Association of alcohol intake with pancreatic cancer mortality in never smokers PDF Print E-mail

Arch Intern Med. 2011 Mar 14;171(5):444-51.
Association of alcohol intake with pancreatic cancer mortality in never smokers.
Gapstur SM, Jacobs EJ, Deka A, McCullough ML, Patel AV, Thun MJ.
Epidemiology Research Program, American Cancer Society, 250 Williams St NW, Atlanta, GA 30303-1002. This e-mail address is being protected from spambots. You need JavaScript enabled to view it .
BACKGROUND: An international panel of experts characterized the evidence linking alcoholic beverage consumption to pancreatic cancer as limited. Primary concerns include inconsistent results from underpowered studies, residual confounding by smoking, and the question of whether the association varies by type of alcoholic beverage.
METHODS: The association of alcohol intake with pancreatic cancer mortality was examined using data from the Cancer Prevention Study II, a prospective study of US adults 30 years and older. Alcohol consumption was self-reported on a 4-page questionnaire in 1982. Based on follow-up through December 31, 2006, there were 6847 pancreatic cancer deaths among 1 030 467 participants. Multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs) were computed using Cox proportional hazards regression analysis controlling for age, sex, race/ethnicity, education, marital status, body mass index, family history of pancreatic cancer, and personal history of gallstones, diabetes mellitus, or smoking.
RESULTS: The RRs (95% CIs) of pancreatic cancer mortality associated with current intake of less than 1, 1, 2, 3, and 4 or more drinks per day compared with nondrinkers were 1.06 (0.99-1.13), 0.99 (0.90-1.08), 1.06 (0.97-1.17), 1.25 (1.11-1.42), and 1.17 (1.06-1.29), respectively (P < .001 for trend). Consumption of 3 or more drinks per day was associated with pancreatic cancer mortality in never smokers (RR, 1.36; 95% CI, 1.13-1.62) and in ever smokers (RR, 1.16; 95% CI, 1.06-1.27). This association was observed for consumption of liquor (RR, 1.32; 95% CI, 1.10-1.57) but not beer (RR, 1.08; 95% CI, 0.90-1.30) or wine (RR, 1.09; 95% CI, 0.79-1.49).
CONCLUSION: These results strengthen the evidence that alcohol consumption, specifically liquor consumption of 3 or more drinks per day, increases pancreatic cancer mortality independent of smoking.
PMID: 21403041 [PubMed - in process]

Alcohol intake and risk of oesophageal adenocarcinoma: a pooled analysis from the BEACON Consortium. PDF Print E-mail

Gut. 2011 Mar 14. [Epub ahead of print]
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.
National Cancer Institute, NIH, DHHS, Bethesda, Maryland, USA.
Background and aims 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). Materials and methods 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). Conclusions 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.
PMID: 21406386 [PubMed - as supplied by publisher]

Alcohol consumption and lung cancer risk in never smokers: a meta-analysis. PDF Print E-mail

Ann Oncol. 2011 Mar 22. [Epub ahead of print]
Alcohol consumption and lung cancer risk in never smokers: a meta-analysis.
Bagnardi V, Rota M, Botteri E, Scotti L, Jenab M, Bellocco R, Tramacere I, Pelucchi C, Negri E, La Vecchia C, Corrao G, Boffetta P.
Department of Statistics, University of Milan-Bicocca, Milan.
BACKGROUND: The 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.
METHODS: After 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.
RESULTS: We 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).
CONCLUSIONS: Alcohol 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.
PMID: 21427064 [PubMed - as supplied by publisher]

Lifetime Alcohol Consumption and Risk of Barrett's Esophagus. PDF Print E-mail

Am J Gastroenterol. 2011 Mar 22. [Epub ahead of print]
Lifetime Alcohol Consumption and Risk of Barrett's Esophagus.
Thrift AP, Pandeya N, Smith KJ, Mallitt KA, Green AC, Webb PM, Whiteman DC.
1] School of Population Health, The University of Queensland, Brisbane, Australia [2] Queensland Institute of Medical Research, Brisbane, Australia.
OBJECTIVES: Alcohol is a carcinogen that may increase the risk of Barrett's esophagus (BE) through direct contact with esophageal mucosa. However, few studies have investigated this association and findings have been inconsistent. We sought to examine the association between measures of total and beverage-specific alcohol consumption and BE risk.
METHODS: We conducted a large population-based case-control study that collected information on lifetime alcohol consumption and other exposures from 285 patients with nondysplastic BE, 108 patients with dysplastic BE, and two separate control groups: 313 endoscopy patients with acute inflammatory changes ("inflammation controls") and 644 population controls. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) for categories of average alcohol consumption using unconditional multivariate logistic regression.
RESULTS: Relative to life-long nondrinkers and consumption of <1 drink/week, consumption of 7-20 drinks/week (OR=0.53, 95% CI: 0.31-0.91) and 21-41 drinks/week (OR=0.37, 95% CI: 0.19-0.73) of total alcohol throughout the life was inversely associated with nondysplastic BE, for comparisons with population controls. Lifetime total alcohol consumption was also inversely associated with dysplastic BE (7-20 drinks/week OR=0.52, 95% CI: 0.19-1.43; 21-41 drinks/week OR=0.22, 95% CI: 0.07-0.73). Similarly, reduced risk estimates were found for comparisons with inflammation controls. The inverse associations were observed separately for beer and wine consumption, with a significant linear trend observed with beer consumption. The risks associated with liquor consumption were up to twofold higher; however, they were not statistically significant. We found no evidence for effect modification by factors known (or suspected) to cause BE.
CONCLUSIONS: Overall, alcohol consumption does not increase the risk of BE. Significant inverse associations were observed for beer consumption, the underlying reasons for which remain unclear.Am J Gastroenterol advance online publication, 22 March 2011; doi:10.1038/ajg.2011.89.
PMID: 21427711 [PubMed - as supplied by publisher]

Alcohol drinking and colorectal cancer risk: an overall and dose-response meta-analysis of published studies. PDF Print E-mail

Fedirko V, Tramacere I, Bagnardi V, Rota M, Scotti L, Islami F, Negri E, Straif K, Romieu I, La Vecchia C, Boffetta P, Jenab M
Alcohol drinking and colorectal cancer risk: an overall and dose-response meta-analysis of published studies. [JOURNAL ARTICLE]
Ann Oncol 2011 Feb 9.

BACKGROUND: The 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.
METHODS: Twenty-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.
RESULTS: The 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.
CONCLUSIONS: This meta-analysis provides strong evidence for an association between alcohol drinking of >1 drink/day and colorectal cancer risk.


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