H. pylori, Evil Mastermind or Ally? Part 1

H. pylori, Evil Mastermind or Ally? Part 1

Here at Fix Your Gut we have discussed at length about H. pylori.

There is a lot of ongoing research being done to determine H. pylori’s coexistence with humans.

Is it commensal, or severely opportunistic? Is it normal flora?

Jason Hooper and I have both written about it when it becomes opportunistic. H. pylori, like an evil mastermind, knows when the “shields are down” in the stomach (reduced acid and pepsin production,) and proliferates in the stomach and uppergut to cause numerous digestive woes.

But what about when it coexists with our commensal flora? Can it improve our health?

H. pylori and Humans

H. pylori have coexisted with humans for a very long time. At least 60,000 years of coexistence. 1  Our mouth and stomach are a perfect environment for H. pylori to thrive, easily spread from both organs. 2

H. pylori are believed to be spread through saliva exchange, gastric juice exchange, and fecal contact. 3 It is the true “kissing disease.” H. pylori are believed to have evolved the ability to penetrate the mucosal barrier of the stomach. It loves us so much it evolved to coexist with us. 4

H. pylori colonization at this time is at least half the world’s population. It has however seen a decline in virulence in first world countries, since the dawn of proper hygiene and sanitation. 5

What health conditions have also increased during modernization?

The Esophagus / Lungs Paradox

When you think of someone with a H. pylori infection, you think of gastritis and GERD. 6

You would expect to see people with H. pylori to show issues associated with GERD, including Barrett’s Esophagus and even asthma.

The studies mostly show the exact opposite. 7 8 9 10 11

Barrett’s esophagus is an abnormal mutation to the cells in the lower part of the esophagus. Long-term GERD, LERD, bile acid reflux, or vomiting may cause the stratified squamous epithelium cells to be replaced by simple columnar epithelium with goblet cells. The reasoning behind this replacement of cells is that over time pepsin and stomach acid degrade the cells in the esophagus (chronic inflammation) to the point where the body tries to replace them with cells that secrete more mucus to protect the esophagus from further damage. Even though the body is trying to adapt to protect itself from further damage, it comes at a cost. 12

This change in the cells of the esophagus greatly increases the risk of esophageal cancer formation that has a high mortality rate. The tissue change in Barrett’s esophagus will reverse itself usually after the causes of the disease are remedied, and the risk of cancer then becomes reduced over time. 13

So in people with an H. pylori infection you would believe they would have higher rates of Barrett’s esophagus.

“The effect of H. pylori on Barrett’s esophagus varied by geographic location and in the presence of selection and information biases. Only four studies were found without obvious selection and information bias, and these showed a protective effect of H. pylori on Barrett’s esophagus (Relative risk = 0.46 [95% CI: 0.35, 0.60]).” 14

In other words, if you have H. pylori colonization you may have a lot less risk of developing Barrett’s esophagus. But the type of H. pylori infection may play a role in the reduced risk of Barrett’s esophagus, those include:

  • Strain of H. pylori is CagA positive. 15
  • Location of infection. If you have a duodenal H. pylori infection, bile acid reflux may occur, and the risk of Barrett’s esophagus may increase. You also have an increased risk if the antral part of the stomach (bottom of the stomach) is infected or have atrophic gastritis from the infection. 16

What about asthma?

There are numerous studies linking H. pylori and developing asthma and allergies, but studies have shown its proposed benefits rather than drawbacks.

One study states:

“The loss of this ancient, dominant, and persistent member of the normal biota of humans would be predicted to have consequences, and now there is much information about the beneficial and deleterious aspects of this change on the health and disease of the gastrointestinal tract. However, increasing evidence is pointing to extra-intestinal manifestations of the disappearance of H. pylori, including asthma. An inverse association of H. pylori and childhood asthma, allergic rhinitis, and atopy is becoming increasingly obvious.” 17

But what does H. pylori colonization in early childhood do to prevent the development of allergies and asthma?

“Indeed, its absence is associated with the loss of a metabolically active lymphoid compartment in the stomach. This compartment, with both activator and regulatory T cells, could be involved in setting the age-dependent threshold for allergic sensitization to environmental allergens;” 18

It would appear that a diffuse H. pylori colonization in the stomach helps to create robust low-grade mucosa-associated lymphoid tissue (MALT) which is the first line of defense against allergic proteins that we consume.

There is one study, however, that does attempt to shed some doubt on H. pylori’s protection against asthma and allergies. The study is a meta-analysis based on 770 cases and 785 controls. The study did not find a huge link between H. pylori and asthma and allergies. 19

There were issues with the study because they used serological ELISA tests for H. pylori that would show the body’s reaction to a prior infection but not if the H. pylori were flora.

“In this present study, the included studies used a stable serological method, ELISA, as a unique approach for detecting the presence of H. pylori infection. Nevertheless, the serology of H. pylori is not a reliable criteria for detecting its effect on asthma. The serologic tests could not give us any information on current H. pylori infection. Therefore, a number of further investigations using multi-approaches such as immunhistochemistry, polymerase chain reaction and smears for exploring the presence of H. pylori are required. 20

The study even brings up more limitations:

“The present study has several limitations. Firstly, the papers identified in our study were limited to those openly published up to Jul 2012; it is possible that some related published or unpublished studies that might meet the inclusion criteria were missed, resulting in any inevitable bias, though the funnel plots and the Egger’s tests failed to show any significant publication bias. Secondly, the results may be interpreted with care because of the limited number and small sample sizes of each included studies. Thirdly, subgroup analyses regarding other confounding factors such as smoking status, age and gender have not been conducted in the present study because sufficient information could not be extracted from the primary literature.” 21

It appears that colonization may be beneficial when it is a part of normal flora.

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