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Duodenal ulcer: the helicobacterization of a psychosomatic disease?

The discovery of Helicobacter pylori has revolutionized thinking about the etiology of duodenal ulcer, where it is thought to play a central role in the vast majority of cases. The colonization of the gastric antrum by Helicobacter now explains a number of the principal changes of gastric physiology in patients with duodenal ulcers, especially those related to the secretion of gastrin and acid and their regulation, as well as of serum pepsinogen levels. One principal effect of this discovery has been to trivialize the role of psychosocial factors in ulcer causation, as reflected by a dramatic reduction in the number of published papers on this aspect of the problem in the years following 1983, the year in which the first report of Helicobacter appeared. However, given the widespread occurrence of infection with H. pylori in first and third world country populations, only very small numbers of subjects actually develop duodenal ulcers. The epidemiological, clinical and genetic evidence strongly suggests that host factors, especially the effects of stress (in the broadest psychosocial sense) may be decisive in determining who develops a duodenal ulcer. This therefore seems an appropriate time to devote greater research efforts at better understanding how stress influences the essential stability of the Helicobacter-host interaction to promote the development of duodenal ulcers.