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 byin vitroevidence of toxicity of such substances toHelicobacter pylori.The objective of the present study was to establish whether this association is causal. Forty patients with proven infection withH. pyloriand 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 H2antagonist therapy. Efficacy of therapy was determined endoscopically by assessment of ulcer healing whileH. pyloristatus was determined by antral biopsy, urease (EC3.5.1.5) culture and histological assessment of the severity ofH. pyloriinfection. Antral levels of prostaglandin E2(PGE2) and leukotriene B4(LTB4) were quantified. Compliance was monitored. Before treatment, both groups were comparable for severity ofH. pyloriinfection, smoking status and levels of LTB4and PGE2. Despite a significant difference in consumption of linoleic acid (19.9 (se) 1.6) g for PUFA group ν. 6.7 (se0.8) g for controls (P< 0.01) and linolenic acid (2.6 (se) 0.2) g ν. 0.6 (se0.03) g (P< 0.01) there was no significant change in either the severity ofH. pyloriinfection or prostaglandin levels in either group at 6 weeks. Consumption of a considerable amount of PUFA does not inhibit the colonization of the stomach byH. pylorinor does this alter the inflammatory changes characteristic ofH. pylorigastritis. 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.
IsHelicobacter pyloriInfection the Primary Cause of Duodenal Ulceration or a Secondary Factor? A Review of the Evidence