Skip to main content
×
Home
    • Aa
    • Aa

Clarification of the link between polyunsaturated fatty acids and Helicobacter pylori-associated duodenal ulcer disease: a dietary intervention study

  • A. E. Duggan (a1), J. C. Atherton (a1), A. Cockayne (a2), M. Balsitis (a3), S. Evison (a4), T. Hale (a1), C. J. Hawkey (a1) and R. C. Spiller (a1)...
Abstract

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 in vitro evidence of toxicity of such substances to Helicobacter pylori. The objective of the present study was to establish whether this association is causal. Forty patients with proven infection with H. pylori 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 H2 antagonist therapy. Efficacy of therapy was determined endoscopically by assessment of ulcer healing while H. pylori status was determined by antral biopsy, urease (EC 3.5.1.5) culture and histological assessment of the severity of H. pylori infection. Antral levels of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) were quantified. Compliance was monitored. Before treatment, both groups were comparable for severity of H. pylori infection, smoking status and levels of LTB4 and PGE2. Despite a significant difference in consumption of linoleic acid (19.9 (se) 1.6) g for PUFA group ν. 6.7 (se 0.8) g for controls (P < 0.01) and linolenic acid (2.6 (se) 0.2) g ν. 0.6 (se 0.03) g (P < 0.01) there was no significant change in either the severity of H. pylori 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 H. pylori nor does this alter the inflammatory changes characteristic of H. pylori 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.

    • Send article to Kindle

      To send this article to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle.

      Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

      Find out more about the Kindle Personal Document Service.

      Clarification of the link between polyunsaturated fatty acids and Helicobacter pylori-associated duodenal ulcer disease: a dietary intervention study
      Available formats
      ×
      Send article to Dropbox

      To send this article to your Dropbox account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your Dropbox account. Find out more about sending content to Dropbox.

      Clarification of the link between polyunsaturated fatty acids and Helicobacter pylori-associated duodenal ulcer disease: a dietary intervention study
      Available formats
      ×
      Send article to Google Drive

      To send this article to your Google Drive account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your Google Drive account. Find out more about sending content to Google Drive.

