DGL Licorice: Deglycyrrhizinated Licorice for Gastric Lining and H. Pylori Research

This article is for informational purposes only and does not constitute medical advice. Always consult your gastroenterologist, physician, or healthcare provider before starting any supplement, especially if you have a digestive condition or take medications. Dietary supplements are not evaluated by the FDA and are not intended to diagnose, treat, cure, or prevent any disease.

MercyIowaCityClinics.org is an independent editorial publication and is not affiliated with any hospital, clinic, or medical provider.

MICC Review Team | July 2026

DGL Licorice: Deglycyrrhizinated Licorice for Gastric Lining and H. Pylori Research

Deglycyrrhizination and Gastric Mucosal Protection

DGL (deglycyrrhizinated licorice) is licorice root (Glycyrrhiza glabra) with glycyrrhizin—the compound responsible for systemic mineralocorticoid effects and hypertension—removed through extraction. Research suggests that DGL may protect and promote repair of gastric and duodenal mucosa through enhanced mucus secretion, increased prostaglandin production, and anti-inflammatory effects independent of acid reduction. Additionally, emerging evidence indicates licorice compounds may inhibit H. pylori colonization and bacterial virulence factors, making DGL of interest in integrated H. pylori management protocols.

Biochemistry and Mucosal Protective Mechanisms

DGL contains flavonoids, saponins, and phenolic compounds that stimulate gastric mucus-secreting cells (surface mucous cells) to increase mucus layer thickness, creating a protective barrier against acid and pepsin attack. Simultaneously, these compounds upregulate prostaglandin (particularly PGE1 and PGE2) production in gastric epithelium, which enhances blood flow to the mucosa and stimulates bicarbonate secretion from gastric mucous cells. This dual mechanism—enhanced mucus production plus increased mucosal blood flow and bicarbonate secretion—provides complementary protection compared to acid-suppressing pharmaceuticals alone. Additionally, licorice flavonoids (chalcones, isoflavonoids) possess direct antimicrobial properties against H. pylori through inhibition of bacterial adhesion molecules and virulence factor expression.

Clinical Evidence for Gastric and H. Pylori Applications

Peptic Ulcer Disease and Gastric Ulcer Healing: Multiple RCTs from the 1970s-1990s, primarily from European and Middle Eastern research centers, demonstrated that DGL accelerated gastric ulcer healing rates compared to placebo and achieved outcomes comparable to H2 receptor blockers (cimetidine, ranitidine). A meta-analysis of 5 RCTs found DGL-treated patients achieved 63-68% ulcer healing at 4-6 weeks versus 38-48% in placebo (NNT approximately 3). These results were obtained at doses of 760-1500 mg daily divided into 2-3 doses, taken 15-30 minutes before meals so that DGL could interact with mucosa before food dilution. Evidence Level: Moderate to Strong

NSAID-Induced Gastric Injury Prevention and Management: Small RCTs suggest DGL (1500 mg daily) reduces NSAID-associated gastric erosion risk by 30-50% when co-prescribed with NSAIDs or taken after NSAID-related symptoms develop. However, PPI therapy remains the established standard for NSAID gastroprotection; DGL is not equivalent and should be considered adjunctive rather than replacement therapy. Evidence Level: Preliminary to Moderate

H. Pylori Eradication and Adjunctive Therapy: Emerging in vitro and animal model evidence indicates that licorice compounds inhibit H. pylori adhesion (through targeting blood group antigen mimicry) and reduce virulence factor expression. Small human trials suggest DGL supplementation (750-1500 mg daily) during standard triple-therapy H. pylori eradication (proton pump inhibitor + two antibiotics) may improve eradication rates by 5-10% and reduce GI side effects (diarrhea, nausea) compared to standard therapy alone. However, RCT evidence is limited and heterogeneous; DGL should not replace standard medical H. pylori therapy but may serve as an adjunctive support agent. Evidence Level: Preliminary

Functional Dyspepsia and Post-Prandial Discomfort: Small RCTs in dyspeptic patients found DGL (760-1500 mg daily) reduced upper abdominal discomfort, bloating, and early satiety by 30-40% compared to placebo at 4-6 weeks. Effect size was comparable to some prokinetic agents. Evidence Level: Preliminary to Moderate

GERD and Esophageal Mucosal Injury: Limited evidence exists specifically for DGL in GERD, though the mucosal protective mechanism theoretically applies to esophageal tissue as well. Most clinical observation comes from inclusion of DGL in multi-herb GERD formulations; isolated DGL RCTs are sparse. Evidence Level: Preliminary

Dosing and Pharmacokinetic Considerations

Clinical trial dosing for gastric ulcer and H. pylori support: 760-1500 mg daily, divided into 2-3 doses, taken 15-30 minutes before meals. This timing is critical—DGL must contact the mucosa before food dilution reduces its effectiveness. Standard formulations (tablets, capsules) dissolve readily in the stomach and provide bioavailability. Chewable tablets that dissolve in the mouth (sometimes advocated by herbalists to stimulate salivary mucin production) are an alternative but unproven superior route.

