Benefits
Digestive and GI mucosal protection (DGL form)
Deglycyrrhizinated licorice (DGL) is the form used in almost all of the human digestive research, because taking most of the glycyrrhizin out removes the blood pressure and potassium effects. Three randomized placebo-controlled trials all tested the same branded extract: 75 mg twice daily for 30 days lowered symptom scores in 50 people with functional dyspepsia; 200 people with reflux symptoms reported earlier relief of heartburn and regurgitation over 28 days; and 150 mg daily for 60 days lowered Helicobacter pylori load on breath and stool testing in 107 people. No other research group has repeated any of them, and none measured ulcer healing. The older ulcer literature is mixed: a 1982 single-blind trial found a tablet combining DGL with antacids healed gastric ulcers at about the same rate as cimetidine, while a 1973 double-blind crossover trial of that same tablet found no healing effect at all.
Cortisol enzyme blockade: the reason for the blood pressure warnings
Glycyrrhizin blocks 11-beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the enzyme that switches cortisol off in the kidney. Blocking it leaves more active cortisol in those tissues, and that is the direct cause of licorice's sodium retention, potassium loss and rise in blood pressure. It is not an adrenal tonic. A systematic review of 58 studies found no evidence that adrenal fatigue exists as a medical condition, and the one controlled study in Addison's disease gave licorice alongside prescription cortisone acetate and reported the result as an interaction for patients and doctors to watch, not as a treatment.
Glycyrrhizin and viruses: mostly laboratory work
Glycyrrhizin slows the replication of several viruses in cell culture, including influenza and herpes viruses. That is laboratory work. The one randomized trial of swallowed licorice in an actual viral illness, in 60 hospitalized adults given 760 mg three times daily for a week during the COVID-19 pandemic, found no effect on oxygen saturation, temperature, breathing rate, length of stay or survival. The hepatitis research people hear about is a different product entirely: a glycyrrhizin solution given by intravenous infusion in Japanese and European hospitals, where the measured effect was on the liver enzyme ALT rather than on the virus, and where it disappeared as soon as the infusions stopped. Licorice supplements are not a treatment for any infection.
Throat and cough: gargles, lozenges, and one small pastille trial
Most of the human throat evidence is not a swallowed supplement. Patients about to be given a breathing tube for surgery rinsed with licorice solution for 30 to 60 seconds and spat it out, and had less sore throat and coughing afterwards: a 2019 meta-analysis of five such trials in 609 patients calls this route topical and found the incidence of postoperative sore throat roughly halved (risk ratio 0.44, 95 percent CI 0.28 to 0.69). Licorice lozenges sucked before surgery cut postextubation cough from 52 to 24 percent in 100 smokers. Away from the operating theatre there is one small trial: 70 people with chronic cough took a licorice pastille or placebo for two weeks in a randomized double-blind trial in Iran, and cough severity scores were lower in the licorice group at four weeks. That is a single unreplicated trial, and licorice on its own has not been tested against placebo for bronchitis or 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
Single-blind, endoscopically controlled trial in 100 patients with benign gastric ulcer: cimetidine 1 g daily versus Caved-S six tablets daily, healing assessed at 6 and 12 weeks. Caved-S is a combination tablet containing deglycyrrhizinated licorice plus antacids, not DGL on its own. (Morgan AG, McAdam WA, Pacsoo C, Darnborough A. Gut 1982;23:545-51)
100 adults with benign gastric ulcer. Endoscopic assessment at 6 weeks and, if unhealed, again at 12 weeks. Fifty-six patients went on to a year of maintenance dosing.
There was no significant difference between the two regimens: about 63 percent of ulcers healed at 6 weeks and about 91 percent at 12 weeks in both groups. Cimetidine relieved night pain better than Caved-S over the first two weeks (p less than 0.02). Recurrences over the first maintenance year were four in each group of 28. Because there was no placebo arm, the trial shows the two treatments performed similarly, not that either beat no treatment, and the licorice arm was a combination tablet rather than DGL alone. It also predates Helicobacter pylori eradication and proton pump inhibitors, which are how gastric ulcers are treated now.
Placebo-controlled trial of intravenous glycyrrhizin given three or six times per week for 4 weeks to European outpatients with chronic hepatitis C who had not responded, or were unlikely to respond, to interferon. (van Rossum TG, Vulto AG, Hop WC, Schalm SW. Am J Gastroenterol 2001;96:2432-7)
72 treatment courses in European adults with chronic hepatitis C, including a placebo group of 13. Four weeks of treatment and four weeks of follow-up.
Mean ALT fell 26 percent with three infusions a week and 47 percent with six, both significant against placebo, with no significant change in the placebo group. Normal ALT was reached by 10 percent and 20 percent of patients respectively, and the reduction disappeared once treatment stopped. This trial did not measure cirrhosis or liver cancer; those claims come from separate Japanese observational work that is not cited here. ALT is a blood marker rather than a clinical outcome, the route is an intravenous hospital preparation rather than oral licorice, and hepatitis C is now cured in most patients by direct-acting antiviral drugs.