Benefits
Digestive and GI mucosal protection (DGL form)
Deglycyrrhizinated licorice (DGL) is one of the most evidence-based natural treatments for peptic ulcer disease, gastritis, and GERD — protecting gastric mucosa by stimulating mucus production, increasing mucosal cell turnover, and inhibiting H. pylori adhesion. Multiple clinical trials show DGL heals gastric ulcers comparable to antacid and H2-blocker therapy without the side effects of glycyrrhizin.
Adrenal support and cortisol prolongation
Glycyrrhizin inhibits 11-beta-hydroxysteroid dehydrogenase (11β-HSD2) — the enzyme that inactivates cortisol. This prolongs cortisol half-life in tissues, providing an adrenal-supportive effect used therapeutically in adrenal fatigue and Addison's disease protocols. Low-dose glycyrrhizin effectively extends the action of endogenous cortisol.
Antiviral activity
Glycyrrhizin has documented antiviral activity against influenza, herpes viruses (HSV-1, HSV-2, VZV), hepatitis C, and HIV in laboratory and clinical studies. IV glycyrrhizin has been used in Japan for decades as a treatment for chronic hepatitis C. The mechanism involves interference with viral entry, replication, and inflammatory signaling.
Respiratory and anti-inflammatory effects
Licorice root is among the most used herbs for respiratory conditions — reducing mucous membrane inflammation, acting as an expectorant, and soothing irritated airways. Anti-inflammatory mechanisms include NF-κB inhibition, COX-2 suppression, and cortisol potentiation in airways — explaining traditional use for cough, bronchitis, and asthma.
Mechanism of action
11β-HSD2 inhibition and cortisol/aldosterone potentiation
Glycyrrhizin and glycyrrhetinic acid inhibit 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) — the enzyme that converts active cortisol to inactive cortisone in kidney, cardiovascular, and other tissues. Inhibition increases local cortisol activity, producing mineralocorticoid-like effects (sodium retention, potassium excretion, blood pressure elevation) that are both therapeutic (in adrenal insufficiency) and adverse (in excess or prolonged use).
DGL mucus stimulation and cytoprotection
DGL stimulates mucosal protective mechanisms in the GI tract independently of glycyrrhizin — increasing mucus gel layer thickness, stimulating prostaglandin E2 production (cytoprotective in mucosa despite being inflammatory elsewhere), and promoting epithelial cell turnover. These effects repair and protect GI mucosa from acid, NSAID, and H. pylori damage.
NF-κB and inflammatory pathway suppression
Glycyrrhetinic acid inhibits NF-κB, reduces TNF-α and IL-6 production, and suppresses 5-LOX and COX-2 — providing broad anti-inflammatory effects that contribute to GI, respiratory, and systemic anti-inflammatory applications.
Clinical trials
Randomized trial of chewable DGL (380 mg three times daily) vs antacid vs cimetidine in 100 patients with gastric ulcer for 12 weeks. (Glick 1982 — older trial)
100 gastric ulcer patients. 12-week intervention.
DGL produced equivalent ulcer healing rates to antacid and cimetidine (H2 blocker) at 12 weeks by endoscopic assessment. Critical context: this is an older trial. Modern peptic ulcer treatment has been transformed by H. pylori eradication therapy (PPI + amoxicillin + clarithromycin or alternatives) and PPI monotherapy (omeprazole, esomeprazole, pantoprazole) — much more effective than older H2 blockers. DGL retains some niche role for symptomatic relief but is not comparable to modern PUD pharmacotherapy.
Long-term observational and clinical study of IV glycyrrhizin (Stronger Neo-Minophagen C) in chronic hepatitis C patients in Japan. (van Rossum et al. 2001, Aliment Pharmacol Ther — or related Arase 1997 follow-up)
Chronic HCV patients receiving IV glycyrrhizin.
Long-term IV glycyrrhizin reduced liver enzyme levels, slowed progression to cirrhosis, and reduced HCC incidence. Critical context: this is an intravenous pharmaceutical preparation used in Japan for decades — not equivalent to oral licorice supplements. Modern HCV care has been REVOLUTIONIZED by direct-acting antivirals (sofosbuvir/ledipasvir, glecaprevir/pibrentasvir) — 95%+ cure rates within 8-12 weeks. Glycyrrhizin's role is essentially historical.