Impact of Alcohol Consumption on Different Types of Esophageal Cancer PDF Print E-mail

Gut. 2011 Aug;60(8):1029-37. Epub 2011 Mar 14.
Alcohol intake and risk of oesophageal adenocarcinoma: a pooled analysis from the BEACON Consortium.
Freedman ND, Murray LJ, Kamangar F, Abnet CC, Cook MB, Nyrén O, Ye W, Wu AH, Bernstein L, Brown LM, Ward MH, Pandeya N, Green AC, Casson AG, Giffen C, Risch HA, Gammon MD, Chow WH, Vaughan TL, Corley DA, Whiteman DC.
Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, Rockville, MD 20852, USA. This e-mail address is being protected from spambots. You need JavaScript enabled to view it
Alcohol intake is a strong and well established risk factor for oesophageal squamous cell carcinoma (OSCC), but the association with oesophageal adenocarcinoma (OA) or adjacent tumours of the oesophagogastric junction (OGJA), remains unclear. Therefore, the association of alcohol intake with OSCC, OA, and OGJA was determined in nine case-control studies and two cohort studies of the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium (BEACON).
Information was collected on alcohol intake, age, sex, education, body mass index, gastro-oesophageal reflux, and tobacco smoking from each study. Along with 10,854 controls, 1821 OA, and 1837 OGJA, seven studies also collected OSCC cases (n=1016). Study specific ORs and 95% CIs were calculated from multivariate adjusted logistic regression models for alcohol intake in categories compared to non-drinkers. Summary risk estimates were obtained by random effects models. Results No increase was observed in the risk of OA or OGJA for increasing levels of any of the alcohol intake measures examined. ORs for the highest frequency category (≥ 7 drinks per day) were 0.97 (95% CI 0.68 to 1.36) for OA and 0.77 (95% CI = 0.54 to 1.10) for OGJA. Suggestive findings linked moderate intake (eg, 0.5 to <1 drink per day) to decreased risk of OA (OR 0.63, 95% CI 0.41 to 0.99) and OGJA (OR 0.78, 95% CI 0.62 to 0.99). In contrast, alcohol intake was strongly associated with increased risk of OSCC (OR for ≥ 7 drinks per day 9.62, 95% CI 4.26 to 21.71).
In contrast to OSCC, higher alcohol consumption was not associated with increased risk of either OA or OGJA. The apparent inverse association observed with moderate alcohol intake should be evaluated in future prospective studies.

Impact of Alcohol Consumption on Gastric Cancer by ALDH allele PDF Print E-mail

Carcinogenesis. 2011 Dec 5. [Epub ahead of print]
Genetic variation in alcohol dehydrogenase (ADH1A, ADH1B, ADH1C, ADH7) and aldehyde dehydrogenase (ALDH2), alcohol consumption, and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.
Duell EJ, Sala N, Travier N, Muñoz X, Boutron-Ruault MC, Clavel-Chapelon F, Barricarte A, Arriola L, Navarro C, Sánchez-Cantalejo E, Quirós JR, Krogh V, Vineis P, Mattiello A, Tumino R, Khaw KT, Wareham N, Allen NE, Peeters PH, Numans ME, Bueno-de-Mesquita HB, van Oijen MG, Bamia C, Benetou V, Trichopoulos D, Canzian F, Kaaks R, Boeing H, Bergmann MM, Lund E, Ehrnström R, Johansen D, Hallmans G, Stenling R, Tjønneland A, Overvad K, Ostergaard JN, Ferrari P, Fedirko V, Jenab M, Nesi G, Riboli E, González CA.
Unit of Nutrition, Environment and Cancer, Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain.
Studies that have examined the association between alcohol consumption and gastric cancer (GC) risk have been inconsistent. We conducted an investigation of 29 genetic variants in alcohol metabolism loci (ADH1 gene cluster: ADH1A, ADH1B, and ADH1C; ADH7; and ALDH2), alcohol intake, and GC risk. We analysed data from a nested case-control study (364 cases and 1272 controls) within the EPIC cohort. Single nucleotide polymorphisms (SNP) were genotyped using a customized array. We observed a statistically significant association between a common 3'-flanking SNP near ADH1A (rs1230025) and GC risk (allelic OR(A v T)=1.30, 95% CI=1.07-1.59). Two intronic variants, one in ADH1C (rs283411) and one in ALDH2 (rs16941667) also were associated with GC risk (OR(T v C)=0.59; 95% CI=0.38-0.91; and OR(T v C)=1.34; 95% CI=1.00-1.79, respectively). Individuals carrying variant alleles at both ADH1 (rs1230025) and ALDH2 (rs16941667) were twice as likely to develop GC (OR(A+T)=2.0; 95% CI=1.25-3.20) as those not carrying variant alleles. The association between rs1230025 and GC was modified by alcohol intake (<5 grams per day: OR(A)=0.89, 95% CI=0.57-1.39; ≥5 grams per day: OR(A)=1.45, 95% CI=1.08-1.94, P-value=0.05). The association was also modified by ethanol intake from beer. A known functional SNP in ADH1B (rs1229984) was associated with alcohol intake (P-value= 0.04), but not GC risk. Variants in ADH7 were not associated with alcohol intake or GC risk. In conclusion, genetic variants at ADH1 and ALDH2 loci may influence GC risk, and alcohol intake may further modify the effect of ADH1 rs1230025. Additional population-based studies are needed to confirm our results.

