{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T10:10:50Z","timestamp":1785924650633,"version":"3.56.0"},"reference-count":37,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:p>\n                    Hans Selye in a note to\n                    <jats:italic>Nature<\/jats:italic>\n                    in 1936 initiated the field of stress research by showing that rats exposed to nocuous stimuli responded by way of a \u2018general adaptation syndrome\u2019 (GAS). One of the main features of the GAS was the \u2018formation of acute erosions in the digestive tract, particularly in the stomach, small intestine and appendix\u2019. This provided experimental evidence for the view based on clinical data that gastro-duodenal (peptic) ulcers could be caused by stress. This hypothesis was challenged by Marshall and Warren\u2019s Nobel Prize (2005)-winning discovery of a causal association between\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    and peptic ulcers. However, clinical and experimental studies suggest that stress can cause peptic ulceration in the absence of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    . Predictably, the etiological pendulum of gastric and duodenal ulceration has swung from \u2018all stress\u2019 to \u2018all bacteria\u2019 followed by a sober realization that both factors play a role, separately as well as together. This raises the question as to whether stress and\n                    <jats:italic>H. pylori<\/jats:italic>\n                    interact, and if so, how? Stress has also been implicated in inflammatory bowel disease (IBD) and related disorders; however, there is no proof yet that stress is the primary etiological trigger for IBD. Central dopamine mechanisms seem to be involved in the stress induction of peptic ulceration, whereas activation of the sympathetic nervous system and central and peripheral corticotrophin-releasing factor appears to mediate stress-induced IBD.\n                  <\/jats:p>","DOI":"10.1530\/joe-16-0547","type":"journal-article","created":{"date-parts":[[2016,12,20]],"date-time":"2016-12-20T21:20:22Z","timestamp":1482268822000},"page":"F1-F5","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":14,"title":["Selye\u2019s general adaptation syndrome: stress-induced gastro-duodenal ulceration and inflammatory bowel disease"],"prefix":"10.1530","volume":"232","author":[{"given":"George","family":"Fink","sequence":"first","affiliation":[{"name":"Florey Institute of Neuroscience and Mental HealthUniversity of Melbourne, Parkville, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"2017011318101388000_232.3.F1.1","unstructured":"Beaumont W 1833 Experiments and Observations on the Gastric Juice and the Physiology of Digestion, pp 280. 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