In 1982, however, the Helicobacter pylori bug was discovered (Marshall and Warren, Nobel Prize in Physiology & Medicine, 2005). This rapidly blurred the importance of psychological stress as a causative agent in peptic ulcers, and soon the Helicobacter became the single, monocausal explanation of this disease. Yet, in the 1990s several studies re-investigated the stress-ulcers link, including one large longitudinal population report, studies related to family and job difficulties and major societal disasters (cf. Susan Levenstein, BMJ 1998; 316:538–41).
Fascinatingly, in 1995, Barry Marshall, discussing whether or not Koch’s postulates have been fulfilled for H. pylori and peptic ulceration, concluded, quote: “only one of the many steps required for the development of peptic ulceration has so far been fulfilled, i.e. the ability of H. pylori to produce histological gastritis in a susceptible host” (BJ Marshall, Ann Med. 1995; 27:565).
As part of the world health organization’s MONICA study, examined a 10 year follow up of 3379 Danish adults without a history of ulcer diagnosis. Blood samples, psychological status and medical data were gathered from this population in 1982-83 and compared to 1993-94 samples.
At the end of the study, 76 participants were diagnosed as having peptic ulcer. The authors report that, based on a stress index scale, subjects in the highest tertile of stress scores, had significantly higher ulcer incidence. Also, their risk to develop ulcer was doubled, when compared to the lowest tertile patients’ group.
Of note, the risk to develop stress-related ulcer was similar in H. pylori seropositive or seronegative subjects. Exposition to NSAIDs did not influence the risk to develop stress-related ulcer either.
These results provide new evidence that psychological stress can increase the risk of peptic ulcer, independently of the presence of H. pylori or NSAIDs use. This also suggests that treatment of psychological stress may represent a therapeutic tool for peptic ulcers.