• Steven Sandberg-Lewis, ND

Helicobacter pylori - Friend or (and) Foe?


Ever since the scientific community accepted the discovery by Marshall and Warren in the late 1970s, H. pylori has been met a with a “test and treat” approach. The present doctrine is basically that “the only good H. pylori is a dead H. pylori”. Martin Blaser, Director of the NYU Human Microbiome Program, and his research associates are among those who have studied both the pathological and the health promoting effects of this important organism. Blaser’s recent book - Missing Microbes – is must reading for healthcare professionals. Although it is clear that H. pylori colonization is associated with peptic ulcers, gastric adenocarcinoma and gastric lymphoma (aka maltoma) there is evidence that it also is an “ancient dominion organism”. H. pylori is likely at the commensal center of the gastrobiota – the normal flora of the stomach (1). Research reveals that it has been an inhabitant of the human stomach for nearly 60,000 years. All mammals have a species specific helicobacter and these organisms may be essential for proper maturation of the gut immune system. Research speaks to this organism’s role in prevention of reflux, Barrett’s esophagus (2) and esophageal adenocarcinoma (3); asthma, eczema and rhinitis (4); laryngeal carcinoma (5); celiac disease (6); Crohn’s disease (7) (8) (9) (10) (11) and possibly obesity (12). It may also protect against fatal cardiovascular events (13).


The term pathobiont is described by Janet Chow et al:

Although the mechanisms that mediate pathology remain largely unclear, it appears that genetic defects and/or environmental factors may predispose mammals to immune-mediated diseases triggered by potentially pathogenic symbionts of the microbiota. We have termed this class of microbes `pathobionts', to distinguish them from acquired infectious agents (14).

Therefore H. pylori may be best considered a commensal which can also transform into a pathobiont – a commensal with important immunomodulatory functions, especially in the neonatal and childhood periods of development. The advent of prescription antibiotics in the early 20th century, increases in Cesarean birth and decreases in breastfeeding rates, smaller family sizes, less crowding and improved water and food sanitation have all decreased transmission of H. pylori to children (15). Although no single antibiotic has been shown to eradicate the organism, Blaser suggests that repeated courses of single antibiotics may eradicate H. pylori in mice. While rates of Helicobacter colonization were originally nearly 100%, in the U.S. only 6% of children have H. pylori colonizing the stomach. This may be one of several reasons why the incidence of allergic diseases, reflux and its complications (including esophageal cancer), obesity and certain autoimmune disease have dramatically increased in the latter 20th century (16).

A theory is that altered gut microbiota lead to a "continuous antigenic stimulation" predisposing to autoimmunity. H. pylori colonization may inhibit this stimulation by activating regulatory T cells. Lack of colonization or early eradication of the organism in children may predispose to Crohn’s disease, etc.


H. pylori is not just one organism, but is very diverse in form (17) has several adaptive features for life in the stomach: the enzyme urease to protect itself from acid by creating a cloud of ammonia, a corkscrew-like morphology which allows it to burrow into mucus and “virulence factors” that allow it to interact closely with the host stomach to downregulate parietal cell acid production and many other functions (18). CagA and vacA are the most studied of the virulence genes. I know of only one commercial lab that currently tests for these (19).

CagA+ and vacA+ virulent strains increase the chance of hypochlorhydria and protect against the development of GERD. Helicobacter eradication in patients with pangastritis has been documented to cause reflux esophagitis. Eradication can also lead to recovery of ghrelin secreting cells and raise plasma ghrelin levels, which may predispose to obesity. It is important to consider the presence or absence of these virulence factors when reading the literature.

It is also important to consider the location of a patient’s bacterial gastritis. Pangastritis (inflammation of the entire gastric lining) is associated with hypochlorhydria whereas antral predominant gastritis is associated with hyperacidity. The antrum is the site of G cells which produce the acid stimulating hormone gastrin. The gastric body is the location of parietal cells which produce acid. When the antrum is inflamed, gastrin can be produced and the gastric body can respond with acid production. When pangastritis is present, the parietal cell mass in the gastric body is decreased and therefore less acid can be made in response to gastrin. The most useful H. pylori research will specify both location of the bacterial gastritis and the presence of virulence factors. Risk of gastric cancer is likely related to specific subtypes of H. pylori (20) .

The clinical question to ponder is when to treat and when to give your patient a “high five” to celebrate the protective presence of this ancient dominion organism?


Based on my study of this conundrum over the last two decades I propose considering the following:

1) Strongly consider eradicating H. pylori when it is present in patients with documented gastric or duodenal ulcers or gastric lymphoma (maltoma). This approach significantly reduces ulcer recurrence and cures maltoma in over 80% of cases (21).


