Exposure 

 

Helicobacter pylori is typically contracted through person-to-person transmission involving contaminated oral or gastrointestinal secretions. 

 

Common transmission routes

 

• Ingestion of food or water contaminated with fecal matter containing H. pylori

• Transmission via saliva, shared utensils, cups, or poor oral hygiene

• Exposure to vomitus or gastric secretions, particularly in household or caregiving settings
   

Hypochlorhydria - Low Stomach Acid

 

Low gastric acid states facilitate more extensive Helicobacter pylori colonisation by reducing one of the stomach’s primary innate defence mechanisms, thereby allowing the organism to persist beyond its usual, and extend into the gastric corpus, a region typically protected by higher acid output. Clinically, corpus colonisation is associated with stomach inflammation (gastritis), parietal cell impairment, and an increased risk of carcinoma. Thus, low stomach acid does not merely permit H. pylori survival, but actively enables broader gastric colonisation.

 

Whereas under normal acidic conditions, most ingested bacteria are rapidly killed or flushed into the intestine; however, when gastric acidity is reduced, H. pylori is less likely to be eliminated during early exposure and can more effectively adhere to the gastric mucosa. [44]

 

Since there are various conditions that lower stomach acid production, eradication and recurrence prevention requires a holistic approach, treating any of the following: 

 

Dysbiosis + Gastric Inflammation 

 

Dysbiosis is characterized by an imbalance in the gastric microbiota with increased populations of bacteria such as Streptococcus, Prevotella, and Haemophilus. Dysbiosis, in turn, contributes to chronic low-grade inflammation through the activation of immune pathways leading to the release of inflammatory cytokines such as TNF-alpha, IL-1, IL-6. These cytokines cause mucosal damage and contribute to the destruction of gastric epithelial cells, including parietal cells, affecting their ability to secrete gastric acid. [38]

 

Small Intestinal Bacterial Overgrowth (SIBO)

 

An overgrowth of bacteria in the small intestine, creates a chronic increase in the production of alkaline gases such as ammonia and methane, as a byproduct of metabolism. As alkaline substances these gases have the capacity to neutralise gastric acid, leading to a chronic reduction in acidity. [36][37]

 

High Sugar Intake

 

D-cells in the stomach produce a hormone known as Somatostatin in response to elevated blood sugar levels. Somatostatin works to inhibit stomach acid production by decreasing the release of gastrin, histamine, and directly inhibiting the parietal cells, thus reducing acid secretion.[35]

 

Chronic Stress [ SNS Hyperactivity ] 

 

Moderate levels of stress increase nitric oxide synthesis, and this causes inhibition of gastric acid secretion. [33]

 

Medications 

 

Long-term use of the following medications suppress stomach acid production via their mechanism of action:

 

Proton Pump Inhibitors (PPIs) -  block the gastric proton pump to strongly suppress acid production

 

• Nexium

• Somac

• Losec
   

H₂ Receptor Antagonists - block histamine receptors in the stomach, reducing acid 

 

• Pepzan, Pepcid

• Tazac
   

Antacids – neutralise existing stomach acid to provide quick, short-term relief
 

• Quick-Eze, Rennie

• Mylanta, Gaviscon Dual Action

• Sodium bicarbonate 

 

Autoimmune Gastritis 

 

Autoimmune gastritis is where the body’s immune system attacks the stomach lining, particularly the parietal cells that produce hydrochloric acid. Over time, this immune damage reduces stomach acid levels long-term. [34]

 

Age 

 

Similarly, the elderly show relatively low stomach acidity. According to a report on 1590 patients, the incidence of low stomach acid was 19% in the fifth decade of life and 69% in the eighth decade of life. [32]