Dietary factors are significantly related to the onset, occurrence and prognosis of gastric cancer. Food type, dietary composition, food processing and storage methods are closely related to the occurrence of gastric cancer. 1997 World Cancer Research Fund and the American Institute for Cancer Research have clearly listed nitrite, salt n food, and smoked meat as causes of gastric cancer, and more and more epidemiological data suggest that heavy salt, smoking, kimchi, and improper food processing and preservation lead to increased incidence of gastric cancer. High-fat and high-cholesterol diets Although there are individual reports of an association between cheese and dairy products and gastric cancer, most studies have concluded that high intake of cheese and dairy products has a protective effect. Overall, it is believed that milk is not consistently associated with gastric cancer, with a protective effect in studies from the Far East, and sporadic reports of an association with gastric cancer may be due to the fact that milk often accompanies a Western diet. In addition, the role of different types of fats in the development of gastric cancer varies widely. Polyunsaturated fats protect against the development of gastric cancer and their regular consumption reduces the incidence of gastric cancer, and the protective effect of polyunsaturated fats is independent of the tissue type of the tumor. Polyunsaturated fats are mainly found in sunflower, vegetable oil and certain nut foods. Poor dietary habits, improper food processing, and food storage methods Epidemiological data show that some country- and region-specific dietary habits and processing methods contribute to the occurrence of gastric cancer. The epidemiological data of gastric cancer in rural and urban areas in China show that poor dietary habits are the risk factors of gastric cancer. Preference for hard food, too dry and too thin food, and too hot and too cold food are obviously related to the occurrence of gastric cancer. Poor dietary habits can easily overload the stomach and cause mechanical damage to the gastric mucosa and disruption of gastric juice secretion, leading to the occurrence of chronic gastric disease over time. The chronic gastric disease, especially atrophic gastritis so that the gastric mucosa protection and barrier role is destroyed, for the role of carcinogenic agents to take advantage of the opportunity. Smoked fish, which is often consumed in many countries, is a risk factor for gastric cancer. Recently, some studies in western countries reported that positive carcinogens were found in smoked fish; polycyclic aromatic hydrocarbons are also produced when fish is grilled, which increases the occurrence of gastric cancer. Frequent consumption of boiled food can increase the relative risk of gastric cancer by 4.16 times; case-control studies show that the percentage of those who frequently consume fried food in the gastric cancer case group is 18.61%, while the percentage of those who frequently consume fried food in the control group is only 5.561%, and frequent consumption of fried food can increase the relative risk of gastric cancer by 3.02 times, and its relative risk increases with the increase of consumption frequency. This may be due to the repeated high temperature of the oil used for frying food, which makes certain components of the oil carbonize and become pre-carcinogens or carcinogens. High-salt diet There is a clear association between the lightness of taste and the relative risk of stomach cancer. There is basically no difference between those with moderate taste and those with light taste, while those with heavy salt increase the relative risk of gastric cancer by 191% compared with those with light taste. The role of salt n food on gastric cancer is very large. A case-control study on gastric cancer in Harbin, China showed that the proportion from not eating salt n food was 2.22% and 9.17% in the case group and control group, respectively, while the frequent consumption of salt n food was 33.06% and 15.00%, respectively, which was significantly higher in the case group than in the control group, and the OR value increased significantly with the increase in the frequency of salt n food consumption. An epidemiological survey in an area with high incidence of gastric cancer in Shandong Province also suggested that heavy salt and salt-n foods were risk factors for gastric cancer. The Japanese National Nutrition Survey showed that the mortality rate of gastric cancer was positively correlated with per capita salt consumption, and the relative risk of gastric cancer increased significantly in those who consumed high-salt foods daily. In Henan Province, a rank correlation analysis was conducted between salt sales and adjusted mortality rates of several major malignancies, and it was found that high-salt foods, such as salted meat, alkaline meat, shrimp oil, and fish sauce, had an increased risk of gastric cancer. In a case-control study, the relative risk of salted meat consumption in Shanghai was 4.75, salted fish was 3.14, and shrimp oil in Fuzhou was 1.73. In Changle, Fujian, an area with a high incidence of gastric cancer in China, fish dew, made by soaking and fermentation of miscellaneous fish with large amounts of salt, is consumed with extremely high salt content. However, direct calculation of salt consumption revealed that the amount of salt consumed did not change much despite the fact that the mortality rate of gastric cancer among Japanese people decreased year by year. Crude sea salt contains nitrates. Salted fish and cured meat are rich in amides. Long-term intake of high salt can corrode and damage the gastric mucosa, leading to chronic gastritis. High salt promotes nitrosamines absorption and direct contact and action on the gastric mucosa by repeatedly breaking the gastric mucosal barrier. In animal experiments, salt in combination with N-methyl-N-nitro-N-nitrosoguanidine increased the occurrence of tumors. It can be seen that high salt is mainly a co-carcinogenic factor contributing to the development of gastric cancer. Nitrite, N-nitroso complexes In recent years, much attention has been paid to the carcinogenesis of N-nitroso compounds, and important progress has been made in the research work on the etiology of nitrosamines in gastric cancer. n-Nitroso compounds include two major groups: nitrosamines and nitrosamides. Nitrosamines are formed easily by nitrite at pH 1-4 and amines in the stomach, and can directly induce tumors in the stomach without any metabolic activation. For example, N-methyl-N-nitroso-N-acetyl urea induces up to 100% of gastric adenocarcinoma in rats, and the direct carcinogenic activity of nitrosamides has special significance in the etiology of gastric cancer. Dietary proteins can be nitrosylated