H. pylori
Helicobacter pylori virulence↓
Also searched as Helicobacter pylori virulence.
This is a testable, treatable cause — not a lifestyle factor. If it is present, it can be found and cleared, and the inflammation clears with it. That is why it sits at the top of the map with the things you can act on.
In depth
A bacterium that colonizes the stomach lining and sustains chronic inflammation there.
What drives it
Bacterial urease increases it.
The enzyme that lets the organism hold a compartment that kills almost everything else. Verbatim, J Ethnopharmacol 2024 S0378874124006950 (Phellodendron chinense; urease enzyme kinetics + RT-qPCR of virulence genes): it ‘induced alterations in bacterial morphology and structure, downregulated the expression of various virulence genes, and inhibited urease enzyme activity.’ independent group (KoreaMed RID 2256470, Korean red ginseng): protopanaxatriol ‘remarkably suppressed H. pylori urease and H+/K+ ATPase’. For scale, doi 10.1128/aac.43.7.1788: of 77 plant-derived foodstuffs screened, green tea extract was the strongest urease inhibitor, IC50 13 ug/mL, catechins the active principle. Scope stated before anyone asks: urease inhibition is a colonization mechanism, not eradication — the same AAC paper says ‘clinical trials with such an antibacterial agent alone have mostly failed to eradicate H. pylori.’ measured negative kept on the record: Saussurea lappa costunolide inhibits growth but ‘had NO inhibitory effect of H. pylori urease activity’. doi 10.1128/aac.43.7.1788:
Bacterial adhesion increases it.
The grip that keeps the organism in place instead of being swept away with the mucus. Verbatim, PMC3307715 (P. freudenreichii JS, single agent): it ‘decreased the adhesion of Helicobacter pylori to Caco-2 intestinal cells when used individually’. independent group, PMID 30806251 (Hericium erinaceus): it ‘inhibited H. pylori adhesion capacity to human gastric epithelial cell line (AGS), even when added at a concentration that affected neither H. pylori nor AGS viability’ — adhesion blockade independent of killing. Third stream, J Ethnopharmacol 2024 S0378874124006950 (Phellodendron chinense, immunofluorescence adhesion assay). Why it is a colonization lever and not an eradication claim, in the literature’s own words: these agents are ‘less likely to generate resistance... since adhesion is a nonlethal function’. PMID 30806251 · PMC3307715
What it drives
It reduces Digestion.
About as close to proof as medicine gets, and it was obtained both ways: experimental ingestion of H. pylori caused gastritis in humans, and eradicating the organism resolved the inflammation (NCBI Bookshelf NBK2445). H. pylori infection causes chronic gastritis which can progress to peptic ulcer, gastric cancer and MALT lymphoma (PMC11558793), and it is a major cause of recurrent peptic ulcer disease. After eradication, ulcer rebleeding is close to abolished — cumulative incidence 0.5% over at least 12 months. PMC11558793
It increases Calms inflammation.
The damage is inflammatory and it does not stop at the stomach lining: chronic H. pylori gastritis drives gastric atrophy and, through the resulting achlorhydria, a dysbiotic gastric microbiome that carries the process toward neoplasia (PMC11558793). In a pivotal trial, eradication after endoscopic removal of early gastric cancer reduced metachronous gastric cancer versus placebo; in an earlier cohort, no second cancer occurred in the eradicated group against 9% in the non-eradicated group over five years. PMC11558793
It reduces Gut barrier.
10.1016/j.nbd.2024.106458 — https://www.merckmanuals.com/professional/gastrointestinal-disorders/gastritis-and-peptic-ulcer-disease/helicobacter-pylori-infection — The aging outcome lists the thirteen hallmarks themselves, each mapped to its pathway and labeled with its hallmark number. (from the reviews of this outcome). doi 10.1016/j.nbd.2024.106458
It reduces Stomach contents rising.
10.1007/s10388-018-0637-5 — Drawn from reviews of neighboring outcomes rather than from studies of this outcome itself, which is weaker evidence, and the map marks it so. Verbatim: “When comparing to controls, the network meta-analysis of 6 studies showed that H. pylori infection was associated with a lower risk of GERD (OR=0.68) or be (OR=0.59) or EAC (OR=0.54)”. doi 10.1007/s10388-018-0637-5
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.