|
|
Background and AimsAlcohol has been declared a carcinogen for cancers of the esophagus, although the evidence relates largely to the squamous subtype. Evidence for an effect on adenocarcinomas is scant and inconsistent. MethodsWe compared nationwide samples of patients with esophageal adenocarcinoma (EAC) (n = 365) or esophagogastric junction adenocarcinoma (EGJAC) (n = 426) or esophageal squamous cell carcinoma (ESCC) (n = 303) with controls sampled from a population register (n = 1580). We used generalized additive models to assess nonlinear effects of self-reported alcohol intake on cancer risk, and calculated odds ratios (ORs) and 95% confidence intervals (CIs) using multivariate logistic and piecewise regression. ResultsWe observed no association between average weekly alcohol intake and EAC or EGJAC risk. For ESCC, the relationship with alcohol was nonlinear. At intakes of less than 170 g/wk there was no significant association; at greater than this level, there was a significant linear effect (OR, 1.03; 95% CI, 1.02–1.05 per 10 g alcohol/wk). For ESCC, but not EAC or EGJAC, a statistically significant multiplicative interaction between smoking and alcohol was observed (P = .02). In analyses by beverage type, ESCC risks, but not EAC or EGJAC, increased linearly with beer intake (OR, 1.05; 95% CI, 1.04–1.07). Those who drank modest levels of wine (<50–90 g/wk) or port or spirits (<10–20 g/wk) had significantly lower risks of all 3 cancers than nondrinkers; higher intakes were associated with increased risks of ESCC only. ConclusionsAlcohol intake above the recommended US dietary guidelines significantly increases the risk of ESCC, but not EAC or EGJAC. Smoking modifies the effect of alcohol intake on ESCC risk. Abbreviations used in this paper: CI, confidence interval, EAC, esophageal adenocarcinoma, EGJAC, esophagogastric junction adenocarcinoma, ESCC, esophageal squamous cell carcinoma, OR, odds ratio ⁎ Queensland Institute of Medical Research, Brisbane, Australia ‡ School of Population Health, The University of Queensland, Brisbane, Australia
This article has an accompanying continuing medical education activity on page 1444. Learning Objective: Upon completion of this CME activity, successful learners will be able to differentiate the effects of alcohol consumption on the risks of different histologic subtypes of esophageal cancer. Successful learners will also be able to describe the way in which tobacco smoking modifies the effects of alcohol with respect to risk of esophageal cancer. Conflict of interest The authors disclose no conflicts. Funding This study was supported by the Queensland Cancer Fund and the National Health and Medical Research Council of Australia (program no. 199600). David Whiteman and Penelope Webb are supported by Senior Research Fellowships from the National Health and Medical Research Council of Australia. Nirmala Pandeya is supported by a PhD scholarship from the National Health and Medical Research Council of Australia. The funding bodies played no role in the design or conduct of the study; the collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript. PII: S0016-5085(08)02310-X doi:10.1053/j.gastro.2008.12.052 © 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.
| ||||||||||||||||||||||||||||
ABSTRACT
Alcohol Consumption and the Risks of Adenocarcinoma and Squamous Cell Carcinoma of the Esophagus