50% Globally Infected

Globally, more than 50% of all people are infected [8], with the prevalence of escalating with age. [9]

Helicobacter Pylori is a gram-negative bacterium that colonises within the human gastrointestinal tract (this includes the mouth).


  • Belching
  • Nausea
  • Vomiting
  • Difficulty swallowing
  • Abdominal discomfort
  • Upper abdominal bloating
  • Decreased appetite
  • Peptic ulcers
  • Bad breath
  • Heartburn
  • Reoccurring oral plaque
  • Gingivitis
  • Tooth cavities

H. Pylori infection is the main cause of chronic gastritis, with an infection rate between 80%-95% in sufferers. [7]

It is present in almost all cases of duodenal ulcers and most cases of gastric ulcer [10] with as many as 90% of individuals with ulcers being infected.

H. Pylori is a significant contributing factor for the risk of gastric cancers.

H. Pylori burrows deep within parietal cells (cells that secrete stomach acid), not only does this make it harder to eradicate, but this also leads to unique symptoms within the host. One factor being hypochlorhydria (low levels of stomach acid secreted within the body); this prevents the host from sterilising bacteria in food, reduces the ability to obtain nutrients desired from food and the inability to assimilate certain key minerals, such as zinc or iron.

Reduced intrinsic factor (IF) production is also likely for individuals suffering from a H. Pylori infection. IF is essential to bind with vitamin B12, preventing further breakdown from stomach acid along with attaching to the surface of the ileum to allow for absorption of B12 into the body.

H. Pylori can also block vitamin C absorption, thus compounding to the amount of oxidative damage inflicted onto the body.

H. Pylori infection augments the gastric mucosal damage induced by NSAIDs.

H. Pylori antagonise Aspirin-induced delayed ulcer healing due to suppression of acid secretion by the enhancement of PGE2 possibly derived by COX2 expression.

Due to the nature of the parasite being a gram-negative bacteria, it shifts the immune system more towards a Th1 mediated response as opposed to Th2 – this can reduce the severity of allergies, asthma and other humeral/mucosal reactions.


  1. Morales-Espinosa R, et al., Oral Microbiol Immunol. 2009
  2. Nguyen AM, et al., Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995
  3. Miyabayashi H, et al., Helicobacter. 2000
  4. Gebara EC, et al., J Clin Periodontol. 2006
  5. Dye BA, et al., Am J Public Health. 2002
  6. Eskandari A, et al. Med Oral Patol Oral Cir Bucal.
  7. Abro AH, et al. J Ayub Med Coll Abbottabad. 2011
  8. Saudi J Gastroenterol. 2014
  9. J Gastrointestin Liver Dis. 2011
  10. J Gastroenterol Hepatol. 2011
  11. Surveillance of Helicobacter pylori antibiotic resistance in England and Wales; Public Health England, 2008
  12. Jernberg, C, et al. 2010