DGL is not absorbed systemically (unlike whole licorice glycyrrhizin, which is absorbed and can cause sodium retention and hypertension). It functions entirely through local GI mucosal mechanisms. This makes DGL free from systemic side effects and safe even in patients with hypertension or cardiac conditions—the primary advantage over whole licorice supplementation.

Forms and Product Standardization

DGL is available as: chewable tablets (750 mg per tablet typical), swallowable capsules (375-750 mg per capsule), and powder (loose or in packets). Products are typically labeled by total DGL content with standardization to minimum 1% flavonoids. Most commercial DGL supplements contain precisely standardized amounts (usually 750 mg or 1500 mg per dose). Unlike many herbal extracts, DGL standardization is relatively consistent across manufacturers. The most studied formulations in clinical trials (Caved-S brand) contained 760 mg per dose; modern products often use 750 mg or 1500 mg equivalents. Third-party testing for purity and potency provides additional assurance.

Drug Interactions and Special Populations

Medications Requiring Gastric pH: DGL enhances gastric bicarbonate and mucus production, subtly raising local pH. This may modestly reduce absorption of pH-dependent medications (iron supplements, bisphosphonates, ketoconazole). Separating DGL and these medications by 1-2 hours is prudent.

Antibiotics for H. Pylori Therapy: No direct pharmacokinetic interaction. However, if DGL is used adjunctively during H. pylori eradication therapy, close monitoring of treatment success via post-therapy urea breath test or stool antigen testing is essential to confirm eradication.

Aspirin and NSAIDs: When co-prescribed, DGL may enhance NSAID gastroprotection, though effects are additive rather than synergistic. This combination requires GI team oversight.

Corticosteroids and Immunosuppression: Licorice compounds have mild immunostimulatory properties. In severely immunocompromised patients (post-transplant, advanced HIV, acute chemotherapy), high-dose DGL supplementation warrants caution, though clinical evidence of significant adverse interaction is lacking.

Blood Pressure and Hypertension Medications: Unlike whole licorice glycyrrhizin (which causes sodium and water retention), DGL has no systemic mineralocorticoid effect and does not raise blood pressure. This is safe even in hypertensive patients—a critical distinction from standard licorice.

Warfarin and Anticoagulants: No direct interaction with warfarin or other anticoagulants. However, licorice's antimicrobial effects may modestly alter gut microbiota vitamin K production; INR monitoring is prudent if starting DGL in anticoagulated patients.

Who Should Consider / Who Should Avoid

Excellent candidates: Peptic ulcer disease (gastric or duodenal ulcer) patients seeking mucosal healing support adjunctive to standard therapy. NSAID users with gastric irritation or ulcer history. H. pylori-positive patients undergoing eradication therapy seeking adjunctive support. Functional dyspepsia with post-prandial discomfort. GERD patients with esophageal mucosal injury seeking complementary support. Hypertensive patients who need ulcer healing support (DGL safe, unlike whole licorice).

Use cautiously or avoid: Severe hypokalemia or electrolyte imbalances (licorice flavonoids may have mild mineralocorticoid-like effects at very high doses, though DGL is much safer than whole licorice). Severe renal disease requiring mineral restriction (consult nephrologist). Medications with narrow therapeutic windows requiring gastric pH for absorption (separate dosing by 1-2 hours). Pregnancy (insufficient safety data; consult obstetrician, though DGL has better safety profile than many alternatives). Estrogen-dependent cancers or hormone-sensitive conditions (licorice may have mild estrogenic activity; consult oncology if applicable).

Clinical Bottom Line

DGL represents one of the best-researched herbal agents for peptic ulcer healing and gastric mucosal protection, with moderate RCT evidence supporting accelerated ulcer healing at 760-1500 mg daily. Emerging data suggest adjunctive value in H. pylori management, though it must not replace standard eradication therapy. Its unique profile—mucosal protective via mucus/prostaglandin enhancement rather than acid suppression—makes it complementary to conventional gastroenterology and potentially useful in patients seeking alternatives or adjunctive support to PPIs and H2 blockers. Critical advantages over whole licorice: no systemic mineralocorticoid effects, hypertension-safe, no sodium retention risk. Proper timing (15-30 minutes before meals) and adequate dosing (≥760 mg daily) are essential for efficacy.

For more information on ulcer management and H. pylori protocols, explore our comprehensive digestive research library and evidence-based ingredient profiles.

This ingredient profile is provided for educational purposes only. It does not constitute medical advice, a treatment recommendation, or a substitute for evaluation by a qualified gastroenterologist, physician, or healthcare provider. Patients with digestive conditions should discuss all supplement use with their GI care team before starting, stopping, or changing any supplement. Individual responses to supplements vary. MercyIowaCityClinics.org is an independent editorial publication and is not affiliated with any hospital, clinic, or medical provider.