Helicobacter pylori prophylaxis

Infections of the human gut with the bacterium Helicobacter pylori, and the fact that it can result in stomach cancer, have only been recognized since the organism’s discovery three decades ago. Since then, clinical trials and basic research on the organism and its close relatives have so thoroughly validated its public health importance that it resulted in a Nobel Prize for the original researchers. Helicobacter pylori is now recognized by the World Health Organization as a Class I human carcinogen. Alongside a dramatically increased awareness of this infectious agent, there is a proliferation of strategies for cures, some real and many imagined, to eradicate H. pylori infection.

Stomach cancer, as well as gastritis, gastric ulcers, and duodenal ulcers (much of which are caused by H. pylori infection), are diseases of both the industrialized and the developing world. Although infection with H. pylori is rapidly declining in Western nations, the prevalence of infection is greater than 90% in much of the developing world and greater than 60% in Japan and S. Korea. Globally, gastric cancer is the second leading cause of cancer mortality, and it is still the leading cause of cancer death in many countries. About half a million new cases of gastric cancer yearly (about 55% of the total number of cases), are directly attributable to infection with H. pylori. Societal costs, not only of these cancers, but of gastric and duodenal ulcer, are enormous.

The development or identification of ways in which to lower the prevalence of H. pylori infection and the consequent risk of cancer is of compelling importance. There are currently no vaccines against this infection and none are expected in the near future. Because of the development of such antibiotics as metronidazole, omeprazole, clarithromycin, and the proton pump inhibitors, effective antibiotic therapies now exist for those who can afford them (e.g. residents of industrialized countries). However, antibiotic therapy of infected individuals in most of the developing world is impractical due to complex economic, social and logistic considerations. There are other problems with antibiotic treatment in that the development of antibiotic resistance is of considerable concern, and eradication rates in many studies is as low as 70%. This bodes ill for a strategy of treating entire populations with antibiotics.

Complete eradication of H. pylori in symptom-free people might not be prudent due to the intriguing, but not yet proven possibilities of adverse side-effects. Additionally, although over half of the world’s population is infected by H. pylori, the vast majority of infected individuals never develop gastric cancer. The concept that a diet-based treatment could reduce levels of H. pylori colonization or virulence, mitigate gastritis, inhibit progression of corpus atrophy, and perhaps eventually delay or prevent development of gastric cancer — without completely eradicating the organism in treated individuals, is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. A number of potential dietary treatments (e.g. Lactobacillus spp., broccoli sprouts, honey, cranberries and garlic) have been suggested in the scientific literature. Scores of other indigenous plants have been used for many centuries by native and traditional healers as cures for syndromes that are likely to involve H. pylori infection.

A question that underlies much of the dietary strategy to reduce the incidence of gastritis, ulcers, or stomach cancer, can be very simply stated as follows: Is it necessary to completely prevent or eradicate infection with H. pylori, or will reducing the level and/or virulence of colonization (of the gastric mucosae), result in a reduced risk of disease or reduced disease severity? Martin Blaser (of New York University) has provided a cogent analysis of this issue and he concludes: “Although further research may show that human beings are better off without their long-time companions H pylori, I maintain that we are at present too ignorant of the diversity of H. pylori strains and their interactions with human beings to advocate their total elimination.”

1. Blaser MJ. (1997) Not all Helicobacter pylori strains are created equal: Should all be eliminated? Lancet 349:1020-22. [Abstract]
2. Blaser MJ, Berg DE. (2001) Helicobacter pylori genetic diversity and risk of human disease. J Clin Invest 107:767-73. [Abstract]
3. Blaser MJ. (2005) An endangered species in the stomach. Sci Amer February:38-45. [Abstract]

If we accept this statement, then we must identify suitable endpoints for interventions designed to reduce damage to the human stomach resulting from infection with H. pylori, without necessarily eradicating the bacterium. Several primary non-invasive endpoints for detecting eradication of infection have been used in recent years, however, the adaptability of such tests to the accurate measurement of a reduction of bacterial levels or bacterial virulence-related genotypes is problematic.

If by following a dietary regimen one can achieve a reduction in indicators of inflammation and of colonization, but not complete resolution of that infection (since complete resolution may be undesirable), then is this dietary strategy not worthy of further development, either by itself or in a combinative approach? I submit that a number of foods may each have a small but measurable effect on the severity of infection and/or the risk of gastritis, ulcers, or stomach cancer, and that it is therefore worthwhile to utilize the available biomarkers of H. pylori colonization in order to evaluate the efficacy of this incremental effect in vivo. This question of course must be considered in the context of rapid development of H. pylori strains resistant to synthetic antibiotics, oppressive poverty in many of the areas with very high prevalence of H. pylori infection, and the huge cost of any long-term pharmaceutical preventive strategy.

Compared with the use of synthetic pharmaceuticals, a dietary approach to prevention can be very inexpensive, and may be the only practical or affordable approach to take in areas underserved by healthcare. If indigenous plants and/or foods can be identified which are effective in preventing or reducing H. pylori infection, these could be introduced in such areas. For example, potent anti-inflammatory activity and rapid uptake by cells and organs has been demonstrated for certain phytochemicals (e.g. sulforaphane from broccoli sprouts). There is also considerable precedent for treating and ameliorating gastritis and digestive disorders with foods (e.g. garlic, honey, Lactobacillus spp.).

Copyright 2014 Jed W. Fahey

Copyright 2014 Jed W. Fahey

Related Publications

Fahey JW, KK Stephenson, AJ Wallace. (2015) Dietary amelioration of Helicobacter infection.  Nutrition Research DOI:http:/dx.doi.org/10.1016/j.nutres.2015.03.001.[Abstract]
Fahey JW, KK Stephenson, KL Wade, P Talalay. (2013) Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates. Biochemical & Biophysical Research Communications 435: 1-7. [Abstract]
Farag, TH, JW Fahey, SS Khalfan and JM Tielsch. (2008) Diet as a factor in unexpectedly low prevalence of Helicobacter pylori infection. Transactions of the Royal Society of Tropical Medicine and Hygiene 102(11): 1164-1165. [Abstract]
Yanaka A, JW Fahey, A Fukumoto, M Nakayama, S Inoue, S Zhang, M Tauchi, H Suzuki, I Hyodo and M Yamamoto. (2009) Dietary sulforaphane-rich broccoli sprouts reduce colonization and attenuate gastritis in Helicobacter pylori-infected mice and humans. Cancer Prevention Research 2(4): 353-360. [Abstract] [Full Article]
Haristoy, X, JW Fahey, I Scholtus and A Lozniewski. (2005) Evaluation of antimicrobial effect of several isothiocyanates on Helicobacter pylori. Planta Medica 71: 326-330. [Abstract]
Fahey, JW, A Munoz, Y Matsuzaki, H Suzuki, P Talalay, M Tauchi, S Zhang, C Hurt and A Yanaka. (2004) Dietary amelioration of Helicobacter pylori infection: Design criteria for a clinical trial. Cancer Epidemiol. Biomark. Prevent. 13(10): 1610-1616. [Abstract] [Full Article]
Fahey, JW, X Haristoy, PM Dolan, TW Kensler, I Scholtus , KK Stephenson, P Talalay and A Lozniewski. (2002) Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. Proc. Natl. Acad. Sci. USA 99: 7610-7615. [Abstract] [Full Article]
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