N-Nitroso compounds (NOC) are potent animal carcinogens and potential human carcinogens. The primary source of exposure for most individuals may be endogenous formation, a process that can be inhibited by dietary polyphenols. To estimate the risk of gastric cancer (GC) in relation to the individual and combined consumption of polyphenols and NOC precursors (nitrate and nitrite), a population-based case-control study was carried out in Mexico City from 2004 to 2005 including 257 histologically confirmed GC cases and 478 controls. Intake of polyphenols, nitrate and nitrite were estimated using a food frequency questionnaire. High intakes of cinnamic acids, secoisolariciresinol and coumestrol were associated with an 50% reduction in GC risk. A high intake of total nitrite as well as nitrate and nitrite from animal sources doubled the GC risk. Odds ratios around 2-fold were observed among individuals with both low intake of cinnamic acids, secoisolariciresinol or coumestrol and high intake of animal-derived nitrate or nitrite, compared to high intake of the polyphenols and low animal nitrate or nitrite intake, respectively. Results were similar for both the intestinal and diffuse types of GC. Our results show, for the first time, a protective effect for GC because of higher intake of cinnamic acids, secoisolariciresinol and coumestrol, and suggest that these polyphenols reduce GC risk through inhibition of endogenous nitrosation. The main sources of these polyphenols were pears, mangos and beans for cinnamic acids; beans, carrots and squash for secoisolariciresinol and legumes for coumestrol. '
UICCKey words: nitrate; nitrite; diet; polyphenols; gastric cancer In Mexico, gastric cancer (GC) rates show an increasing trend with time, 1 in contrast to other countries, and remains the 2nd leading cause of cancer mortality. 2 Nitrate and nitrite are precursors for the endogenous formation of N-nitroso compounds (NOC), which are carcinogenic in animals and, potentially, in humans. 3 Ingested nitrate is absorbed in the small intestine and 25% is excreted in the mouth, where oral bacteria reduce about 20% to nitrite (about 5% of ingested nitrate).In the acidic stomach, nitrite forms nitrous acid, which decomposes into various reactive nitrogen species (RNS). Nitrite and RNS react with nitrosatable compounds, mainly amines and amides, to form NOC. 4 The formation of NOC is inhibited by some antioxidants, such as polyphenols 5,6 and vitamins C and E. 4,7 For this reason, a low consumption of these inhibitors of NOC formation, (INC) together with a high consumption of nitrate and/or nitrite, results in an increase in the endogenous formation of NOC. 3 Contrasting with consistent results showing an increase in the risk of GC because of nitrite consumption, 8 the association with nitrate intake is less certain. Some investigators observed no association with nitrate consumption 9-16 ; whereas, others have observed a decrease in GC risk with increasing nitrate consumption. 17,18 These apparent contradictory results reflect the...