Helicobacter pylori

Licorice is the one H. pylori herb with human trials, and it works as an add-on rather than an antimicrobial. Two randomised trials found that adding licorice to a standard eradication regimen improved eradication rates — one against the standard regimen alone ^{1Reference 1Hajiaghamohammadi et al. · 2016RCTEffect of adding licorice to the standard treatment regimen of Helicobacter pylori — randomised controlled trialView study →}, one comparing licorice with bismuth ^{2Reference 2Momeni et al. · 2014RCTEffect of licorice versus bismuth on eradication of Helicobacter pylori in patients with peptic ulcer disease — randomised controlled trialView study →}. Licorice polysaccharides block H. pylori adhesion to human gastric mucosa in vitro ^{3Reference 3Wittschier et al. · 2009In vitroAqueous extracts and polysaccharides from liquorice roots inhibit adhesion of Helicobacter pylori to human gastric mucosa — in vitroView study →}, so rather than killing the organism it loosens its grip on the epithelium while the antibiotics work.

Licorice separately has a classic antiulcer record — deglycyrrhizinated licorice (DGL) showed endoscopic healing in controlled gastric and duodenal ulcer trials from the late 1960s ^{4,5Reference 4Turpie et al. · 1969Clinical trialClinical trial of deglycyrrhizinized liquorice in gastric ulcer — controlled trialView study →Reference 5D’Imperio et al. · 1978RCTDouble-blind trial in duodenal and gastric ulcers: cimetidine and deglycyrrhizinized liquorice — randomised controlled trialView study →} and reduced aspirin-induced mucosal bleeding ^{6Reference 6Rees et al. · 1979AnimalEffect of deglycyrrhizinated liquorice on gastric mucosal damage by aspirin — animal modelView study →}, via prostaglandin-mediated mucus and cell proliferation.

The eradication trials are small and single-centre. The DGL ulcer trials predate modern methodology and PPIs, and one found DGL ineffective. Preparations are not interchangeable: whole-root licorice at sustained therapeutic doses causes pseudo-aldosteronism — raised blood pressure and potassium loss — which is why DGL exists.

Coptis acts on urease. Epiberberine — one of coptis’s whole-rhizome alkaloids — inhibits H. pylori and reduces host apoptosis and inflammatory damage by down-regulating urease expression, shown in vitro and in a mouse model ^{7Reference 7Wu et al. · 2024In vitroEpiberberine inhibits Helicobacter pylori and reduces host apoptosis and inflammatory damage by down-regulating urease expression — in vitro and mouse modelView study →}. Urease is the bacterium’s central survival adaptation. Whole coptis extract outperforms isolated berberine against H. pylori urease, which suggests the traditional whole-rhizome preparation does something the single famous alkaloid does not.

Coptisine separately alleviates colitis in mice via the TXNIP/NLRP3 inflammasome ^{8Reference 8Li et al. · 2024AnimalCoptisine alleviates colitis through modulating gut microbiota and inhibiting the TXNIP/NLRP3 inflammasome — mouse modelView study →}. There is no human trial for this indication. Like other berberine-containing herbs, coptis is not used in pregnancy or in newborns.

A dedicated in-vitro study found taheebo bark extract active against H. pylori ^{9Reference 9Park et al. · 2006In vitroAntibacterial activity of Tabebuia impetiginosa Martius ex DC (Taheebo) against Helicobacter pylori — in vitroView study →}, part of a broader and well-replicated antibacterial profile driven by the bark’s naphthoquinones — the same chemistry that covers Staphylococcus aureus including MRSA. The work is in vitro only, with no animal infection model and no human data for this indication.

The naphthoquinone lapachol is the source of pau d’arco’s toxicity concerns at higher doses; broad in-dish potency is not evidence of a safe, effective oral dose.

Ashwagandha acts on the inflammation H. pylori provokes rather than on the bacterium. Withaferin A inhibits H. pylori-induced IL-1β production in dendritic cells by regulating NF-κB and NLRP3 inflammasome activation ^{10Reference 10Kim et al. · 2015In vitroWithaferin A inhibits Helicobacter pylori-induced production of IL-1β in dendritic cells by regulating NF-κB and NLRP3 inflammasome activation — in vitroView study →}. Most H. pylori pathology — the gastritis, the atrophy, the long road to malignancy — is driven by the host inflammatory response rather than by the bacterium directly, so damping that response is a rational target.

The evidence is a single in-vitro study in isolated immune cells. There is no evidence ashwagandha affects the infection, the gastritis or any clinical outcome in a person.

The leaf and bark decoction is traditionally used for stomach ulcers alongside mouth ulcers, diarrhoea and colic — a tannin-rich astringent applied to an ulcerated surface. Consistent with the pattern of the astringent barks, but there is no trial and no H. pylori-specific testing. Anacardiaceae family, containing the contact allergen urushiol.