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Plasma and dietary vitamin C levels and risk of gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST)

Vitamin C is an antioxidant and inhibitor of carcinogenic N-nitroso compound production in the stomach. Higher dietary vitamin C consumption is associated with decreased risk of gastric cancer (GC) in numerous case–control studies, but data from prospective studies are limited, particularly so for blood measures of vitamin C. The objective of this study was to determine the association of plasma and dietary vitamin C levels with the risk of GC in a case–control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), a large cohort involving 10 European countries. Using a fluorometric method, vitamin C was measured in pre-diagnostic plasma from 215 GC cases (matched controls = 416). Conditional logistic regression models adjusted by body mass index, total energy intake, smoking status/duration/intensity and Helicobacter pylori infection status were used to estimate relative cancer risks. No association with GC risk was observed for dietary vitamin C, whereas an inverse GC risk was observed in the highest versus lowest quartile of plasma vitamin C [odds ratio (OR) = 0.55, 95% confidence interval (CI) = 0.31–0.97, Ptrend = 0.043], which was maintained after exclusion of cases with 2 years follow-up (OR = 0.40, 95% CI = 0.19–0.83, Ptrend = 0.064). The inverse association was more pronounced in subjects consuming higher levels of red and processed meats, a factor that may increase endogenous N-nitroso compound production. The effect of plasma vitamin C was not different by GC anatomical subsite (cardia/non-cardia) or histological subtype (diffuse/intestinal), and there was no significant interaction of effect with H.pylori. The results of this study show, in a prospective setting, an inverse association of GC risk with high levels of plasma vitamin C and suggest an interaction with the intake of red and processed meats, whose consumption may elevate endogenous N-nitroso compound production.

Published on 11-24-2008
Authors: Mazda Jenab1,*, Elio Riboli2, Pietro Ferrari1, Joan Sabate1,3, Nadia Slimani1, Teresa Norat1, Marlin Friesen1, Anne Tjonneland4, Anja Olsen4, Kim Overvad5, Marie-Christine Boutron-Ruault6, Francoise Clavel-Chapelon6, Mathilde Touvier6, Heiner Boeing7, Mandy Schulz7, Jakob Linseisen8, Gabriele Nagel8, Antonia Trichopoulou9, Androniki Naska9, Eleni Oikonomou9, Vittorio Krogh10, Salvatore Panico11, Giovanna Masala12, Carlotta Sacerdote13, Rosario Tumino14, Petra H. Peeters15, Mattijs E. Numans15, Hendrik B. Bueno-de-Mesquita16, Frederike L. Buchner16, Eiliv Lund17, Guillem Pera18, Carmen Navarro Sanchez19, Maria-Jose Sanchez20, Larraitz Arriola21, Aurelio Barricarte22, Jose Ramon Quiros23, Goran Hallmans24, Roger Stenling25, Goran Berglund26, Sheila Bingham27, Kay-Tee Khaw28, Timothy Key29, Naomi Allen29, Fatima Carneiro30, U. Mahlke31, Guiseppe Del Giudice32, Domenico Palli12, Rudolf Kaaks1 and Carlos A. Gonzalez18
Source: Carcinogenesis Advance Access originally published online on June 14, 2006