Alcohol Consumption and Liver Cancer PDF Print E-mail

Br J Cancer. 2011 Oct 25;105(9):1430-5. doi: 10.1038/bjc.2011.360. Epub 2011 Sep 13.
Smoking as an independent risk factor for hepatocellular carcinoma: the Singapore Chinese Health Study.
Koh WP, Robien K, Wang R, Govindarajan S, Yuan JM, Yu MC.
Department of Epidemiology and Public Health, Yong Loo Lin School of Medicine, National University of Singapore, MD3, Singapore 117597, Singapore. This e-mail address is being protected from spambots. You need JavaScript enabled to view it
Given the close correlation between smoking and alcohol intake in most epidemiologic studies, it is difficult to exclude the residual confounding effect of alcohol in the association between smoking and hepatocellular carcinoma (HCC).
We evaluated the association between smoking and risk of HCC in the Singapore Chinese Health Study, a prospective cohort with a low prevalence of alcohol intake. Information on cigarette smoking and alcohol consumption was obtained through in-person interviews conducted at enrolment.
After a mean of 11.5 years of follow-up, there were 394 incident cases of HCC. Participants who consumed more than two alcoholic drinks per day showed an increased risk for HCC (hazard ratio (HR)=2.24; 95% confidence interval (CI)=1.46-3.41). After adjusting for alcohol consumption and other potential confounders, current vs never smokers had a statistically significant, increased risk of HCC (HR=1.63; 95% CI=1.27-2.10) that was dose-dependent (number of cigarettes per day, P for trend<0.001). The observed tobacco-HCC association also was duration-dependent (years of smoking in ever smokers, P for trend=0.002). When we excluded daily drinkers from the analysis, all risk estimates remained essentially the same and statistically significant.
Our findings strongly implicate tobacco smoke as a causal factor of HCC development.

No association between alcohol consumption and risk of bladder cancer PDF Print E-mail

Ann Oncol. 2011 Oct 29. [Epub ahead of print]
Alcohol drinking and bladder cancer risk: a meta-analysis.
Pelucchi C, Galeone C, Tramacere I, Bagnardi V, Negri E, Islami F, Scotti L, Bellocco R, Corrao G, Boffetta P, La Vecchia C.
Department of Epidemiology, Mario Negri Institute for Pharmacological Research, Milan.
We aimed at investigating the risk of bladder cancer at different levels of alcohol consumption by conducting a meta-analysis of epidemiological studies.
In 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.
Compared 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).
This 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.

Alcohol consumption and the risk of endometrial cancer: a meta-analysis. PDF Print E-mail

Asia Pac J Clin Nutr. 2011;20(1):125-33.
Alcohol consumption and the risk of endometrial cancer: a meta-analysis.
Sun Q, Xu L, Zhou B, Wang Y, Jing Y, Wang B.
Department of Pharmacy, the Affiliated Wuxi Hospital for Maternal and Child Health Care of Nanjing Medical University, Jiangsu 214002, China. This e-mail address is being protected from spambots. You need JavaScript enabled to view it .
Epidemiologic findings are inconsistent concerning the association of endometrial cancer risk with alcohol consumption. Therefore, we conduct a meta-analysis of studies that assessed the association of alcohol consumption and the risk of endometrial cancer. A systematic literature search up to April 2010 was performed in MEDLINE and EMBASE, and study-specific risk estimates were pooled using a random-effects model. In the present study, six prospective and 14 case-control studies were included. Alcohol intake was not significantly associated with the risk of endometrial cancer among prospective studies (relative risk (RR): 1.04; 95% confidence interval (CI): 0.91-1.18) or among case-control studies (odds ratio (OR): 0.89; 95% CI: 0.76-1.05). However evidence from the results of our stratified analyses revealed that increased risk of endometrial cancer was associated with liquor consumption (RR: 1.22; 95% CI: 1.03-1.45) but null association with wine and beer consumption. In conclusion, alcohol consumption is not associated with the risk of endometrial cancer. Future studies should also examine whether the relation varies according to different type of alcoholic beverages.
PMID: 21393120 [PubMed - in process]


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