CI = 1.2–2.9; Ganyu OR = 3.1 95% CI = 2.2–4.3). However, after further adjustment for tea temperature, ever drinking tea was not related to cancer in either county (Dafeng: OR = 1.0, 95% CI = 0.7–1.3; Ganyu: OR = 1.3, 95% CI = 0.9–1.7). For dose‐response relationships, we observed positive relationship with monthly consumption of tea (p for trend = 0.067) and tea concentration (p for trend = 0.006) after further adjustment for tea temperature. In conclusion, green tea drinking was not inversely associated with esophageal cancer in this study. However, drinking tea at high temperatures significantly increased esophageal cancer risk. There was no obvious difference of green tea drinking between low‐ and high‐risk areas. © 2008 Wiley‐Liss, Inc.     

Lifetime alcohol intake and risk of non‐Hodgkin lymphoma: Findings from the Melbourne Collaborative Cohort Study

Cohort studies have reported inconsistent evidence regarding alcohol intake and risk of non‐Hodgkin lymphoma (NHL), mostly based on alcohol intake assessed close to study enrolment. We examined this association using alcohol intake measured from age 20 onwards. We calculated usual alcohol intake for 10‐year periods from age 20 using recalled frequency and quantity of beverage‐specific consumption for 37,990 participants aged 40–69 years from the Melbourne Collaborative Cohort Study. Cox regression was performed to derive hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between alcohol intake (g/day) and NHL risk. After a mean follow‐up of 19.3 years, 538 NHL cases were diagnosed. Approximately 80% of participants were either lifetime abstainers or consumed below 20 g of ethanol/day. All categories of lifetime alcohol intake were associated with about 20% lower incidence of NHL compared with lifetime abstention, but there was no evidence of a trend by amount consumed (HR = 0.97 per 10 g/day increment in intake, 95% CI: 0.92–1.03; p value = 0.3). HRs for beer, wine and spirits were 0.91 (95% CI: 0.83–1.00; p value = 0.05), 1.03 (95% CI: 0.94–1.12; p value = 0.6), and 1.06 (95% CI: 0.83–1.37; p value = 0.6), respectively, per 10 g/day increment in lifetime intake. There were no significant differences in associations between NHL subtypes. In this low‐drinking cohort, we did not detect a dose‐dependent association between lifetime alcohol intake and NHL risk.     

Circulating sex hormone levels and colorectal cancer risk in Japanese postmenopausal women: The JPHC nested case–control study

Previous epidemiological studies evaluated endogenous sex hormone levels and colorectal cancer (CRC) risk have yielded inconsistent results. Also, it is unknown if consumption of dietary isoflavones may influence the endogenous sex hormones and CRC relationships. We conducted a nested case–control study within the JPHC Study Cohort II wherein 11,644 women provided blood samples at the 5-year follow-up survey. We selected two matched controls for each case from the cohort (185 CRC cases and 361 controls). Multivariable conditional logistic regression was used to estimate odds ratios (ORs), 95% confidence intervals (CIs) for the association between circulating sex hormone levels and CRC risk. Comparing extreme tertiles, circulating testosterone levels were positively associated with CRC risk (OR = 2.10, 95% CI = 1.11–3.99, p for trend = 0.03). Levels of estradiol, SHBG, and progesterone were not associated with CRC risk. In a subgroup analysis by dietary isoflavone intake, SHBG levels were positively associated with CRC risk among those with low total isoflavone intake (p for trend = 0.03), with a statistically nonsignificant inverse association among those with high total isoflavone intake (p for trend = 0.22; p for interaction = 0.002). Endogenous levels of testosterone were positively associated with CRC among postmenopausal women. The association of endogenous SHBG with CRC development may be altered by the level of dietary isoflavone intake.     

Alcohol drinking and bladder cancer risk: a meta-analysis

BackgroundWe aimed at investigating the risk of bladder cancer at different levels of alcohol consumption by conducting a meta-analysis of epidemiological studies.Patients and methodsIn October 2010, we carried out a systematic literature search in the Medline database, using PubMed. We identified 16 case–control and 3 cohort studies, including a total of 11 219 cases of bladder cancer, satisfying the inclusion criteria for this meta-analysis. Moderate alcohol intake was defined as <3 drinks per day (i.e. <37.5 g of ethanol per day) and heavy intake as ≥3 drinks/day. Pooled estimates of the relative risks (RR) and the corresponding 95% confidence intervals (CI) were calculated using random effects models.ResultsCompared with non-drinkers, the pooled RRs of bladder cancer were 1.00 (95% CI 0.92–1.09) for moderate and 1.02 (95% CI 0.78–1.33) for heavy alcohol drinkers. When we excluded four studies that did not adjust for tobacco smoking, the corresponding estimates were 0.98 (95% CI 0.89–1.07) and 0.97 (95% CI 0.72–1.31).ConclusionsThis meta-analysis of epidemiological studies provides definite evidence on the absence of any material association between alcohol drinking and bladder cancer risk, even at high levels of consumption.     

