How diet, nutrition and physical activity affect stomach cancer risk. In total, we analysed 89 studies from around the world, comprising 17.5 million adults and nearly 77,000 cases of stomach cancer.
The stomach is part of the digestive system, located between the oesophagus and the small intestine. It secretes enzymes and gastric acid to help food digestion, as well as the intrinsic factor necessary for absorption of vitamin B12.
The stomach acts as an interim storage area for chewed food, before it’s sent to the small intestines though muscular contractions. The body of the stomach is lined with a mucous membrane consisting of columnar epithelial cells and glands, surrounded by muscle.
In addition to the findings on diet, nutrition and physical activity outlined above, other established causes of bladder cancer include:
Smoking is a cause of stomach cancer. It is estimated that 11% of cases worldwide are attributable to tobacco use.
Helicobacter pylori infection is a cause of stomach non-cardia cancer. Also, infection with Epstein-Barr virus is under investigation as a contributor to stomach cancer.
Industrial chemical exposure
Occupational exposure to dusty and high-temperature environments – such as woodprocessing and food-machine operators – has been associated with an increased risk of stomach cancer. Other industries including rubber manufacturing, coal mining, metal processing and chromium production have also been associated with an elevated risk of this cancer.
Pathogenesis: how does stomach cancer develop?
The lining of the stomach is exposed to carcinogens present in foods, which are held in the stomach for a period of up to five hours during digestion.
More than 95% of stomach cancers are adenocarcinomas, with primary gastric lymphoma being the second most common malignancy. Pathogenesis and aetiology differ between cardia and non-cardia cancers.
Chronic gastritis, inflammation brought about by a variety of environmental factors and ageing can eventually lead to changes in the characteristics of the stomach mucosal cells. These changes appear to be precursor conditions to the development of non-cardia cancer.
Non-cardia cancers may be either intestinal (well-differentiated) or diffuse (undifferentiated, from mucus-producing cells). Intestinal types commonly undergo a cascade from normal mucosa through chronic gastritis to atrophic gastritis, intestinal dysplasia, and then adenocarcinoma. This progression may take several years. Intestinal types are more common in males and older adults, whereas diffuse types may occur in all age groups with equal sex distribution and show more rapid progression and poorer prognosis.
H. pylori infection is strongly implicated in the aetiology of intestinal non-cardia cancer. Infection appears to interact with dietary factors. One pooled analysis reported an increased stomach cancer risk with H. pylori infection (RR = 2.9), increasing to RR = 5.9 when the analysis was restricted to cases occurring at least 10 years after infection diagnosis. A rare, genetically inherited form of diffuse stomach cancer also exists, which is unrelated to H. pylori infection. Rare hereditary variants contribute to about 1–3 per cent of stomach cancers.
The pathogenesis of cardia cancer is less well established, although it is associated with inflammation of the cardia. There are similarities between cardia cancer and oesophageal adenocarcinoma, which is inversely associated with H. pylori infection and positively with Barrett’s oesophagus. However, evidence for Barrett’s oesophagus as a causal factor in cardia cancer is not conclusive. Cardia cancer may, in some populations, be inversely associated with H. pylori infection, but cardia cancer in the presence of H. pylori infection shows an association with gastric atrophy. A dual aetiology, with some tumours linked to H. pylori infection and some to reflux injury, is emerging.
Inherited mutations of certain genes, particularly the GSTM1-null phenotype, are associated with elevated risk of stomach cancer. Certain polymorphisms of interleukin genes (IL-17 and IL-10) have also been associated with increased risk of stomach cancer, particularly in Asian populations. These polymorphisms may interact with H. pylori infection and smoking to affect cancer risk.
Full references and a summary of the mechanisms underpinning all the findings can be found in the stomach cancer report.
In 2018, World Cancer Research Fund International published Diet, Nutrition, Physical Activity and Cancer: a Global Perspective on behalf of AICR, WCRF and WKOF. This was the third in our series of major reports looking at the many ways in which our diets, and how active we are, affect our cancer risk. You can find out much more about bladder cancer by downloading a pdf of the relevant chapter in the 2018 report. Please note, however, that this webpage may have been updated since the report was published.
Published findings in peer-reviewed journals
Selected findings from this report have been published in peer-reviewed journals. Details of the papers and links to the abstract in PubMed are below:
An update of the WCRF/AICR systematic literature review and meta-analysis on dietary and anthropometric factors and esophageal cancer risk. S Vingeliene, DSM Chan, AR Vieira, E Polemiti, C Stevens, L Abar, D Navarro Rosenblatt, DC Greenwood, T Norat. Ann Oncol. 2017 Oct 1;28(10):2409-2419. Abstract