Updated: Jul 31
Among trillions of various gut microorganisms, including viruses, bacteria, archaea, and fungi, Helicobacter pylori (HP) is considered one of the cancer-causing bacterial inhabitants that lives in the stomach. There are multiple pathological mechanisms of how HP can contribute to various cancers, such as gastric, esophageal, liver, and pancreatic cancer:
HP infection can damage the gastric mucosal lining, leading to gastritis, peptic ulcers, and duodenal ulcers. This damage can stimulate an immune response, leading to local and systemic chronic inflammation.
HP can neutralize gastric acid that’s needed for proper digestion. This potentially can result in hypochlorhydria or achlorhydria, epithelial atrophy, and dysplasia.
Oncoprotein cytotoxin-associated genes, such as CagA and VacA, are critical virulence factors of HP. HP infections with positive Cag strains are often associated with a highly increased risk of gastric cancers by increasing the accumulation of inflammatory cytokines, which, as a result, upregulates the activity of oncogenic pathways and inactivates tumor suppressor pathways.
HP infection can potentially induce methylations on CpG islands of E-cadherin (a cell adhesion molecule) and tumor-suppressor genes, increasing the risk of developing adenocarcinoma in the stomach (Meng et al., 2018).
Besides gastric cancer, research also has shown HP infection is also linked to the following types of cancer:
Esophageal cancer: It’s been observed that the esophageal cancer incidence rate has reduced in populations with HP infection. The assumption made to explain this is that HP reduces stomach acid release, therefore increasing the pH in the gastric tract. However, I don’t believe this is always true, considering a reduction of gastric acid could cause indigestion, causing foods to sit in the stomach longer than they are supposed, which could then cause acid reflux, leading to the corrosion of the esophageal lining.
Liver cancer: It’s been shown that HP bacteria can reach the liver tissue through the bloodstream, as VacA and CagA have been found in liver tissues with hepatocellular carcinoma. Additionally, LPS and other inflammatory cytokines released by HP directly promote the growth of liver cancer.
Pancreatic cancer: The pathogenic compounds HP releases, including ammonia, lipopolysaccharide (LPS), and inflammatory cytokines, can damage the pancreas. LPS from HP has been confirmed to overstimulate KRAS gene mutation, initiating the development of pancreatitis or pancreatic cancer (Meng et al., 2018).
The good news is that there are many preventative measures to reduce HP-related cancer risk, and here are some examples:
At least half of the world's population has HP, but most people are unaware they have it. It’s crucial to screen for HP infection. The available tools include stool tests, blood tests, and breath tests. These conventional and functional test options are widely available and can be ordered by primary care doctors or holistic health practitioners.
Most people with HP don’t present symptoms and may not need to be treated. However, those with symptoms may need to consider implementing natural or antibiotic therapy to eradicate HP infection. HP, in general, is tough to treat nowadays, but it’s at least necessary to apply therapeutic tools to control the bacteria load of HP.
Diet: It’s recommended to avoid excess intake of salty and fatty foods if HP-associated symptoms are present. Certain foods, such as cruciferous vegetables, cranberries, cabbage juice, ginger, and pomegranate juice/peel, can be beneficial as symptom-alleviating agents or treatment options.
Lifestyle: Simple lifestyle changes can drastically reduce these risk cancers risks. Regular exercise, avoiding late-night eating, and eating smaller frequent meals can improve digestion and acid reflux and protect the esophageal lining.
Jenny Noland, MS, CNS, CNGS, CKNS, LDN, MBA
Functional Nutritionist in Eugene, Oregon
Board-Certified Nutrition Specialist
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Meng, C., Bai, C., Brown, T. D., Hood, L. E., & Tian, Q. (2018). Human Gut Microbiota and Gastrointestinal Cancer. Genomics, Proteomics & Bioinformatics, 16(1), 33. https://doi.org/10.1016/J.GPB.2017.06.002