Single nucleotide polymorphisms of ADH1B,ADH1C and ALDH2 genes and esophageal cancer: A population‐based case–control study in China

Alcohol drinking is a major risk factor for esophageal cancer (EC) and the metabolism of ethanol has been suggested to play an important role in esophageal carcinogenesis. Epidemiologic studies, including genomewide association studies (GWAS), have identified single nucleotide polymorphisms (SNPs) in alcohol dehydrogenases (ADHs) and aldehyde dehydrogenases (ALDHs) to be associated with EC. Using a population‐based case–control study with 858 EC cases and 1,081 controls conducted in Jiangsu Province, China, we aimed to provide further information on the association of ADH1B (rs1229984), ADH1C (rs698) and ALDH2 (rs671) polymorphisms with EC in a Chinese population. Results showed that ADH1B (rs1229984) was associated with EC with odds ratios (ORs) of 1.34 [95% confidence interval (CI): 1.08–1.66] for G‐allele carriers compared to A/A homozygotes. No heterogeneity was detected on this association across different strata of alcohol drinking and tobacco smoking. Statistical interaction between ALDH2 (rs671) and alcohol drinking on EC susceptibility in both additive and multiplicative scales was observed. Compared to G/G homozygotes, A‐allele carriers were positively associated with EC among moderate/heavy drinkers (OR = 1.64, 95% CI: 1.12–2.40) and inversely associated with EC among never/light drinks (OR = 0.75, 95% CI: 0.54–1.03). In addition, statistical interaction between ALDH2 and ADH1B polymorphisms on EC susceptibility among never/light drinkers was indicated. We did not observe association of ADH1C polymorphism with EC. In conclusion, our findings indicated that ADH1B (rs1229984) was associated with EC independent of alcohol drinking and tobacco smoking status and alcohol drinking interacted with ALDH2 (rs671) on EC susceptibility in this high‐risk Chinese population.     

Consumption of meat,traditional and modern processed meat and colorectal cancer risk among the Moroccan population: A large-scale case–control study

The current study aimed to investigate the relationship between red and white meat subtypes, processed meat (divided into traditional “Khlii, Kaddid” and industrially processed meat) and colorectal cancer (CRC) risk, considering CRC subsites, in Moroccan adults. A case–control study was conducted including 2,906 matched case–control pairs recruited from the five largest university hospitals in Morocco. Dietary data were collected through a validated Food Frequency Questionnaire (FFQ). Multivariable odds ratios (OR) and 95% confidence intervals (CI), for the association of CRC risk with meat consumption (high vs. low intake), were estimated using conditional logistic regression models, adjusted for relevant confounding variables. Overall, consumption of red meat was positively associated with colon cancer and CRC risk (OR = 1.23, 95% CI = 1.05–1.44; OR = 1.14, 95% CI = 1.02–1.27), respectively. In contrast, no significant association was observed between the consumption of red meat and rectal cancer risk (OR = 1.05, 95% = 0.90–1.23). Interestingly, while processed meat from industrial processes was positively associated with colon cancer, rectal cancer and CRC (OR = 1.61, 95% CI = 1.27–2.04; OR = 1.73, 95% CI = 1.34–2.23; OR = 1.67, 95% CI = 1.41–1.98), processed meat prepared using traditional methods was inversely associated with colon cancer and CRC risk (OR = 0.74, 95% CI = 0.57–0.98; OR = 0.77, 95% CI = 0.64–0.93), respectively. Furthermore, positive associations were observed between poultry intake and colon cancer risk among men (OR = 1.27, 95% CI = 1.01–1.59). Our study showed similar associations between the consumption of red meat and CRC risk in Morocco as in developed countries, while inverse associations were found for traditionally processed meat products. This is the first study to investigate the differential effects of traditional vs. westernized processed meat products in a developing country. Other studies are needed to confirm these findings and to understand the physiological pathways underlying these associations.     

Alcohol consumption and mammographic density in the Danish Diet,Cancer and Health cohort

Purpose

We examined the association between alcohol consumption and mammographic density (MD) considering in detail the time of exposure and the type of alcohol.

Methods

Of 5,356 women (4,489 post-menopausal) from the Danish Diet, Cancer and Health cohort (1993–1997) who attended mammographic screening in Copenhagen (1993–2001), we used MD (mixed/dense or fatty) assessed at the first screening after cohort entry. Alcohol consumption was assessed at the time of recruitment. Logistic regression was used to estimate associations [odds ratios (OR), 95% confidence intervals (CI)] between alcohol consumption and MD.

Results

The mean age was 56.2 years, 56.5% of women had mixed/dense MD, and 91.8% were alcohol consumers. There was no association between current alcohol consumption and MD at baseline (age 50–65, on average 1 year before MD assessment) neither between age at drinking initiation and MD, in the fully adjusted model. There was a borderline statistically significantly increased OR of having mixed/dense MD in women who consumed?>?7 drinks/week at age 20–29 (1.31, 95% CI 1.00–1.72) compared to non-drinkers in this age group, and no effect of drinking at age 30–39, 40–49 or after >?50 years, when adjusting for current drinking. However, when considering different types of alcohol, drinking spirits at age 20–29 was positively associated with mixed/dense breast (3–7 drinks/week: OR 1.74, 95% CI 1.12–2.72); >7 drinks/week: (OR 1.76, 95% CI 0.73–4.23). No consistent pattern was found with beer, wine, or fortified wine.

Conclusions

We found higher MD among women with high alcohol consumption in early adulthood (ages 20–29), in those drinking spirits.