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Helicobacter pylori – a real pathogen?

Doctors commonly rule out infection by the bacterium Helicobacter pylori (H. pylori) when a patient has stomach pain. It is probably the most widely studied and treated bacterium, and has been named the “prize bug of all time[1]” despite that it is quite controversial. If the vast majority of us have it and remain unaffected by it, why does mainstream medicine call this bacterium a pathogenic infection that must be eradicated? Let me tell you what mainstream doctors don’t have time to mention to patients about H. pylori.

H. pylori prevalence exceeds 50% of the general population

Pain in the epigastric region of the abdomen (below your sternum and above your umbilicus) is by far most likely to emanate from your stomach; in comparison, pancreatitis (which causes similar pain) is quite rare. Stomach pain is also called dyspepsia, heartburn, gastritis, or a stomach acid disorder.

We know that by quickly reversing the acidity of the stomach and correcting offending diet and stress, that such pain usually resolves. Do you ever wonder why doctors so commonly test for H. pylori whenever a patient feels stomach pains? Ever since Barry Marshall and Robin Warren discovered this curved gram-negative bacillus 1982, Helicobacter pylori has become the most studied and yet elusive bacterium of all time. Despite the mainstream adoption of testing for and treating H. pylori, the question remains, is stomach pain caused by H. pylori?

Let’s look at the prevalence of this bacterium. An extensive systematic investigation of stomach disease in China reported[2] H. pylori prevalence of 73.3% by blood testing, and 71.7% by endoscopic biopsy. Subjects tested from Korea,[3] Vietnam,[4] and Turkey[5] revealed an H. pylori prevalence of 50–70% of the population. In people from Eastern Siberia[6] the rate of H. pylori infection exceeded 90%. Several studies of Asian,[7] Indian,[8] African[9] and Iranian[10] children and adolescents showed prevalence rates that ranged from 20% to 84%.

Based on its high prevalence among mostly all asymptomatic individuals, would you even consider H. pylori to be an “infection”?

Associations with gastritis, peptic ulcers, and gastric cancer

Up until 2005 the research on this bug lead to approximately 25,000 scientific publications.[11] It is true that scientists have found an association between the presence of h. pylori bacteria and stomach inflammation (gastritis), ulceration (peptic ulcer disease), and stomach cancer. They have gone so far as to even report that these stomach illnesses are the direct result of “infection” with h. pylori.

Gastritis and peptic ulcer disease have been shown to be decreased in populations after treatment of H. pylori. In addition to treatment with two antibiotics, one proton-pump inhibitor, and bismuth (e.g. Pepto Bismol), the authors recommend, “Public health measures should be targeted to alleviate poor living conditions which will in turn result in decreased transmission and reduction of the reservoir of infection.”[12]

How does this fit with the fact that most of us have H. pylori “infection?”

Stomach cancer is the most serious allegation of H. pylori infection. One large Finnish study[13] followed subjects for 10 years and found a marked decline in stomach cancer incidence after H. pylori eradication, but then a second study[14] from Japan showed that stomach cancer continued to develop at a rate of 0.3% per year—even after H. pylori eradication. As a stomach cancer risk reduction measure, some authors suggest that, “H. pylori eradication for all infected subjects will prevent not only H. pylori related diseases but also the spread of bacterium in [the] future.”[15] The problem here is that I don’t see mention of other risk factors such as inflammatory lifestyle and dietary habits that would be confounding factors before H. pylori could be directly blamed.

The data on H. pylori is a bit confusing

After H. pylori had been intensely studied, researchers went about finding ways to implicate it as the cause of disease. Pathogenic mechanisms were described to fortify the H. pylori story. It was found that only certain H. pylori subtypes were considered dangerous.[16]

Some studies show the possibility that H. pylori is a beneficial bacterium in some humans[17] and that H. pylori even protects against reflux and cancer of the esophagus[18] causing these authors to report, “…our entire approach to the worldwide elimination of this organism, sometimes indiscriminately, will need critical reevaluation.” For example, there is a study that shows that H. pylori may be beneficial to humans: children with H. pylori had fewer cases of diarrhea than children without H. pylori infection in this study.[19]

We know that that most people who test positive for H. pylori are asymptomatic.[20] Consider the fact that my patients who can simply identify the offending trigger (see below) and eliminate it, usually resolve their symptoms. Those triggers are:

  • foods that you know stir up excessive stomach acid: spicy foods, carbonated drinks, coffee, sweet foods on an empty stomach, citrus such as strong orange juice, or possibly cow's milk or excessive bread. I have patients who can simply identify the offending food, eliminate it, and resolve their symptoms

  • eating late at night or under stress

  • prolonged painful emotions or a major stress/illness

I’ve found that H. pylori could be a contributing factor to stomach illnesses, but certainly not the cause.

To healing and feeling good.

Michael Cutler, M.D.


