Gastritis

References & Evidence Notes

Each numbered entry below is either a source you can follow or a note setting out what the evidence does and does not support. Both are numbered together so the markers in the text line up.

Last reviewed 26 August 2026. Supplement entries are cross-checked against the NIH National Center for Complementary and Integrative Health and the Linus Pauling Institute Micronutrient Information Center.⁸ The single most useful thing on this page is this: if you have persistent indigestion, get tested for Helicobacter pylori. It is a treatable bacterial infection, it is the leading modifiable cause of stomach cancer, and clearing it removes that risk factor. Eradication means a course of antibiotics with acid suppression, prescribed and confirmed afterwards with a test of cure. Nothing on this page eradicates it, and the supplements here earn their place by supporting the stomach lining alongside that treatment, never in place of it. Some symptoms mean endoscopy rather than any diet: vomiting blood or coffee-ground material, black tarry stools, difficulty swallowing, unintentional weight loss, persistent vomiting, anaemia, or new indigestion starting in later life. Those need assessment now, not a trial of something gentle first.

1. On H. pylori and cancer risk: the International Agency for Research on Cancer classifies Helicobacter pylori as a Group 1 carcinogen, the same certainty category as tobacco smoke. This is a statement about how confident we are that it causes cancer, not about how large the risk is for any individual: most infected people never develop gastric cancer. Infection drives a progression from chronic gastritis through atrophy and intestinal metaplasia, and eradication reduces subsequent gastric cancer risk, with greater benefit the earlier in that sequence it happens. ↩
2. On testing: urea breath test and stool antigen test both detect active infection and are used to confirm eradication. Both require stopping proton pump inhibitors for around two weeks and antibiotics for four beforehand, or they produce false negatives. Serology detects past exposure, cannot distinguish active from resolved infection, and is not used to confirm cure. A test of cure after treatment is standard and frequently skipped, which matters because resistance means a meaningful proportion of first-line courses fail. ↩
3. On endoscopy and alarm features: haematemesis or coffee-ground vomiting, melaena, dysphagia, unintentional weight loss, persistent vomiting, iron deficiency anaemia, a palpable mass, or new-onset dyspepsia in an older adult all warrant endoscopy rather than empirical treatment. Age thresholds differ between guidelines, with current US guidance commonly citing 60. Endoscopy also identifies atrophic gastritis, intestinal metaplasia and dysplasia, which change follow-up. ↩
4. On mastic gum, stated plainly because the stakes are unusual here. Mastic resin has demonstrable activity against H. pylori in laboratory conditions. Translating that into eradication in people has not succeeded. A controlled study by Bebb and colleagues found that mastic gum did not eradicate H. pylori in any participant (J Antimicrob Chemother. 2003;52(3):522–523. PubMed 12888582). A later small study reported eradication in roughly a third of patients on monotherapy at best, well below the rates expected of antibiotic regimens. Claims circulating online of 70 to 80% eradication are not supported by the trial literature. Mastic may still be reasonable for symptom relief and mucosal support, and it is retained here on that basis. It is not an alternative to eradication therapy, and treating it as one leaves a Group 1 carcinogen in place. ↩ ↩
5. On sulforaphane and manuka honey: broccoli sprout sulforaphane has human data showing reduced markers of H. pylori colonisation and gastric inflammation during intake, with effects that diminish after stopping, and it does not clear the infection. Manuka honey inhibits H. pylori in laboratory culture; there is no clinical trial evidence that eating it eradicates the organism. Both are reasonable foods. Neither is treatment. ↩ ↩
6. On the other causes: NSAIDs and aspirin cause gastric mucosal injury by inhibiting prostaglandin-mediated protection, and this is dose-related and often silent until bleeding occurs. Alcohol, bile reflux, severe physiological stress and radiation are other recognised causes. Autoimmune gastritis destroys parietal cells, producing achlorhydria and loss of intrinsic factor, and therefore vitamin B12 deficiency and pernicious anaemia; it also carries increased risk of gastric neuroendocrine tumours and adenocarcinoma, both quantified in a meta-analysis of follow-up studies, PubMed 41398405, so it warrants surveillance and B12 replacement rather than dietary management. ↩
7. On acid suppression and nutrition: long-term proton pump inhibitor use is associated with reduced absorption of vitamin B12, magnesium, iron and calcium, and with an increased risk of enteric infection including C. difficile. These are reasons for periodic review of whether the drug is still needed and for monitoring, not reasons to stop a PPI that is treating something; gastroenterology guidance sets out how that review is done, PubMed 35183361. Stopping abruptly after prolonged use causes rebound acid hypersecretion, which is well described and is why discontinuation is tapered rather than sudden, PubMed 38791497. ↩
8. National Center for Complementary and Integrative Health (NIH), nccih.nih.gov, and the Linus Pauling Institute Micronutrient Information Center, lpi.oregonstate.edu/mic.