The incidence of cancer of the proximal stomach has increased markedly over the past 20 years. Unlike cancer of the more distal stomach, it is not related to Helicobacter pylori infection and occurs in healthy non-atrophic acid secreting stomachs. While the responsible agent remains unidentified, it is likely that environmental factors, such as the diet, play a role in the rising incidence of these cancers. Saliva contains high concentrations of nitrite derived from the enterosalivary recirculation of dietary nitrate and its reduction by buccal bacterial. For many years, there has been interest in nitrite as a potential pre-carcinogen for gastric cancer. Acidification of nitrite in the stomach produces nitrosative species, which can form potentially carcinogenic N-nitroso compounds. Antioxidants such as ascorbic acid protect against this nitrosative chemistry by converting the nitrosative species to nitric oxide. However, nitric oxide diffuses rapidly to lipids, where it reacts with oxygen to form further nitrosative species (N₂O₃). Using gas chromatography – ion trap tandem mass spectrometry (GC-MS/MS), we have investigated the effect of lipid on the formation of N-nitroso compounds from nitrite in a model of the human stomach. While we successfully demonstrated the inhibitory effect of ascorbic acid on N-nitrosation in a single-phase system, N-nitrosation was not inhibited by ascorbic acid in presence of 10% lipid. These results indicate that the presence of lipid can markedly alter the protective effects of antioxidants with respect to potentially carcinogenic nitrosative chemistry occurring in the human stomach, and illustrate how diet can influence gastric biochemistry.