Dietary intake of polyphenols, nitrate and nitrite and gastric cancer risk in Mexico City

Abstract

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...

Dietary intakes and food sources of phytoestrogens in the European Prospective Investigation into Cancer and Nutrition (EPIC) 24-hour dietary recall cohort

“…51 In other Western countries such as Mexico, US and Canada, lignan intakes were much lower than our results (from 0.35 to 0.86 mg/day). 20,37,52 To our knowledge, there are not descriptive data on dietary lignan intake in Asian populations, but probably their contribution to the total phytoestrogen intake would be low like in our UK health-conscious group (o16%). Several papers have reported on intakes of secoisolariciresinol and matairesinol, 34,60 but most of them did not consider lariciresinol and pinoresinol, which contributed 470% to the total lignans in our cohort.…”

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“…Vegetable intake accounts for ∼80% of dietary nitrate consumption in human diets 10; dietary nitrates can be reduced to nitric oxide (NO) via non‐enzymatic reduction by lingual bacteria and a variety of mammalian reductases and increase NO bioavailability through the nitrate‐nitrite‐NO pathway 11, 12. Gastric metabolism of nitrate and nitrite is associated with both health benefits and risks 13, including the formation of potentially carcinogenic nitrosamines promoted by nitrites in processed meats which can be inhibited by flavonoids and other compounds in vegetables 14. Importantly, both the European Food Standards Agency (EFSA) and a recent NHLBI panel concluded that current research does not support a role for nitrate consumed as vegetables as a carcinogen 10.…”

Alimentary factors in the development of gastric intestinal metaplasia in functional dyspeptic patients

“…More recently begun to be recognized the potential carcinogenic effects of nitrosamines and nitrosamides, generically called N-compounds, substances formed in the interaction between a group of secondary nitrogen (which can be an amine or amide, a urea or an alkyl-ring peptide) and a nitrite. The evidence that the populations most at risk for gastric cancer have diets rich in substrates for the process of endogenous N-compounds triggered the interest in the evaluation of these substances in the genesis of gastric cancer (6) . The N-nitroso compounds, the main source for most people, the endogenous formation, a process that can be inhibited by polyphenols.…”

“…The N-nitroso compounds, the main source for most people, the endogenous formation, a process that can be inhibited by polyphenols. A case-control study in Mexico City in 2004-2005, including 257 cases with gastric cancer (histologically confirmed) and 478 controls was conducted to estimate the risk of gastric cancer in relation to individual and combined consumption of polyphenols and precursors N-compounds (6) . The intake of polyphenols, nitrate and nitrite were estimated by a food frequency questionnaire.…”

“…Epidemiological studies demonstrate the importance of ambiental factors, especially alimentary, in its pathogenesis. A factor that has been investigated in gastric oncogenesis is the infection by Helicobacter pylori leading to chronic gastritis, atrophy of the mucosa and intestinal metaplasia; having, thus, participation in the chain of events leading to gastric cancer (6,21,23) .…”