2) When considering the risk for gastric adenocarcinoma, the risk is about 1% for patients with H. pylori pangastritis. This is the hypochlorhydric patient presentation and not necessarily the same patient that develops duodenal ulcers. None of this is settled science, but consider these facts when discussing treatment options with your patient. Note: One study showed that early treatment of H. pylori in gastric ulcer patients significantly reduced the risk of gastric cancer more than early treatment of duodenal ulcer (22). This makes sense since gastric ulcer patients may have hypochlorhydria or achlorhydria whereas duodenal ulcer patients are more likely to be hyperchlorhydric.


3) Strongly consider avoiding H. pylori treatment in a patient who does not have the typical diseases associated with this organism. Stool, breath, saliva or serum testing a patient suffering from functional dyspepsia or gastroesophageal reflux for H. pylori status also makes little sense considering the protective effect of this organism against GERD and GERD associated complications.


References


1. Maldonado-Contreras, A. Structure of the human gastric bacterial community in relation to Helicobacter pylori status. ISME J. . Apr 5, 2011, Vol. 4, 574-9.

2. Helicobacter pylori infection and the risks of Barrett's oesophagus: a population-based case-control study. Thrift, AP. 2011, Int J Cancer. , pp. 130(10):2407-16.

3. Esophageal Adenocarcinoma Developing after Eradication of Helicobacter pylori. Abe, Y. 2011, Case Rep Gastroenterol. , pp. 5(2):355-60.

4. Inverse associations of Helicobacter pylori with asthma and allergy. Chen, Y. 2007, Arch Intern Med. , pp. 167(8):821-7.

5. Is there any association between Helicobacter Pylori infection and laryngeal carcinoma? Pirzadeh, A. 2011, Asian Pac J Cancer Prev. , pp. 12(4):897-900.

6. Decreased risk of celiac disease in patients with Helicobacter pylori colonization. Lebwohl, B. 2013, Am J Epidemiol. , pp. 178(12):1721-30.

7. Inflammatory Bowel Diseases: Review of Known Environmental Protective and Risk Factors Involved. vandersloot, KWJ. 2017, Inflamm Bowel Dis., pp. 23(9):1499-1509.

8. Protective effects of Helicobacter pylori for IBD are related to the cagA-positive strain. Lord, AR. 2017, Gut. , pp. pii: gutjnl-2017-313805.

9. Association of Helicobacter pylori and Crohn's Disease Incidence: An Inversion Reaction? Bartels, LE. 2017, Dig Dis Sci. , pp. doi: 10.1007/s10620-017-4561-7.

10. Is There a Link Between H. Pylori and the Epidemiology of Crohn's Disease? Shah, A. 2017, Dig Dis Sci. , pp. doi: 10.1007/s10620-017-4496-z.

11. Does Helicobacter pylori eradication therapy trigger or protect against Crohn's disease? Murad, HA. 2016, Acta Gastroenterol Belg. , pp. 79(3):349-354.

12. Does Helicobacter pylori infection protect against esophageal diseases in Asia? Wu, JC. 2011, Indian J Gastroenterol. , pp. 30(4):149-53.

13. Helicobacter pylori infection, chronic atrophic gastritis and major cardiovascular events: a population-based cohort study. Schöttker, B. 2011, Atherosclerosis. , pp. 220(2):569-74.

14. Pathobionts of the Gastrointestinal Microbiota and Inflammatory Disease. Chow, J. 2011, Curr Opin Immunol. , pp. 23(4): 473–480.

15. The theory of disappearing microbiota and the epidemics of chronic diseases. Blaser, MJ. 2017, Nat Rev Immunol. , pp. 17(8):461-463. .

16. The Role of Environmental Factors in the Pathogenesis of Inflammatory Bowel Diseases: A Review. Shouval, DS. 2017, JAMA Pediatr. , p. doi: 10.1001/jamapediatrics.2017.

17. Heterogeneity of Helicobacter pylori. Blaser, MJ. 2012, Eur J Gastroenterol Hepatol., pp. Suppl 1:S3-6; discussion S6-7.

18. The Role of CagA in the Gastric Biology of Helicobacter pylori. Backert, S. 2016, Cancer Res. , pp. 76(14):4028-31.

19. Diagnostic solutions. Diagnostic solutions Lab. [Online] June 19, 2015. www.diagnosticsolutionslab.com/gi-map™.

20. Peek, RM Jr. Helicobacter pylori and gastrointestinal tract adenocarcinomas. Nat Rev Cancer. . Jan , 2002, Vol. 2, (1);28-37.

21. Sumida, T. Antibodies to Helicobacter pylori and CagA protein are associated with the response to antibacterial therapy in patients with H. pylori-positive API2-MALT1-negative gastric MALT lymphoma. Cancer Sci. 2009 Jun;100(6):1075-81. . Jun;, 2009, Vol. 100, (6); 1075-81.

*I would like to thank Dickson Thom, DDS, ND for introducing me to the idea of H. pylori as a commensal over a decade ago. We team taught the Gastroenterology course at the National College of Naturopathic Medicine (now National University of Natural Medicine) for many years.

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