Testing for and treating H. pylori for gastroesophageal disease is now the mainstream standard of care. However, study results show two sides of H. pylori; it is both protective and harmful. Let’s look for further evidence to sort this out.

H. pylori protects against some G.I. cancers

A study[1] reported in 1998 showed that certain H. pylori strain to contain the “Cag-A protein” to protect from stomach acid diseases. That’s because these strains can lower stomach acidity (i.e. raise pH) and were found to prevent Gastroesophageal Reflux Disease (GERD), Barrett's esophagus (pre-cancerous changes), and esophageal cancer. Other reports corroborated this fact, demonstrating a protective role for H. pylori in GERD (gastroesophageal reflux disease).[2]

Moreover, in 2005 researchers reported[3] that it was the absence, not the presence of H. pylori that increased the risk of developing esophageal cancer. Of 128,992 patients who were followed up with nearly 40 years later, 52 developed esophageal adenocarcinoma. Researchers matched control subjects according to age, gender, and race; then they compared alcohol consumption, body mass index (BMI), cigarette smoking, education level, and blood tests for H. pylori IgG antibodies and H. pylori Cag-A protein. The researchers concluded that being overweight and cigarette smoking were strong independent risk factors for esophageal adenocarcinoma—but the presence of H. pylori infection markedly decreased that cancer risk.

Interesting, huh? Here is ample evidence that the absence (not the presence) of H. pylori in the stomach leads to cancers of the esophagus!

H. pylori may cause some G.I. cancers

Although H. pylori seems to prevent acid reflux-associated diseases of the stomach and esophagus, the risk of developing stomach cancer via H. pylori infection outweighs the benefits of H. pylori infection.[4] In a 2017 report,[5] Japanese researchers intricately described the mechanism by which H. pylori apparently directly causes stomach cancer, concluding that “Chronic infection with Helicobacter pylori cag-A positive strains is the strongest risk factor of gastric cancer.”

While this intense examination of H. pylori virulence factors is valuable, how should we look upon H. pylori infection now in light of the fact that H. pylori infection is extremely common; plus, few colonized persons ever develop cancer?

I see a big need for research to include other risk factors for stomach cancer along with testing for H. pylori with cag-A protein. For example, environment (diet and lifestyle), genetics, and other confounding factors appear to be omitted in these analyses.

In fact, we could look at populations where stomach cancer is rare and yet also have heavy H. pylori infection rates. For example, Indians rarely develop this cancer. Their incidence of stomach cancer is almost negligible, at about 3 per 100, 000 people[6] while in Japan, it is the most common of all cancers with an incidence almost 10 times higher than in the United States.

H. pylori a cause of halitosis?

A 2016 meta-analysis[7] of the data on this subject shows us that H. pylori probably does play a significant role in bad breath. The authors looked at 115 articles, 21 of which met their inclusion criteria. As I understand their analysis, they found that among H. pylori-infected individuals, the rate of halitosis was four times more than those without it (Odds Ratio 4.03, P=0.009). Also, among halitosis patients, H. pylori infection was found to be nearly three times more than in those without H. pylori infection (Odds Ratio 2.85, P=0.004). Also, the relative risk of having persistent halitosis after successful H pylori eradication in people with H pylori infection was only 17% (P <0.0001), compared to patients without successful H. pylori eradication. The authors concluded, “There is clear evidence that H pylori infection correlates with halitosis. H pylori infection might be important in the pathophysiological mechanism of halitosis, and H pylori eradication therapy may be helpful in those patients with refractory halitosis.”

To put things into better perspective, the authors of a more recent analysis[8] in 2017 tell us that in previous studies on this subject, “…the role of oral factors (oral hygiene and bacterial counts, and decayed, missing, or filled teeth, or DMFT) as the most important cause of halitosis has been neglected.” These researchers analyzed 100 patients with dyspepsia and H. pylori – positive antibody tests. They found a “direct and significant relationship” between halitosis with oral factors—more so than with H. pylori and halitosis. They concluded, “…we cannot attribute halitosis in patients with H. pylori infection to the presence of this microorganism with certainty.”

In summary, the full story on whether H. pylori is the villain or simply guilty by association is still not conclusive.

Michael Cutler, M.D.

[1] Chow WH, Blaser MJ, et al. An Inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res. 1998;58:588–590. https://www.ncbi.nlm.nih.gov/pubmed/9485003

[2] Warburton-Timms VJ, Charlett A, Valori RM, Uff JS, Shepherd NA, Barr H, McNulty CA. The significance of cagA (+) Helicobacter pylori in reflux oesophagitis. Gut. 2001;49:341–346. https://www.ncbi.nlm.nih.gov/pubmed/11511554

[3] de Martel C, Llosa AE, Farr SM, Friedman GD, Vogelman JH, Orentreich N, Corley DA, Parsonnet J. Helicobacter pylori infection and the risk of development of esophageal adenocarcinoma. J Infect Dis. 2005;191:761–767. https://www.ncbi.nlm.nih.gov/pubmed/15688293

[4] Graham DY. Helicobacter pylori, GERD, NSAIDs, and cancer: where we really stand. Am J Gastroenterol. 1999;94:1420–1421. https://www.ncbi.nlm.nih.gov/pubmed/10235238

[5] Structure and function of Helicobacter pylori CagA, the first-identified bacterial protein involved in human cancer. Proc Jpn Acad Ser B Phys Biol Sci. 2017;93(4):196-219. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489429/

[6] Pavithran K, Doval DC, Pandey KK. Gastric cancer in India. Gastric Cancer. 2002;5:240–243. https://www.ncbi.nlm.nih.gov/pubmed/12491084

[7] Dou W, Li J, Xu L, Zhu J, Hu K, Sui Z, Wang J, Xu L, Wang S, Yin G. Halitosis and helicobacter pylori infection: A meta-analysis. Medicine (Baltimore). 2016 Sep;95(39):e4223. https://www.ncbi.nlm.nih.gov/pubmed/27684792

[8] Anbari F, Ashouri Moghaddam A, Sabeti E, Khodabakhshi A. Halitosis: Helicobacter pylori or oral factors. Helicobacter. 2018 Nov 15:e12556. https://www.ncbi.nlm.nih.gov/pubmed/?term=30440100