Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.
The American Journal of Clinical Nutrition 2011 ; 94: 1266-75.
Duell EJ, Travier N, Luján-Barroso L, Clavel-Chapelon F, Boutron-Ruault MC, Morois S, Palli D, Krogh V, Panico S, Tumino R, Sacerdote C, Quirós JR, Sánchez-Cantalejo E, Navarro C, Gurrea AB, Dorronsoro M, Khaw KT, Allen NE, Key TJ, Bueno-de-Mesquita HB, Ros MM, Numans ME, Peeters PH, Trichopoulou A, Naska A, Dilis V, Teucher B, Kaaks R, Boeing H, Schütze M, Regnér S, Lindkvist B, Johansson I, Hallmans G, Overvad K, Egeberg R, Tjønneland A, Lund E, Weiderpass E, Braaten T, Romieu I, Ferrari P, Jenab M, Stenling R, Aune D, Norat T, Riboli E, and González CA
DOI : 10.3945/ajcn.111.012351
PubMed ID : 21993435
Gastric cancer (GC) is the second leading cause of cancer death worldwide. The association between alcohol consumption and GC has been investigated in numerous epidemiologic studies with inconsistent results.
We evaluated the association between alcohol consumption and GC risk.
We conducted a prospective analysis in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, which included 444 cases of first primary gastric adenocarcinoma. HRs and 95% CIs for GC were estimated by using multivariable Cox proportional hazards regression for consumption of pure ethanol in grams per day, with stratification by smoking status, anatomic subsite (cardia, noncardia), and histologic subtype (diffuse, intestinal). In a subset of participants, results were further adjusted for baseline Helicobacter pylori serostatus.
Heavy (compared with very light) alcohol consumption (≥60 compared with 0.1-4.9 g/d) at baseline was positively associated with GC risk (HR: 1.65; 95% CI: 1.06, 2.58), whereas lower consumption amounts (<60 g/d) were not. When we analyzed GC risk by type of alcoholic beverage, there was a positive association for beer (≥30 g/d; HR: 1.75; 95% CI: 1.13, 2.73) but not for wine or liquor. Associations were primarily observed at the highest amounts of drinking in men and limited to noncardia subsite and intestinal histology; no statistically significant linear dose-response trends with GC risk were observed.
Heavy (but not light or moderate) consumption of alcohol at baseline (mainly from beer) is associated with intestinal-type noncardia GC risk in men from the EPIC cohort.