      Clarification of the link between polyunsaturated fatty acids and Helicobacter pylori-associated duodenal ulcer disease: a dietary intervention study
      Available formats
      ×
Copyright
References
Hide All
Carriere F., Barrowman J., Verger R. & Laugier R. (1993) Secretion and contribution to lipolysis of gastric and pancreatic lipases during a test meal in humans. Gastroenterology 105, 876888.
Coggan D., Lambert P. & Langman M. J. S. (1981) 20 Years of hospital admissions for peptic ulcer in England and Wales. Lancet i, 13021305.
Fineberg H. & Pearlman L. A. (1981) Surgical treatment of peptic ulcer in the United States. Trends before and after the introduction of cimetidine. Lancet i, 13051307.
Goggan P., Marrero J., Spychal R., Jackson P., Corbishley C. & Northfield T. (1992). Surface hydrophobicity of gastric mucosa in Helicobacter pylori infection: effect of clearance and eradication. Gastroenterology 103, 14861490.
Grant H., Palmer K., Kelly R., Wilson N. & Misiewicz J. (1988) Dietary linoleic acid and prostaglandin secretion. Gastroenterology 94, 955959.
Grant H. W., Palmer K. R., Riermesma R. R. & Oliver M. F. (1990) Duodenal ulcer is associated with low dietary linoleic acid intake. Gut 31, 997998.
Hawkey C. J. (1986) Synthesis of prostaglandins E2 and thromboxane B2 and prostaglandin catabolism in gastritis and gastric ulcer. Gut 27, 14841492.
Hollander D. & Tarnawski A. (1986) Dietary essential fatty acids and decline in peptic ulcer disease – a hypothesis. Gut 27, 239242.
Hollander D., Tarnawski A., Ivey K., DeZeery A., Zipser R., McKenzie W. & McFarland W. (1982) Arachidonic acid protection of rat gastric mucosa against ethanol injury. Journal of Laboratory and Clinical Medicine 100, 296308.
Hunt M., Hillier K. & Jewell R. (1988) Modification of upper gastrointestinal prostaglandin synthesis by dietary fatty acids. Prostaglandins 35, 597608.
Kearney J., Kennedy N. P., Keeling P. W. N., Keating J. J., Grubb L., Kennedy M. & Gibney M. J. (1989) Dietary intakes and adipose tissue levels of linoleic acid in peptic ulcer disease. British Journal of Nutrition 62, 699706.
Khulusi S. (1995) Duodenal ulceration. Pathogenesis and the role of Helicobacter pylori. MD Thesis submitted to the Faculty of Medicine, University of Bristol.
Maczulak A. E., Dehority B. A. & Palmquist D. L. (1981) Effects of long-chain fatty acids on growth of rumen bacteria. Applied Microbiology 42, 856862.
Mauch F., Bode G., Ditschuneit H. & Malfertheiner P. (1993). Demonstration of a phospholipid-rich zone in the human gastric epithelium damaged by Helicobacter pylori. Gastroenterology 105, 16981704.
Miller T. (1983) Protective effects of prostaglandins against gastric mucosal damage: current knowledge and proposed mechanisms. American Journal of Physiology 245, G601G623.
Oliver M. F. (1989) Cigarette smoking, polyunsaturated fats, linoleic acid, and coronary heart disease. Lancet i, 12411242.
Robert A., Nezamis J., Lancaster C. & Hanchar A. (1979) Cytoprotection by prostaglandins in rats. Gastroenterology 77, 433443.
Sonnenberg A., Muller H. & Fabio P. (1985) Birth-cohort analysis of peptic ulcer mortality in Europe. Journal of Chronic Diseases 38, 309317.
Spychal R., Groggan P., Marrero J. M., Saverymuttu S., Yu C., Corbishley C., Maxwell J. & Northfield T. (1990) Surface hydrophobicity of gastric mucosa in peptic ulcer disease. Relationship to gastritis and Campylobacter pylori infection. Gastroenterology 98, 12501254.
Staveren W., Deurenberg P., Katan M., Burema J., de Groot L. & Hoffmans A. (1986) Validity of the fatty acid composition of subcutaneous fat tissue microbiopsies as an estimate of the long term average fatty acid composition of the diet of separate individuals. American Journal of Epidemiology 123, 455463.
Tarnawski A., Hollander D. & Gergely H. (1987) Protection of the gastric mucosa by linoleic acid – a nutrient essential fatty acid. Clinical and Investigative Medicine 3, 132135.
Thompson L., Cockayne A. & Spiller R. C. (1994). Inhibitory effect of polyunsaturated fatty acids on the growth of Helicobacter pylori: a possible explanation of the effect on peptic ulcer. Gut 35, 15571561.
Thompson L., Edwards R., Greenwood D. & Spiller R. C. (1992) Possible mechanisms of alterations in colonic flora by diets high in polyunsaturated fatty acids. In Medical and Environmental Aspects of Anaerobes, pp. 144148 [B. I., Duerden J. S., Brazier S. V., Seddon and W. G. Wade, editors]. Petersfield: Wrightson Biomedical Publishing Ltd.
Recommend this journal

Email your librarian or administrator to recommend adding this journal to your organisation's collection.

British Journal of Nutrition
  • ISSN: 0007-1145
  • EISSN: 1475-2662
  • URL: /core/journals/british-journal-of-nutrition
Please enter your name
Please enter a valid email address
Who would you like to send this to? *
×

Keywords:

Metrics

Full text views

Total number of HTML views: 4
Total number of PDF views: 30 *
Loading metrics...

Abstract views

Total abstract views: 73 *
Loading metrics...

* Views captured on Cambridge Core between September 2016 - 20th October 2017. This data will be updated every 24 hours.