{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T00:46:13Z","timestamp":1791074773175,"version":"4.1.0"},"reference-count":23,"publisher":"Cambridge University Press (CUP)","issue":"4","license":[{"start":{"date-parts":[[2007,3,9]],"date-time":"2007-03-09T00:00:00Z","timestamp":1173398400000},"content-version":"unspecified","delay-in-days":3446,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Br J Nutr"],"published-print":{"date-parts":[[1997,10]]},"abstract":"<jats:p>Epidemiological evidence has suggested that the declining prevalence of duodenal ulcer disease may be attributable to rising consumption of polyunsaturated fatty acids, a hypothesis supported by<jats:italic>in vitro<\/jats:italic>evidence of toxicity of such substances to<jats:italic>Helicobacter pylori.<\/jats:italic>The objective of the present study was to establish whether this association is causal. Forty patients with proven infection with<jats:italic>H. pylori<\/jats:italic>and endoscopic evidence of past or present duodenal ulcer disease were randomized to receive either polyunsaturated fatty acids (PUFA group), in the form of capsules and margarine, or a placebo (control). Both groups received concurrent H<jats:sub>2<\/jats:sub>antagonist therapy. Efficacy of therapy was determined endoscopically by assessment of ulcer healing while<jats:italic>H. pylori<\/jats:italic>status was determined by antral biopsy, urease (<jats:italic>EC<\/jats:italic>3.5.1.5) culture and histological assessment of the severity of<jats:italic>H. pylori<\/jats:italic>infection. Antral levels of prostaglandin E<jats:sub>2<\/jats:sub>(PGE<jats:sub>2<\/jats:sub>) and leukotriene B<jats:sub>4<\/jats:sub>(LTB<jats:sub>4<\/jats:sub>) were quantified. Compliance was monitored. Before treatment, both groups were comparable for severity of<jats:italic>H. pylori<\/jats:italic>infection, smoking status and levels of LTB<jats:sub>4<\/jats:sub>and PGE<jats:sub>2<\/jats:sub>. Despite a significant difference in consumption of linoleic acid (19.9 (<jats:sc>se<\/jats:sc>) 1.6) g for PUFA group \u03bd. 6.7 (<jats:sc>se<\/jats:sc>0.8) g for controls (<jats:italic>P<\/jats:italic>&lt; 0.01) and linolenic acid (2.6 (<jats:sc>se<\/jats:sc>) 0.2) g \u03bd. 0.6 (<jats:sc>se<\/jats:sc>0.03) g (<jats:italic>P<\/jats:italic>&lt; 0.01) there was no significant change in either the severity of<jats:italic>H. pylori<\/jats:italic>infection or prostaglandin levels in either group at 6 weeks. Consumption of a considerable amount of PUFA does not inhibit the colonization of the stomach by<jats:italic>H. pylori<\/jats:italic>nor does this alter the inflammatory changes characteristic of<jats:italic>H. pylori<\/jats:italic>gastritis. We conclude that the association between duodenal ulceration and a low level of dietary PUFA is likely to be spurious, probably reflecting the effect of confounding factors such as affluence, social class or smoking.<\/jats:p>","DOI":"10.1079\/bjn19970171","type":"journal-article","created":{"date-parts":[[2005,6,9]],"date-time":"2005-06-09T07:49:51Z","timestamp":1118303391000},"page":"515-522","source":"Crossref","is-referenced-by-count":19,"title":["Clarification of the link between polyunsaturated fatty acids and<i>Helicobacter pylori<\/i>-associated duodenal ulcer disease: a dietary intervention study"],"prefix":"10.1017","volume":"78","author":[{"given":"A. E.","family":"Duggan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. C.","family":"Atherton","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Cockayne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Balsitis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Evison","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Hale","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. J.","family":"Hawkey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. C.","family":"Spiller","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"56","published-online":{"date-parts":[[2007,3,9]]},"reference":[{"key":"S000711459700158X_ref002","first-page":"1302","article-title":"Lancet","volume":"i","author":"Coggan","year":"1981","journal-title":"20 Years of hospital admissions for peptic ulcer in England and Wales"},{"key":"S000711459700158X_ref013","doi-asserted-by":"crossref","first-page":"856","DOI":"10.1128\/AEM.42.5.856-862.1981","article-title":"Effects of long-chain fatty acids on growth of rumen bacteria","volume":"42","author":"Maczulak","year":"1981","journal-title":"Applied Microbiology"},{"key":"S000711459700158X_ref019","first-page":"1250","article-title":"Surface hydrophobicity of gastric mucosa in peptic ulcer disease","volume":"98","author":"Spychal","year":"1990","journal-title":"Relationship to gastritis and Campylobacter pylori infection"},{"key":"S000711459700158X_ref012","unstructured":"Khulusi S. 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