Coronary artery disease associated with Helicobacter pylori infection is at least partially due to inadequate folate status.

The numerous effects of Helicobacter pylori have attracted significant attention. The most consistent and well appreciated effect is peptic ulcer. However, gastric cancer, growth retardation and coronary artery disease are among other sequelae of this chronic infection. This discussion describes a potential relationship among risk of coronary artery disease, the changes caused in gastric juice by H. pylori-induced gastritis, and the bioavailability of folates. Reduced folate absorption can occur in an environment of increased gastric juice pH and/or decreased ascorbic acid. This can, relatively rapidly, result in inadequate folate status which inhibits the methionine synthase reaction. Reduced methionine synthase activity increases the blood concentration of homocyst(e)ine which is known to be toxic to endothelial cells, and an independent risk factor for atherosclerosis. Decreased folate bioavailability may help explain the increased risk of coronary artery disease which has been observed in populations infected with H. pylori. It would also be consistent with the increased occurrence of this association in lower socioeconomic groups, and may also help explain the low incidence of gastric cancer in Africa, despite the high prevalence of H. pylori infection.