Demographic factors: demographic factors such as age and gender are the risk factors of gastric cancer. The incidence rate and mortality rate of gastric cancer increase with age. In China, the incidence rate of gastric cancer increases significantly after the age of 40 and gradually decreases after reaching the peak. The incidence rate and mortality rate of gastric cancer are higher in men than in women in all countries in the world. 2008 IARC data show that the ratio of men to women with gastric cancer is 1.8:1, and the ratio of men to women is (1.1-2.3):1 in different countries, and the ratio of men to women in regions with high incidence of gastric cancer is also relatively high. In China, the cumulative incidence and mortality rates are about two times higher in men than in women. The trend of high male to low female incidence does not depend on the difference in smoking, but the influence of genetic factors and other exogenous factors (such as differences in sex hormone secretion, dietary habits and behavioral differences, etc.) may lead to gender differences in the distribution of gastric cancer. A large prospective follow-up study in Japan found that a daily salt intake of more than 10 g significantly increased the incidence of gastric cancer, and patients with atrophic gastritis with infection were more significantly associated with gastric cancer. A high-salt diet not only directly damages the gastric mucosa and increases susceptibility to carcinogens, but also contains high amounts of nitrates, which are reduced in the stomach and combined with amines in food to form N-nitroso compounds such as amyl nitrite. An ecological study conducted in 39 groups of people in 24 countries found that the mortality rate of gastric cancer in men and women was significantly associated with sodium and nitrate, and the relationship with sodium was stronger than that with nitrate. 1.Cured, smoked, fried and deep-fried foods. Such foods produce carcinogens such as PAHs and N-nitroso compounds, which have been shown to be closely related to gastric cancer in several studies in Iceland, Japan, Uruguay and ethnic minority areas in China. Bad eating habits. 2. Bad dietary habits can lead to repeated damage and repair of gastric mucosa and reduce the protective effect of gastric mucosa, which can cause cancer in the long term. A Meta-analysis suggests that Chinese people skip breakfast, eat irregularly, eat fast, overeat and eat leftovers are risk factors for stomach cancer. Smoking: Several prospective studies have found that smoking has a dose-response relationship with the risk of gastric cancer, and the risk of gastric cancer increases with the increase in daily smoking volume and duration, and is associated with higher recurrence and mortality of gastric cancer. Alcohol consumption: Ethanol can damage the gastric mucosa, but its effect on gastric cancer is inconclusive, and is related to the type of alcohol and the amount and duration of consumption. Infectious factors: In the 1990s, IARC and WHO classified carcinogenic factors, and Meta-analysis showed that H. pylori infection could increase the risk of gastric cancer by two times. A prospective study found that 2.9% of H. pylori-positive patients eventually progressed to gastric cancer, whereas none of the negative patients developed gastric cancer.12 A pooled analysis of nested case-control studies showed that the incidence of non-cardia gastric cancer was 2.97 times higher in the H. pylori-positive population than in the negative population. Although 2 billion people worldwide are infected with H. pylori, less than 1% of the H. pylori-infected population eventually develop gastric cancer, suggesting that H. pylori infection is not a sufficient condition for gastric carcinogenesis, which is the result of the interaction of bacterial virulence factors with the genetic background and environmental factors associated with the host inflammatory response. A variety of H. pylori virulence factors, such as virulence gene islands (cagA), vacuolar toxin (VacA), partial adhesins and outer membrane protein (OMP), are involved in gastric carcinogenesis. Nevertheless, the Maastricht Consensus Report concluded that there is no specific bacterial virulence factor marker available for clinical use and that H. pylori infection is the most important risk factor for gastric cancer and eradication would be the most promising strategy to reduce the incidence of gastric cancer. Whether H. pylori eradication can reduce gastric cancer mortality, effectively reduce atrophy and intestinal epithelial metaplasia, and whether H. pylori eradication after endoscopic resection of early gastric cancer can prevent heterochronic carcinogenesis are inconsistent and need to be confirmed by further studies. Genetic factors: Epidemiological data suggest that some gastric cancers have a tendency to gather in families, among which hereditary diffuse gastric cancer (about 1%-3% of all gastric cancers) is caused by mutations in the CDH1 gene encoding epithelial calreticulin (E-cadherin), and germline mutation carriers have an 80% chance of developing hereditary infiltrative gastric cancer in their lifetime. Other familial diseases are associated with an increased risk of gastric cancer, such as Lynch syndrome and familial adenomatous polyposis. The genetic factors of sporadic gastric cancer are of greater interest due to the low proportion of hereditary gastric cancers with clear mutations. Recent genome-wide association studies have identified some susceptibility loci for diffuse gastric cancer, pancreatic cancer and gastric body cancer, revealing the complexity of gastric cancer and the existence of genetic heterogeneity among its subtypes, but the specific mechanisms and clinical implications remain to be investigated. The genetic susceptibility of first-degree relatives of patients with sporadic gastric cancer is high. Although it is difficult to change this genetic susceptibility, eradication can eliminate important factors for the development of gastric cancer, thus improving the prevention effect. V. Other factors: Environmental factors such as geology and drinking water may influence the occurrence of gastric cancer through interaction with genetic background H. pylori infection and host immunity. Psychosocial factors (such as mental stimulation or depression) and immune factors may have some association with the occurrence of gastric cancer, but whether they are confirmed risk factors needs further study. The knowledge of the population about gastric cancer prevention and treatment is also an important factor affecting the early diagnosis and treatment of gastric cancer. VI. Protective factors: Fruit and vegetable intake is a protective factor for gastric cancer. A large-scale prospective study found that the risk of gastric cancer was reduced by 44% in the high intake group compared to the low daily fruit and vegetable intake group, and a recent Meta-analysis showed that dietary fiber intake was negatively associated with gastric cancer risk, and consumption of onion and garlic vegetables could also reduce the occurrence of gastric cancer. Meta-analyses on the association between green tea and gastric cancer have not yet reached a favourable conclusion. Some epidemiological studies have found a negative association between vitamin C, carotenoids, vitamin E, and the trace element selenium and the risk of gastric cancer, but the results of randomized controlled trials (RCTs) are not uniform. There is an association between increased use of food refrigeration technologies such as refrigerators and decreased risk of gastric cancer.