Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort

  • Eric J. Duell
  • , Noémie Travier
  • , Leila Lujan-Barroso
  • , Françoise Clavel-Chapelon
  • , Marie Christine Boutron-Ruault
  • , Sophie Morois
  • , Domenico Palli
  • , Vittorio Krogh
  • , Salvatore Panico
  • , Rosario Tumino
  • , Carlotta Sacerdote
  • , J. Ramón Quirós
  • , Emilio Sánchez-Cantalejo
  • , Carmen Navarro
  • , Aurelio Barricarte Gurrea
  • , Miren Dorronsoro
  • , Kay Tee Khaw
  • , Naomi E. Allen
  • , Timothy J. Key
  • , H. Bas Bueno-De-Mesquita
  • Martine M. Ros, Mattijs E. Numans, Petra H.M. Peeters, Antonia Trichopoulou, Androniki Naska, Vardis Dilis, Birgit Teucher, Rudolf Kaaks, Heiner Boeing, Madlen Schütze, Sara Regner, Björn Lindkvist, Ingegerd Johansson, Göran Hallmans, Kim Overvad, Rikke Egeberg, Anne Tjønneland, Eiliv Lund, Elisabete Weiderpass, Tonje Braaten, Isabelle Romieu, Pietro Ferrari, Mazda Jenab, Roger Stenling, Dagfinn Aune, Teresa Norat, Elio Riboli, Carlos A. González

Risultato della ricerca: Contributo su rivistaArticolo in rivistapeer review

Abstract

Background: 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. Objective: We evaluated the association between alcohol consumption and GC risk. Design: 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. Results: 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. Conclusion: 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.

Lingua originaleInglese
pagine (da-a)1266-1275
Numero di pagine10
RivistaAmerican Journal of Clinical Nutrition
Volume94
Numero di pubblicazione5
DOI
Stato di pubblicazionePubblicato - 1 nov 2011
Pubblicato esternamente

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