[1] 23 years of the discovery of Helicobacter pylori: is the debate over?. Ann Clin Microbiol Antimicrob. 2005;4:17. Published 2005 Oct 31.

[2] Li Z, Zou D, Ma X, Chen J, Shi X, Gong Y, Man X, et al. Epidemiology of peptic ulcer disease: endoscopic results of the systematic investigation of gastrointestinal disease in China. Am J Gastroenterol. 2010;105:2570–7.

[3] Nam SY, Choi IJ, Ryu KH, Kim BC, Kim CG, Nam BH. Effect of Helicobacter pylori infection and its eradication on reflux esophagitis and reflux symptoms. Am J Gastroenterol. 2010;105:2153–62.

[4] Nguyen TL, Uchida T, Tsukamoto Y, Trinh DT, Ta L, Mai BH, et al.Helicobacter pylori infection and gastroduodenal diseases in Vietnam: a cross-sectional, hospital-based study. BMC Gastroenterol. 2010;10:114.

[5] Ozdil K, Sahin A, Kahraman R, Yuzbasioglu B, Demirdag H, Calhan T, et al. Current prevalence of intestinal metaplasia and Helicobacter pylori infection in dyspeptic adult patients from Turkey. Hepatogastroenterology. 2010;57:1563–6.

[6] Tsukanov VV, Butorin NN, Maady AS, Shtygasheva OV, Amelchugova OS, Tonkikh JL, et al. Helicobacter pylori Infection, Intestinal Metaplasia, and Gastric Cancer Risk in Eastern Siberia. Helicobacter. 2011;16:107–12.

[7] Ozen A, Furman A, Berber M, Karatepe HO, Mutlu N, Saricoban HE, et al. The effect of Helicobacter pylori and economic status on growth parameters and leptin, ghrelin, and insulin-like growth factor (IGF)-I concentrations in children. Helicobacter. 2011;16:55–65.

[8] Thankachan P, Muthayya S, Sierksma A, Eilander A, Thomas T, Duchateau GS, et al. Helicobacter pylori infection does not influence the efficacy of iron and vitamin B(12) fortification in marginally nourished Indian children. Eur J Clin Nutr. 2010;64:1101–7.

[9] Cherian S, Burgner DP, Cook AG, Sanfilippo FM, Forbes DA. Associations between Helicobacter pylori infection, co-morbid infections, gastrointestinal symptoms, and circulating cytokines in African children. Helicobacter. 2010;15:88–97.

[10] Abdollahi A, Morteza A, Khalilzadeh O, Zandieh A, Asgarshirazi M. The role of Helicobacter pylori infection in gastro-oesophageal reflux in Iranian children. Ann Trop Paediatr. 2011;31:53–7.

[11] 23 years of the discovery of Helicobacter pylori: is the debate over?. Ann Clin Microbiol Antimicrob. 2005;4:17. Published 2005 Oct 31.

[12] Goh KL, Chan WK, Shiota S, Yamaoka Y. Epidemiology of Helicobacter pylori infection and public health implications. Helicobacter. 2011;16 Suppl 1(0 1):1-9.

[13] Kosunen TU, Pukkala E, Sarna S, Seppala K, Aromaa A, Knekt P, et al. Gastric cancers in Finnish patients after cure of Helicobacter pylori infection: a cohort study. Int J Cancer. 2011;128:433–9.

[14] Take S, Mizuno M, Ishiki K, Yoshida T, Ohara N, Yokota K, et al. The long-term risk of gastric cancer after the successful eradication of Helicobacter pylori. J Gastroenterol. 2011;46:318–24.

[15] Goh KL, Chan WK, Shiota S, Yamaoka Y. Epidemiology of Helicobacter pylori infection and public health implications. Helicobacter. 2011;16 Suppl 1(0 1):1-9.

[16] Ahmed N, Sechi LA. Helicobacter pylori and gastroduodenal pathology: new threats of the old friend. Ann Clin Microbiol. 2005;4:1. doi: 10.1186/1476-0711-4-1.

[17] Putsep K, Branden CI, Boman HG, Normark S. Antibacterial peptide from H. pylori. Nature. 1999;398:671–672.

[18] Richter JE, Folk GW, Vaezi MF. Helicobacter pylori and gastroesophageal reflux disease: the bug may not be all bad. Am J Gastroenterol. 1999;93:1800–1802.

[19] Rothenbacher D, Blaser MJ, Bode G, Brenner H. Inverse relationship between gastric colonization of Helicobacter pylori and diarrheal illnesses in children: results of a population-based cross-sectional study. J Infect Dis. 2000;182:1446–1449.

[20] Oztürk H, Senocak ME, Uzunalimoğlu B, Hasçelik G, Büyükpamukçu N, Hiçsönmez A. Helicobacter pylori infection in symptomatic and asymptomatic children: a prospective clinical study. Eur J Pediatr Surg. 1996 Oct;6(5):265-9.

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