{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,27]],"date-time":"2025-09-27T01:13:16Z","timestamp":1758935596597},"reference-count":62,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2018,3,12]],"date-time":"2018-03-12T00:00:00Z","timestamp":1520812800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Humans and <jats:styled-content style=\"fixed-case\"><jats:italic>Helicobacter pylori<\/jats:italic><\/jats:styled-content> have evolved and adapted over tens of thousands of years. Yet peptic ulcer disease appeared to be rare prior to the 19th century. The prevalence of peptic ulcer disease increased between 1850 and 1900 and culminated in a cohort at high risk that was born at the end of the 19th century. This coincided with the provision of safe water and improvements in sanitation and personal hygiene. One hypothesis for the emergence of peptic ulcer disease focuses on the rate of development of atrophic gastritis induced by <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u00a0pylori<\/jats:italic><\/jats:styled-content>. The hypothesis developed in this article focuses on delay in the age of acquisition of <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u00a0pylori<\/jats:italic><\/jats:styled-content> to a time when immune and inflammatory responses to the infection were more mature. Whereas the acquisition of <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u00a0pylori<\/jats:italic><\/jats:styled-content> in infancy usually resulted in mild pangastritis, hypochlorhydria, and a low risk for peptic ulcer disease, delayed acquisition could cause either more severe pangastritis (predisposing to gastric ulceration) or gastritis largely restricted to the antrum of the stomach (predisposing to duodenal ulceration). The decline in the prevalence of peptic ulcer disease over the past 100\u00a0years parallels the decline in the prevalence of <jats:styled-content style=\"fixed-case\"><jats:italic>H.\u00a0pylori<\/jats:italic><\/jats:styled-content>. The epidemic of ulcer disease in the first half of the 20th century seems likely to be an adverse effect of important public health measures undertaken in the latter half of the 19th century.<\/jats:p>","DOI":"10.1111\/jgh.14090","type":"journal-article","created":{"date-parts":[[2018,1,10]],"date-time":"2018-01-10T16:53:47Z","timestamp":1515603227000},"page":"1321-1326","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Rise and fall of peptic ulceration: A disease of civilization?"],"prefix":"10.1111","volume":"33","author":[{"given":"Ian C","family":"Roberts\u2010Thomson","sequence":"first","affiliation":[{"name":"University of Adelaide  Adelaide South Australia Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2018,3,12]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(00)70433-8"},{"key":"e_1_2_10_3_1","unstructured":"MoynihanBGA.Duodenal ulcer. 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