CLARIFICATION OF THE LINK BETWEEN POLYUNSATURATED FATTY-ACIDS AND HELICOBACTER-PYLORI-ASSOCIATED DUODENAL-ULCER DISEASE - A DIETARY INTERVENTION STUDY

Citation
Ae. Duggan et al., CLARIFICATION OF THE LINK BETWEEN POLYUNSATURATED FATTY-ACIDS AND HELICOBACTER-PYLORI-ASSOCIATED DUODENAL-ULCER DISEASE - A DIETARY INTERVENTION STUDY, British Journal of Nutrition, 78(4), 1997, pp. 515-522
Citations number
23
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00071145
Volume
78
Issue
4
Year of publication
1997
Pages
515 - 522
Database
ISI
SICI code
0007-1145(1997)78:4<515:COTLBP>2.0.ZU;2-R
Abstract
Epidemiological evidence has suggested that the declining prevalence o f duodenal ulcer disease may be attributable to rising consumption of polyunsaturated fatty acids, a hypothesis supported by in vitro eviden ce of toxicity of such substances to Helicobacter pylori. The objectiv e of the present study was to establish whether this association is ca usal. Forty patients with proven infection with H. pylori and endoscop ic evidence of past or present duodenal ulcer disease were randomized to receive either polyunsaturated fatty acids (PUFA group), in the for m of capsules and margarine, or a placebo (control). Both groups recei ved concurrent Hz antagonist therapy. Efficacy of therapy was determin ed endoscopically by assessment of ulcer healing while H. pylori statu s was determined by antral biopsy, urease (EC 3.5.1.5) culture and his tological assessment of the severity of H. pylori infection. Antral le vels of prostaglandin E-2 (PGE2) and leukotriene B-4 (LTB4) were quant ified. Compliance was monitored. Before treatment, both groups were co mparable for severity of H. pylori infection, smoking status and level s of LTB4 and PGE(2). Despite a significant difference in consumption of linoleic acid (19.9 (SE 1.6) g for PUFA group v. 6.7 (se 0.8) g for controls (P < 0.01) and linolenic acid (2.6 (SE 0.2) g nu. 0.6 (SE 0. 03) g (P < 0.01) there was no significant change in either the severit y of H. pylori infection or prostaglandin levels in either group at 6 weeks. Consumption of a considerable amount of PUFA does not inhibit t he colonization of the stomach by H. pylori nor does this alter the in flammatory changes characteristic of H. pylori gastritis. We conclude that the association between duodenal ulceration and a low level of di etary PUFA is likely to be spurious, probably reflecting the effect of confounding factors such as affluence, social class or smoking.