to secondary and tertiary amines when high concentrations of nitrite are present in the stomach, and bacteria in a large Italian study and other related studies suggest an association between dietary proteins, especially of animal origin, and gastric cancer, and similarly, a case-control study in Mexico showed an increased risk of gastric cancer with some variation in a high-protein diet and correlated with the tissue type of gastric cancer, with a diffuse gastric cancer risk mildly increased, while intestinal-type gastric cancer was statistically significant. In Shaanxi Jia County, a county with a high incidence of gastric cancer, a survey in 1990 saw that farmers were fed a mixture of flour, mainly sorghum flour, mixed with potato flour and bean flour, which had a significantly higher nitrate content, 7.1 times that of maize flour, 8.2 times that of sorghum rice and 15.2 times that of millet, with a very significant difference (P<0.01)< span="">. Jia County is located in the Loess Plateau, the climate is dry and cold, vegetable consumption time is short, generally 3 to 4 months a year, so the autumn masses of homemade sauerkraut, consumed for more than six months. Locally consumed vegetables qQ grow quickly and for a long time (4-5 months), so they are more commonly consumed by farmers, and their nitrate and nitrite contents were determined to be significantly higher than those of locally consumed beans and tomatoes (P < 0.01). Some case-control studies have shown that the intake of N-nitroso complex precursors is also associated with the development of gastric cancer. Moldy foods The decline in gastric cancer in the United States in recent decades is thought to be related to the promotion of refrigerators, fresh food storage, and a reduction in moldy foods. The National Comprehensive Stomach Cancer Study Group observed that the level of gastric cancer deaths at each IMC site was positively correlated with the consumption of moldy food. According to the external environmental fungal survey at each high incidence site, it was found that fungal contamination of grain was common at each site. From the fungus isolated from the gastric juice of patients with chronic gastric disease, it was also found that there can be toxic-producing species such as Aspergillus heterocystis, Aspergillus oryzae, Aspergillus flavus and Fusarium. In addition, in the absence of gastric acid, the total number of bacteria in the gastric juice and nitrate reductase positive bacteria are increased. Preliminary consideration of Aspergillus or its metabolites and the synergistic effect of bacteria and nitrogen may be one of the causes of gastric cancer, pending further study. Fujian Changle male gastric cancer adjusted mortality rate of 120.47/100,000, ranking first in the country, and is still on the rise. Local mold-prone days are long, grain mold is quite common, and the study found that with the increased intake of moldy food, the risk of gastric cancer increases, in a dose-effect relationship. High incidence points in Gansu Wuwei, Shaanxi Jia County residents commonly consume sauerkraut, by which toxic fungi were also detected. China's gastric cancer comprehensive study group reported that the high incidence of gastric cancer area grain mold is more common, chronic gastric disease patients with gastric fluid detection of toxic fungi Aspergillus oryzae accounted for the first, and the severity of gastric mucosal lesions and gastric fluid NO2-content is significantly related to the detection rate is significantly higher than in low incidence areas. Animal experiments have demonstrated that Aspergillus or aflatoxin can induce adenogastric cancer in rats, and certain fungi can produce carcinogenic mycotoxins under suitable conditions and can promote the synthesis of N-nitroso compounds. Fungi may play a role in the development of gastric cancer. Alcohol, tobacco and other factors For many years, tobacco and alcohol have been considered as the causes of gastric cancer. meta-analysis shows that smokers increase the risk of gastric cancer by 50%-60% compared with nonsmokers, and some studies point out that smoking smokeless tobacco can cause more carcinogenic nitrosamines than smoked tobacco, and an epidemiological survey in a high incidence area of gastric cancer in Shandong Province in China also suggests that smoking is a risk factor for gastric cancer. et al. reported a Swedish case-control study on the relationship between smoking, alcohol consumption, and gastric cancer, and found that any type of smoking increased the risk of all three types of gastric cancer, with diffuse gastric cancer being the highest and gastric cardia cancer the lowest. There was no significant difference between quitters (≥2 years) and never smokers, while there was a significant difference between cardia-type and diffuse gastric cancer and smokers. There was a significant dose-dependent relationship between the risk of developing gastric cancer and the amount of smoking. Smoking ≥15 cigarettes/d increased the risk of these three types of gastric cancer by twofold or more. The study showed no effect of beer and hard liquor on these three types of gastric cancer. Other studies on alcohol consumption and gastric cancer have come to different conclusions, with Kato et al. suggesting that alcohol is not associated with intestinal and diffuse gastric cancer, while Jedrychowski et al. reported that vodka increased the risk of both types of gastric cancer. The relationship between alcohol and gastric cancer awaits the conclusion of further epidemiological studies and case-control studies. The mechanism by which tobacco causes gastric cancer is unknown. It is believed that tobacco-specific nitrosamines, nitroso complexes and other carcinogens swallowed during smoking are involved in the process of gastric cancer formation. Smokers have higher levels of DNA synthesis. A Chinese study showed that smoking increases intestinal chemosis and atypical hyperplasia in chronic atrophic gastritis. Paper cigarette smoke contains oxidants and free radicals that deplete protective antioxidants such as ascorbic acid and carotenoids, and Buiatti detected lower levels of certain antioxidants in the blood of smokers compared to nonsmokers. It is further assumed that the risk factors for gastric cancer from smoking can be neutralized by antioxidants in food, and in fact, several studies, including Hansson et al, have shown that fresh vegetables and fruits can counteract the gastric cancer risk of tobacco. Alcoholic beverages and tobacco smoke can contain carcinogens such as PAH and NOC, in addition to affecting the in vivo metabolism of NOC and other carcinogens, and promoting NOC synthesis. At the same time, they are gastric mucosa irritants and have cancer-promoting effects in animal experiments.