Gastric cancer is on the decline with improved hygiene, and some authors now suggest it can prevented in up to 99 percent of cases. Genetic factors, diet, and inflammation of the stomach walls all play a role in the development of this cancer. The inflammation is caused predominantly by Helicobacter pylori (H. pylori) infection. Other bacterial infections and Epstein-Barr viral infections are associated with a minority of cases. According to Reference 1, estimates range from 36 to 99 percent of gastric cancers that are attributed to Helicobacter pylori.
Infection with H. pylori usually occurs in early childhood. The sequence of events leading to gastric cancer is very slow, requiring decades. Only 1 percent of those infected reach the final stage. Reference 1 outlines the process as follows:
1. Infection with Helicobacter pylori.
2. Chronic superficial gastritis, which may have no symptoms, develops in 100 percent.
3. Chronic atrophic gastritis affects 50 percent.
4. Intestinal metaplasia affects 40 percent.
5. Dysplasia develops in 8 percent.
6. Adenocarcinoma develops in 1 percent.
Researchers at the Harvard School of Public Health analyzed the cost-effectiveness of screening for H. pylori infection in two different locations: a high-risk area in China, and the United States, where the risk is much lower. In China, the optimum predicted screening program would be to check everyone at age 20 and treat those who are infected. In the United States, the analysis favors endoscopic screening only for patients with gastric dysplasia.
A paper from Japan warned that for patients with peptic ulcers, eradication of H. pylori does not reduce the risk of gastric cancer. This is consistent with other reports that different strains of H. pylori produce different effects: infections with excess stomach acid production increase the risk of ulcers, while infections with reduced stomach acid production increase the risk of cancer.
Diet may be as important as H. pylori infection, according to Reference 5. This paper lists 38 studies on the relationship between dietary factors and gastric cancer, conducted over the last 25 years. Results are mixed, but generally show a protective effect from diets high in fruits and vegetables.
References:
1. Tepes B, “Can gastric cancer be prevented?”, Journal of Physiology and Pharmacoloty 2009; 60(Supplement 7): 71-77.
2. Yeh JM et al, “Cost-effectiveness of treatment and endoscopic surveillance of precancerous lesions to prevent gastric cancer”, Cancer. 2010 Jun 15; 116(12): 2941-53.
3. Yeh JM et al, “Exploring the cost-effectiveness of Helicobacter pylori screening to prevent gastric cancer in China in anticipation of clinical trial results”, Int J Cancer. 2009 Jan 1; 124(1): 157-66.
4. Mabe K et al, “Does Helicobacter pylori eradication therapy for peptic ulcer prevent gastric cancer?” World J Gastroenterol. 2009 Sep 14; 15(34): 4290-7.
5. Rocco A et al, “Diet, H pylori infection and gastric cancer: Evidence and controversies”, World Journal of Gastroenterology 2007 June 7; 13(21): 2910-2912.
Linda Fugate is a scientist and writer in Austin, Texas. She has a Ph.D. in Physics and an M.S. in Macromolecular Science and Engineering. Her background includes academic and industrial research in materials science. She currently writes song lyrics and health articles.